Lung Cancer

Overview

Literature Analysis

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Tag cloud generated 10 March, 2017 using data from PubMed, MeSH and CancerIndex

Mutated Genes and Abnormal Protein Expression (753)

How to use this data tableClicking on the Gene or Topic will take you to a separate more detailed page. Sort this list by clicking on a column heading e.g. 'Gene' or 'Topic'.

GeneLocationAliasesNotesTopicPapers
SCLC1 3p23-p21 SCCL, SCLC -SCLC1 and Lung Cancer
3000
EGFR 7p12 ERBB, HER1, mENA, ERBB1, PIG61, NISBD2 -EGFR and Lung Cancer
2685
TP53 17p13.1 P53, BCC7, LFS1, TRP53 -TP53 mutations in Lung Cancer
1314
KRAS 12p12.1 NS, NS3, CFC2, KRAS1, KRAS2, RASK2, KI-RAS, C-K-RAS, K-RAS2A, K-RAS2B, K-RAS4A, K-RAS4B -KRAS and Lung Cancer
989
ALK 2p23 CD246, NBLST3 -ALK and Lung Cancer
555
MKI67 10q26.2 KIA, MIB-, MIB-1, PPP1R105 -MKI67 and Lung Cancer
509
ERBB2 17q12 NEU, NGL, HER2, TKR1, CD340, HER-2, MLN 19, HER-2/neu -ERBB2 and Lung Cancer
489
CDKN2A 9p21.3 ARF, MLM, P14, P16, P19, CMM2, INK4, MTS1, TP16, CDK4I, CDKN2, INK4A, MTS-1, P14ARF, P19ARF, P16INK4, P16INK4A, P16-INK4A -CDKN2A and Lung Cancer
453
PTEN 10q23.31 BZS, DEC, CWS1, GLM2, MHAM, TEP1, MMAC1, PTEN1, 10q23del -PTEN and Lung Cancer
404
GSTM1 1p13.3 MU, H-B, GST1, GTH4, GTM1, MU-1, GSTM1-1, GSTM1a-1a, GSTM1b-1b -GSTM1 and Lung Cancer
-Tabacco smoke, GSTM1 Polymorphisms and Suceptability to Lung Cancer
259
EML4 2p21 C2orf2, ELP120, EMAP-4, EMAPL4, ROPP120 -EML4 and Lung Cancer
290
MET 7q31 HGFR, AUTS9, RCCP2, c-Met -C-MET and Lung Cancer
289
CTNNB1 3p22.1 CTNNB, MRD19, armadillo -CTNNB1 and Lung Cancer
260
ROS1 6q22.1 ROS, MCF3, c-ros-1 -ROS1 and Lung Cancer
241
ERCC1 19q13.32 UV20, COFS4, RAD10 -ERCC1 and Lung Cancer
223
CYP1A1 15q24.1 AHH, AHRR, CP11, CYP1, P1-450, P450-C, P450DX -CYP1A1 and Lung Cancer
217
AKT1 14q32.32 AKT, PKB, RAC, CWS6, PRKBA, PKB-ALPHA, RAC-ALPHA -AKT1 and Lung Cancer
204
PROC 2q13-q14 PC, APC, PROC1, THPH3, THPH4 -PROC and Lung Cancer
191
BAX 19q13.33 BCL2L4 -BAX and Lung Cancer
190
BRAF 7q34 NS7, BRAF1, RAFB1, B-RAF1 -BRAF and Lung Cancer
188
CD9 12p13.3 MIC3, MRP-1, BTCC-1, DRAP-27, TSPAN29, TSPAN-29 -CD9 and Lung Cancer
174
KIT 4q12 PBT, SCFR, C-Kit, CD117 -KIT and Lung Cancer
170
CASP3 4q34 CPP32, SCA-1, CPP32B -CASP3 and Lung Cancer
164
TNF 6p21.3 DIF, TNFA, TNFSF2, TNF-alpha -TNF and Lung Cancer
152
CDKN1A 6p21.2 P21, CIP1, SDI1, WAF1, CAP20, CDKN1, MDA-6, p21CIP1 -CDKN1A and Lung Cancer
149
PIK3CA 3q26.3 MCM, CWS5, MCAP, PI3K, CLOVE, MCMTC, p110-alpha -PIK3CA and Lung Cancer
146
KITLG 12q22 SF, MGF, SCF, FPH2, FPHH, KL-1, Kitl, SHEP7 -KITLG and Lung Cancer
143
MTOR 1p36.2 FRAP, FRAP1, FRAP2, RAFT1, RAPT1 -MTOR and Lung Cancer
142
XRCC1 19q13.2 RCC -XRCC1 and Lung Cancer
139
GSTT1 22q11.23 -GSTT1 and Lung Cancer
136
BIRC5 17q25 API4, EPR-1 -Survivin Expression in Non Small Lung Cancer
134
NODAL 10q22.1 HTX5 -NODAL and Lung Cancer
133
PTGS2 1q25.2-q25.3 COX2, COX-2, PHS-2, PGG/HS, PGHS-2, hCox-2, GRIPGHS -PTGS2 (COX2) and Lung Cancer
124
SRC 20q12-q13 ASV, SRC1, c-SRC, p60-Src -SRC and Lung Cancer
123
STAT3 17q21.31 APRF, HIES, ADMIO -STAT3 and Lung Cancer
121
RET 10q11.2 PTC, MTC1, HSCR1, MEN2A, MEN2B, RET51, CDHF12, CDHR16, RET-ELE1 -RET-KIF5B fusion in Adenocarcinoma Lung Cancer
-RET and Lung Cancer
96
RASSF1 3p21.3 123F2, RDA32, NORE2A, RASSF1A, REH3P21 -RASSF1 and Lung Cancer
119
ERCC2 19q13.3 EM9, TTD, XPD, TTD1, COFS2, TFIIH -ERCC2 and Lung Cancer
118
RRM1 11p15.4 R1, RR1, RIR1 -RRM1 and Lung Cancer
115
STK11 19p13.3 PJS, LKB1, hLKB1 -STK11 and Lung Cancer
109
CEACAM5 19q13.2 CEA, CD66e -CEACAM5 and Lung Cancer
106
RB1 13q14.2 RB, pRb, OSRC, pp110, p105-Rb, PPP1R130 -RB1 and Lung Cancer
103
MYC 8q24.21 MRTL, MYCC, c-Myc, bHLHe39 -MYC and Lung Cancer
96
HIF1A 14q23.2 HIF1, MOP1, PASD8, HIF-1A, bHLHe78, HIF-1alpha, HIF1-ALPHA -HIF1A and Lung Cancer
94
KIF5B 10p11.22 KNS, KINH, KNS1, UKHC, HEL-S-61 -KIF5B and Lung Cancer
-RET-KIF5B fusion in Adenocarcinoma Lung Cancer
-KIF5B-ALK Rearrangements in Lung Cancer
40
VEGFA 6p12 VPF, VEGF, MVCD1 -VEGFA and Lung Cancer
88
PCNA 20pter-p12 ATLD2 -PCNA and Lung Cancer
84
TERT 5p15.33 TP2, TRT, CMM9, EST2, TCS1, hTRT, DKCA2, DKCB4, hEST2, PFBMFT1 -TERT and Lung Cancer
73
HGF 7q21.1 SF, HGFB, HPTA, F-TCF, DFNB39 -HGF and Lung Cancer
70
CCND1 11q13.3 BCL1, PRAD1, U21B31, D11S287E -CCND1 and Lung Cancer
70
FTCDNL1 2q33.1 FONG -FONG and Lung Cancer
68
MUC1 1q21 EMA, MCD, PEM, PUM, KL-6, MAM6, MCKD, PEMT, CD227, H23AG, MCKD1, MUC-1, ADMCKD, ADMCKD1, CA 15-3, MUC-1/X, MUC1/ZD, MUC-1/SEC Overexpression
Prognostic
-MUC1 and Lung Cancer
67
CYP2E1 10q26.3 CPE1, CYP2E, P450-J, P450C2E -CYP2E1 and Lung Cancer
64
FOS 14q24.3 p55, AP-1, C-FOS -FOS and Lung Cancer
61
BCL2 18q21.3 Bcl-2, PPP1R50 -BCL2 and Lung Cancer
61
TGFB1 19q13.1 CED, LAP, DPD1, TGFB, TGFbeta -TGFB1 and Lung Cancer
60
BAD 11q13.1 BBC2, BCL2L8 -BAD and Lung Cancer
60
IGF1R 15q26.3 IGFR, CD221, IGFIR, JTK13 -IGF1R and Lung Cancer
60
FGFR1 8p11.23-p11.22 CEK, FLG, HH2, OGD, FLT2, KAL2, BFGFR, CD331, FGFBR, FLT-2, HBGFR, N-SAM, FGFR-1, HRTFDS, bFGF-R-1 -FGFR1 and Lung Cancer
59
OGG1 3p26.2 HMMH, MUTM, OGH1, HOGG1 -OGG1 and Lung Cancer
56
CHRNA5 15q24 LNCR2 -CHRNA5 and Lung Cancer
54
NQO1 16q22.1 DTD, QR1, DHQU, DIA4, NMOR1, NMORI -NQO1 and Lung Cancer
53
XRCC3 14q32.3 CMM6 -XRCC3 and Lung Cancer
53
TGFBR2 3p22 AAT3, FAA3, LDS2, MFS2, RIIC, LDS1B, LDS2B, TAAD2, TGFR-2, TGFbeta-RII -TGFBR2 and Lung Cancer
53
ACHE 7q22 YT, ACEE, ARACHE, N-ACHE -ACHE and Lung Cancer
52
BCL2L1 20q11.21 BCLX, BCL2L, BCLXL, BCLXS, Bcl-X, bcl-xL, bcl-xS, PPP1R52, BCL-XL/S -BCL2L1 and Lung Cancer
52
MIR21 17q23.1 MIRN21, miR-21, miRNA21, hsa-mir-21 -MicroRNA miR-21 and Lung Cancer
51
TTF1 9q34.13 TTF-1, TTF-I -TTF1 and Lung Cancer
50
CCNB1 5q12 CCNB -CCNB1 and Lung Cancer
50
SOX2 3q26.3-q27 ANOP3, MCOPS3 -SOX2 and Lung Cancer
49
NFE2L2 2q31 NRF2 -NFE2L2 and Lung Cancer
46
CALU 7q32.1 -CALU and Lung Cancer
45
ABCG2 4q22 MRX, MXR, ABCP, BCRP, BMDP, MXR1, ABC15, BCRP1, CD338, GOUT1, CDw338, UAQTL1, EST157481 -ABCG2 and Lung Cancer
45
EPHX1 1q42.1 MEH, EPHX, EPOX, HYL1 -EPHX1 and Lung Cancer
44
RELA 11q13.1 p65, NFKB3 -RELA and Lung Cancer
44
HEBP1 12p13.1 HBP, HEBP -HEBP1 and Lung Cancer
44
XPC 3p25.1 XP3, RAD4, XPCC, p125 -XPC and Lung Cancer
44
ABCC1 16p13.1 MRP, ABCC, GS-X, MRP1, ABC29 -ABCC1 (MRP1) and Lung Cancer
42
GAPDH 12p13 G3PD, GAPD, HEL-S-162eP -GAPDH and Lung Cancer
42
RHOA 3p21.3 ARHA, ARH12, RHO12, RHOH12 -RHOA and Lung Cancer
42
CD82 11p11.2 R2, 4F9, C33, IA4, ST6, GR15, KAI1, SAR2, TSPAN27 -CD82 and Lung Cancer
41
RAC1 7p22 MIG5, Rac-1, TC-25, p21-Rac1 -RAC1 and Lung Cancer
41
MYCN 2p24.3 NMYC, ODED, MODED, N-myc, bHLHe37 -MYCN in Lung Cancer
40
CXCR4 2q21 FB22, HM89, LAP3, LCR1, NPYR, WHIM, CD184, LAP-3, LESTR, NPY3R, NPYRL, WHIMS, HSY3RR, NPYY3R, D2S201E -CXCR4 and Lung Cancer
40
CHRNA3 15q24 LNCR2, PAOD2, NACHRA3 -CHRNA3 and Lung Cancer
40
TP63 3q28 AIS, KET, LMS, NBP, RHS, p40, p51, p63, EEC3, OFC8, p73H, p73L, SHFM4, TP53L, TP73L, p53CP, TP53CP, B(p51A), B(p51B) -TP63 and Lung Cancer
39
NAT2 8p22 AAC2, PNAT, NAT-2 -NAT2 and Lung Cancer
39
NME1 17q21.3 NB, AWD, NBS, GAAD, NDKA, NM23, NDPKA, NDPK-A, NM23-H1 -NME1 and Lung Cancer
38
AKT2 19q13.1-q13.2 PKBB, PRKBB, HIHGHH, PKBBETA, RAC-BETA -AKT2 and Lung Cancer
38
PDLIM4 5q31.1 RIL -PDLIM4 and Lung Cancer
36
ERBB3 12q13 HER3, LCCS2, ErbB-3, c-erbB3, erbB3-S, MDA-BF-1, c-erbB-3, p180-ErbB3, p45-sErbB3, p85-sErbB3 -ERBB3 and Lung Cancer
34
TWIST1 7p21.2 CRS, CSO, SCS, ACS3, CRS1, BPES2, BPES3, TWIST, bHLHa38 -TWIST1 and Lung Cancer
34
BAP1 3p21.1 UCHL2, hucep-6, HUCEP-13 -BAP1 and Lung Cancer
34
ASCL1 12q23.2 ASH1, HASH1, MASH1, bHLHa46 -ASCL1 and Lung Cancer
33
CDH13 16q23.3 CDHH, P105 -CDH13 and Lung Cancer
32
CYP1B1 2p22.2 CP1B, GLC3A, CYPIB1, P4501B1 -CYP1B1 and Lung Cancer
32
TNFRSF10B 8p22-p21 DR5, CD262, KILLER, TRICK2, TRICKB, ZTNFR9, TRAILR2, TRICK2A, TRICK2B, TRAIL-R2, KILLER/DR5 -TNFRSF10B and Lung Cancer
32
DROSHA 5p13.3 RN3, ETOHI2, RNASEN, RANSE3L, RNASE3L, HSA242976 -DROSHA and Lung Cancer
31
VEGFC 4q34.3 VRP, Flt4-L, LMPH1D -VEGFC and Lung Cancer
31
MMP1 11q22.2 CLG, CLGN -MMP1 and Lung Cancer
30
PARP1 1q41-q42 PARP, PPOL, ADPRT, ARTD1, ADPRT1, PARP-1, ADPRT 1, pADPRT-1 -PARP1 and Lung Cancer
30
IL6 7p21 HGF, HSF, BSF2, IL-6, IFNB2 -IL6 and Lung Cancer
30
NKX2-1 14q13 BCH, BHC, NK-2, TEBP, TTF1, NKX2A, T/EBP, TITF1, TTF-1, NKX2.1 -NKX2-1 and Lung Cancer
30
POMC 2p23.3 LPH, MSH, NPP, POC, ACTH, CLIP -POMC and Lung Cancer
30
TSC2 16p13.3 LAM, TSC4, PPP1R160 -TSC2 and Lung Cancer
29
CXCL1 4q21 FSP, GRO1, GROa, MGSA, NAP-3, SCYB1, MGSA-a -CXCL1 and Lung Cancer
29
RAD51 15q15.1 RECA, BRCC5, FANCR, MRMV2, HRAD51, RAD51A, HsRad51, HsT16930 -RAD51 and Lung Cancer
29
MCC 5q21 MCC1 -MCC and Lung Cancer
29
SERPINB5 18q21.33 PI5, maspin -SERPIN-B5 and Lung Cancer
29
CYP2A6 19q13.2 CPA6, CYP2A, CYP2A3, P450PB, CYPIIA6, P450C2A -CYP2A6 and Lung Cancer
29
FOXM1 12p13 MPP2, TGT3, HFH11, HNF-3, INS-1, MPP-2, PIG29, FKHL16, FOXM1B, HFH-11, TRIDENT, MPHOSPH2 -FOXM1 and Lung Cancer
28
CXCL12 10q11.1 IRH, PBSF, SDF1, TLSF, TPAR1, SCYB12 -CXCL12 and Lung Cancer
28
RECK 9p13.3 ST15 -RECK and Lung Cancer
28
JUN 1p32-p31 AP1, AP-1, c-Jun -c-Jun and Lung Cancer
28
ZEB1 10p11.2 BZP, TCF8, AREB6, FECD6, NIL2A, PPCD3, ZFHEP, ZFHX1A, DELTAEF1 -ZEB1 and Lung Cancer
28
MIR126 9q34.3 MIRN126, mir-126, miRNA126 -MicroRNA mir-126 and Lung Cancer
27
DICER1 14q32.13 DCR1, MNG1, Dicer, HERNA, RMSE2, Dicer1e, K12H4.8-LIKE -DICER1 and Lung Cancer
27
HMGA2 12q15 BABL, LIPO, HMGIC, HMGI-C, STQTL9 -HMGA2 and Lung Cancer
27
SLC2A1 1p34.2 PED, DYT9, GLUT, DYT17, DYT18, EIG12, GLUT1, HTLVR, GLUT-1, GLUT1DS Prognostic
-GLUT1 Overexpression and Lung Cancer
27
SMARCA4 19p13.2 BRG1, CSS4, SNF2, SWI2, MRD16, RTPS2, BAF190, SNF2L4, SNF2LB, hSNF2b, BAF190A -SMARCA4 and Lung Cancer
27
CYP1A2 15q24.1 CP12, P3-450, P450(PA) -CYP1A2 and Lung Cancer
26
RHOC 1p13.1 H9, ARH9, ARHC, RHOH9 -RHOC and Lung Cancer
26
CLPTM1L 5p15.33 CRR9 -CLPTM1L and Lung Cancer
26
XPA 9q22.3 XP1, XPAC -XPA and Lung Cancer
26
MMP7 11q22.2 MMP-7, MPSL1, PUMP-1 -MMP7 and Lung Cancer
26
TUBB3 16q24.3 CDCBM, FEOM3, TUBB4, CDCBM1, CFEOM3, beta-4, CFEOM3A -TUBB3 and Lung Cancer
25
FAS 10q24.1 APT1, CD95, FAS1, APO-1, FASTM, ALPS1A, TNFRSF6 -FAS and Lung Cancer
25
MCL1 1q21 TM, EAT, MCL1L, MCL1S, Mcl-1, BCL2L3, MCL1-ES, bcl2-L-3, mcl1/EAT -MCL1 and Lung Cancer
25
SMAD4 18q21.1 JIP, DPC4, MADH4, MYHRS -SMAD4 and Lung Cancer
24
CADM1 11q23.3 BL2, ST17, IGSF4, NECL2, RA175, TSLC1, IGSF4A, Necl-2, SYNCAM, sgIGSF, sTSLC-1, synCAM1 -CADM1 and Lung Cancer
24
MMP3 11q22.2 SL-1, STMY, STR1, CHDS6, MMP-3, STMY1 -MMP3 and Lung Cancer
24
PTK2 8q24.3 FAK, FADK, FAK1, FRNK, PPP1R71, p125FAK, pp125FAK -PTK2 and Lung Cancer
24
PPP2CB 8p12 PP2CB, PP2Abeta -PPP2CB and Lung Cancer
24
TSC1 9q34 LAM, TSC -TSC1 and Lung Cancer
24
PPP2CA 5q31.1 RP-C, PP2Ac, PP2CA, PP2Calpha -PPP2CA and Lung Cancer
24
AXL 19q13.1 ARK, UFO, JTK11, Tyro7 -AXL and Lung Cancer
23
CHRNB4 15q24 -CHRNB4 and Lung Cancer
23
SMAD2 18q21.1 JV18, MADH2, MADR2, JV18-1, hMAD-2, hSMAD2 -SMAD2 and Lung Cancer
23
DDR2 1q23.3 TKT, MIG20a, NTRKR3, TYRO10 -DDR2 and Lung Cancer
23
POU5F1 6p21.31 OCT3, OCT4, OTF3, OTF4, OTF-3, Oct-3, Oct-4 -POU5F1 and Lung Cancer
23
ANXA8 10q11.22 ANX8, CH17-360D5.2 -ANXA8 and Lung Cancer
22
DNMT3B 20q11.2 ICF, ICF1, M.HsaIIIB -DNMT3B and Lung Cancer
22
CD24 6q21 CD24A -CD24 and Lung Cancer
22
SKP2 5p13 p45, FBL1, FLB1, FBXL1 -SKP2 and Lung Cancer
22
CBL 11q23.3 CBL2, NSLL, C-CBL, RNF55, FRA11B -CBL and Lung Cancer
22
RAP1A 1p13.3 RAP1, C21KG, G-22K, KREV1, KREV-1, SMGP21 -Lung Cancer and RAP1A
22
TERC 3q26 TR, hTR, TRC3, DKCA1, PFBMFT2, SCARNA19 -TERC and Lung Cancer
22
TYMS 18p11.32 TS, TMS, HST422 -TYMS and Lung Cancer
21
CISH 3p21.3 CIS, G18, SOCS, CIS-1, BACTS2 -CISH and Lung Cancer
21
SLC2A3 12p13.3 GLUT3 -GLUT3 and Lung cancer
21
HNRNPA2B1 7p15 RNPA2, HNRPA2, HNRPB1, SNRPB1, HNRNPA2, HNRNPB1, IBMPFD2, HNRPA2B1 -HNRNPA2B1 and Lung Cancer
21
POLE 12q24.3 FILS, POLE1, CRCS12 -POLE and Lung Cancer
20
CCL2 17q11.2-q12 HC11, MCAF, MCP1, MCP-1, SCYA2, GDCF-2, SMC-CF, HSMCR30 -CCL2 and Lung Cancer
20
EGR1 5q31.1 TIS8, AT225, G0S30, NGFI-A, ZNF225, KROX-24, ZIF-268 -EGR1 and Lung Cancer
20
CDK1 10q21.1 CDC2, CDC28A, P34CDC2 -CDK1 and Lung Cancer
19
CAV1 7q31.1 CGL3, PPH3, BSCL3, LCCNS, VIP21, MSTP085 -CAV1 and Lung Cancer
19
MAGEA3 Xq28 HIP8, HYPD, CT1.3, MAGE3, MAGEA6 -MAGEA3 and Lung Cancer
19
CD74 5q32 II, DHLAG, HLADG, Ia-GAMMA Translocation
-CD74 and Lung Cancer
-CD74-NTRK1 fusion in Lung Cancer
18
FOXO3 6q21 FOXO2, AF6q21, FKHRL1, FOXO3A, FKHRL1P2 -FOXO3 and Lung Cancer
18
SPARC 5q31.3-q32 ON -SPARC and Lung Cancer
18
GSTM3 1p13.3 GST5, GSTB, GTM3, GSTM3-3 -GSTM3 and Lung Cancer
18
ALDH1A1 9q21.13 ALDC, ALDH1, HEL-9, HEL12, PUMB1, ALDH11, RALDH1, ALDH-E1, HEL-S-53e -ALDH1A1 and Lung Cancer
17
TIMP2 17q25 DDC8, CSC-21K -TIMP2 Expression in Lung Cancer
17
ERCC5 13q33 XPG, UVDR, XPGC, COFS3, ERCM2, ERCC5-201 -ERCC5 and Lung Cancer
17
THBS1 15q15 TSP, THBS, TSP1, TSP-1, THBS-1 -THBS1 and Lung Cancer
17
TIMP3 22q12.3 SFD, K222, K222TA2, HSMRK222 -TIMP3 and Lung Cancer
17
NANOG 12p13.31 -NANOG and Lung Cancer
17
FOSL1 11q13.1 FRA, FRA1, fra-1 -FOSL1 and Lung Cancer
17
SSTR2 17q24 -SSTR2 and Lung Cancer
16
MALT1 18q21 MLT, MLT1, IMD12 -MALT1 and Lung Cancer
16
CREB1 2q34 CREB -CREB1 and Lung Cancer
16
SPP1 4q22.1 OPN, BNSP, BSPI, ETA-1 -SPP1 and Lung Cancer
16
MUC5AC 11p15.5 TBM, leB, MUC5, mucin -MUC5AC and Lung Cancer
16
CDC42 1p36.1 G25K, CDC42Hs -CDC42 and Lung Cancer
16
KDR 4q11-q12 FLK1, CD309, VEGFR, VEGFR2 -KDR and Lung Cancer
16
PECAM1 17q23.3 CD31, PECA1, GPIIA', PECAM-1, endoCAM, CD31/EndoCAM -PECAM1 and Lung Cancer
16
CCNA2 4q27 CCN1, CCNA -CCNA2 and Lung Cancer
16
EIF4E 4q23 CBP, EIF4F, AUTS19, EIF4E1, EIF4EL1 -EIF4E and Lung Cancer
16
SIRT1 10q21.3 SIR2, hSIR2, SIR2L1 -SIRT1 and Lung Cancer
16
LOX 5q23.2 -LOX and Lung Cancer
16
MMP12 11q22.2 ME, HME, MME, MMP-12 -MMP12 and Lung Cancer
16
PLK1 16p12.2 PLK, STPK13 -PLK1 and Lung Cancer
16
RAF1 3p25 NS5, CRAF, Raf-1, c-Raf, CMD1NN -RAF1 and Lung Cancer
15
TNFSF11 13q14 ODF, OPGL, sOdf, CD254, OPTB2, RANKL, TRANCE, hRANKL2 -TNFSF11 and Lung Cancer
15
BECN1 17q21 ATG6, VPS30, beclin1 -BECN1 and Lung Cancer
15
SOD2 6q25.3 IPOB, MNSOD, MVCD6 -SOD2 and Lung Cancer
15
EPCAM 2p21 ESA, KSA, M4S1, MK-1, DIAR5, EGP-2, EGP40, KS1/4, MIC18, TROP1, EGP314, HNPCC8, TACSTD1 -EPCAM and Lung Cancer
15
MALAT1 11q13.1 HCN, NEAT2, PRO2853, LINC00047, NCRNA00047 -MALAT1 and Lung Cancer
15
VIP 6q25 PHM27 -VIP and Lung Cancer
15
HES1 3q28-q29 HHL, HRY, HES-1, bHLHb39 -HES1 and Lung Cancer
15
CYP3A4 7q21.1 HLP, CP33, CP34, CYP3A, NF-25, CYP3A3, P450C3, CYPIIIA3, CYPIIIA4, P450PCN1 -CYP3A4 and Lung Cancer
15
PLAUR 19q13 CD87, UPAR, URKR, U-PAR -PLAUR and Lung Cancer
15
TUSC2 3p21.3 PAP, FUS1, PDAP2, C3orf11 -TUSC2 and Lung Cancer
14
TPM3 1q21.2 TM3, TM5, TRK, CFTD, NEM1, TM-5, TM30, CAPM1, TM30nm, TPMsk3, hscp30, HEL-189, HEL-S-82p, OK/SW-cl.5 -TPM3 and Lung Cancer
14
MARCO 2q14.2 SCARA2 -MARCO and Lung Cancer
14
WIF1 12q14.3 WIF-1 -WIF1 and Lung Cancer
14
GPC3 Xq26.1 SGB, DGSX, MXR7, SDYS, SGBS, OCI-5, SGBS1, GTR2-2 -GPC3 and Lung Cancer
14
IGF1 12q23.2 IGFI, IGF-I, IGF1A -IGF1 and Lung Cancer
14
S100A4 1q21 42A, 18A2, CAPL, FSP1, MTS1, P9KA, PEL98 -S100A4 and Lung Cancer
14
YAP1 11q22.1 YAP, YKI, COB1, YAP2, YAP65 -YAP1 and Lung Cancer
14
CDC25C 5q31 CDC25, PPP1R60 -CDC25C and Lung Cancer
14
S100A2 1q21 CAN19, S100L -S100A2 and Lung Cancer
14
CRK 17p13.3 p38, CRKII -CRK and Lung Cancer
14
GPX1 3p21.3 GPXD, GSHPX1 -GPX1 and Lung Cancer
14
H19 11p15.5 ASM, BWS, WT2, ASM1, D11S813E, LINC00008, NCRNA00008 -H19 and Lung Cancer
14
SCGB1A1 11q12.3 UGB, UP1, CC10, CC16, CCSP, UP-1, CCPBP -SCGB1A1 and Lung Cancer
14
CDH2 18q11.2 CDHN, NCAD, CD325, CDw325 -CDH2 and Lung Cancer
14
WARS 14q32.31 IFI53, IFP53, GAMMA-2 -WARS and Lung Cancer
14
DKK1 10q11.2 SK, DKK-1 -DKK1 and Lung Cancer
14
MOS 8q11 MSV -MOS and Lung Cancer
14
CD68 17p13 GP110, LAMP4, SCARD1 -CD68 and Lung Cancer
13
SLC19A1 21q22.3 CHMD, FOLT, IFC1, REFC, RFC1 -SLC19A1 and Lung Cancer
13
RBM5 3p21.3 G15, H37, RMB5, LUCA15 -RBM5 and Lung Cancer
13
DKK3 11p15.3 RIG, REIC -DKK3 and Lung Cancer
13
WNT5A 3p21-p14 hWNT5A -WNT5A and Lung Cancer
13
SEMA3B 3p21.3 SemA, SEMA5, SEMAA, semaV, LUCA-1 -SEMA3B and Lung Cancer
13
IL1B 2q14 IL-1, IL1F2, IL1-BETA -IL1B and Lung Cancer
13
ZEB2 2q22.3 SIP1, SIP-1, ZFHX1B, HSPC082, SMADIP1 -ZEB2 and Lung Cancer
13
PRKDC 8q11 HYRC, p350, DNAPK, DNPK1, HYRC1, IMD26, XRCC7, DNA-PKcs -PRKDC and Lung Cancer
13
VEGFB 11q13.1 VRF, VEGFL -VEGFB and Lung Cancer
13
RRM2 2p25-p24 R2, RR2, RR2M -RRM2 and Lung Cancer
12
ERBB4 2q33.3-q34 HER4, ALS19, p180erbB4 -ERBB4 and Lung Cancer
12
RHOB 2p24 ARH6, ARHB, RHOH6, MST081, MSTP081 -RHOB and Lung Cancer
12
PTHLH 12p12.1-p11.2 HHM, PLP, BDE2, PTHR, PTHRP -PTHLH and Lung Cancer
12
WWOX 16q23 FOR, WOX1, EIEE28, FRA16D, SCAR12, HHCMA56, PRO0128, SDR41C1, D16S432E -WWOX and Lung Cancer
12
COL18A1 21q22.3 KS, KNO, KNO1 -COL18A1 and Lung Cancer
12
MMP14 14q11.2 MMP-14, MMP-X1, MT-MMP, MT1MMP, MTMMP1, WNCHRS, MT1-MMP, MT-MMP 1 -MMP14 and Lung Cancer
12
BMP2 20p12 BDA2, BMP2A -BMP2 and Lung Cancer
12
NOTCH3 19p13.12 IMF2, LMNS, CASIL, CADASIL, CADASIL1 -NOTCH3 and Lung Cancer
11
PPP1R13L 19q13.32 RAI, RAI4, IASPP, NKIP1 -PPP1R13L and Lung Cancer
11
S100P 4p16 MIG9 -S100P and Lung Cancer
11
ABCC4 13q32 MRP4, MOATB, MOAT-B -ABCC4 and Lung Cancer
11
IL17A 6p12 IL17, CTLA8, IL-17, IL-17A -IL17A and Lung Cancer
11
BIRC7 20q13.3 KIAP, LIVIN, MLIAP, RNF50, ML-IAP -BIRC7 and Lung Cancer
11
BRD4 19p13.1 CAP, MCAP, HUNK1, HUNKI -BRD4 and Lung Cancer
11
PDK1 2q31.1 -PDK1 and Lung Cancer
11
IL17C 16q24 CX2, IL-17C -IL17C and Lung Cancer
11
EPHA2 1p36 ECK, CTPA, ARCC2, CTPP1, CTRCT6 -EPHA2 and Lung Cancer
11
ERCC4 16p13.12 XPF, RAD1, FANCQ, ERCC11 -ERCC4 and Lung Cancer
11
MIF 22q11.23 GIF, GLIF, MMIF -MIF and Lung Cancer
11
E2F3 6p22 E2F-3 -E2F3 and Lung Cancer
11
KRT5 12q13.13 K5, CK5, DDD, DDD1, EBS2, KRT5A -KRT5 and Lung Cancer
11
FGFR4 5q35.2 TKF, JTK2, CD334 -FGFR4 and Lung Cancer
11
JUND 19p13.2 AP-1 -JUND and Lung Cancer
11
MAGEA4 Xq28 CT1.4, MAGE4, MAGE4A, MAGE4B, MAGE-41, MAGE-X2 -MAGEA4 and Lung Cancer
11
CTAG1B Xq28 CTAG, ESO1, CT6.1, CTAG1, LAGE-2, LAGE2B, NY-ESO-1 -CTAG1B and Lung Cancer
11
STMN1 1p36.11 Lag, SMN, OP18, PP17, PP19, PR22, LAP18, C1orf215 -STMN1 and Lung Cancer
10
MAML2 11q21 MAM2, MAM3, MAM-3, MLL-MAML2 -MAML2 and Lung Cancer
10
CLDN1 3q28-q29 CLD1, SEMP1, ILVASC -CLDN1 and Lung Cancer
10
PLA2G4A 1q25 PLA2G4, cPLA2-alpha -PLA2G4A and Lung Cancer
10
NEDD9 6p24.2 CAS2, CASL, HEF1, CAS-L, CASS2 -NEDD9 and Lung Cancer
10
PARK2 6q25.2-q27 PDJ, PRKN, AR-JP, LPRS2 -PARK2 and Lung Cancer
10
DLC1 8p22 HP, ARHGAP7, STARD12, p122-RhoGAP -DLC1 and Lung Cancer
10
SLC34A2 4p15.2 NPTIIb, NAPI-3B, NAPI-IIb -SLC34A2 and Lung Cancer
10
ATF1 12q13 TREB36, EWS-ATF1, FUS/ATF-1 -ATF1 and Lung Cancer
10
TNFRSF1A 12p13.2 FPF, MS5, p55, p60, TBP1, TNF-R, TNFAR, TNFR1, p55-R, CD120a, TNFR55, TNFR60, TNF-R-I, TNF-R55, TNFR1-d2 -TNFRSF1A and Lung Cancer
10
SOCS3 17q25.3 CIS3, SSI3, ATOD4, Cish3, SSI-3, SOCS-3 -SOCS3 and Lung Cancer
10
CASP10 2q33-q34 MCH4, ALPS2, FLICE2 -CASP10 and Lung Cancer
10
MIRLET7C 21q21.1 LET7C, let-7c, MIRNLET7C, hsa-let-7c -MicroRNA let-7c and Lung Cancer
10
NAT1 8p22 AAC1, MNAT, NATI, NAT-1 -NAT1 and Lung Cancer
10
TFE3 Xp11.22 TFEA, RCCP2, RCCX1, bHLHe33 -TFE3 and Lung Cancer
10
ACTB 7p22 BRWS1, PS1TP5BP1 -ACTB and Lung Cancer
10
BCAR1 16q23.1 CAS, CAS1, CASS1, CRKAS, P130Cas -BCAR1 and Lung Cancer
10
LGALS1 22q13.1 GBP, GAL1 -LGALS1 and Lung Cancer
10
RBL2 16q12.2 Rb2, P130 -RBL2 and Lung Cancer
10
CD63 12q12-q13 MLA1, ME491, LAMP-3, OMA81H, TSPAN30 -CD63 and Lung Cancer
10
STAR 8p11.2 STARD1 -STAR and Lung Cancer
10
CHFR 12q24.33 RNF116, RNF196 -CHFR and Lung Cancer
10
AVPR1A 12q14.2 V1aR, AVPR1, AVPR V1a -AVPR1A and Lung Cancer
9
MMP11 22q11.23 ST3, SL-3, STMY3 -MMP11 and Lung Cancer
9
GADD45A 1p31.2 DDIT1, GADD45 -GADD45A and Lung Cancer
9
SOX4 6p22.3 EVI16 -SOX4 and Lung Cancer
9
CHIA 1p13.2 CHIT2, AMCASE, TSA1902 -CHIA and Lung Cancer
9
CRKL 22q11.21 -CRKL and Lung Cancer
9
CCR7 17q12-q21.2 BLR2, EBI1, CCR-7, CD197, CDw197, CMKBR7, CC-CKR-7 -CCR7 and Lung Cancer
9
MUC4 3q29 ASGP, MUC-4, HSA276359 -MUC4 and Lung Cancer
9
TOP2A 17q21-q22 TOP2, TP2A -TOP2A Expression in Lung Cancer
9
BDNF 11p14.1 ANON2, BULN2 -BDNF and Lung Cancer
9
GATA3 10p15 HDR, HDRS -GATA3 and Lung Cancer
9
ATF3 1q32.3 -ATF3 and Lung Cancer
9
CEACAM1 19q13.2 BGP, BGP1, BGPI -CEACAM1 and Lung Cancer
9
CFTR 7q31.2 CF, MRP7, ABC35, ABCC7, CFTR/MRP, TNR-CFTR, dJ760C5.1 -CFTR and Lung Cancer
9
POSTN 13q13.3 PN, OSF2, OSF-2, PDLPOSTN, periostin -POSTN and Lung Cancer
9
DIABLO 12q24.31 SMAC, DFNA64 -DIABLO and Lung Cancer
9
BRMS1 11q13.2 -BRMS1 and Lung Cancer
9
ANXA2 15q22.2 P36, ANX2, LIP2, LPC2, CAL1H, LPC2D, ANX2L4, PAP-IV, HEL-S-270 -ANXA2 and Lung Cancer
9
RARB 3p24.2 HAP, RRB2, NR1B2, MCOPS12 -RARB and Lung Cancer
9
NDRG1 8q24.3 GC4, RTP, DRG1, NDR1, NMSL, TDD5, CAP43, CMT4D, DRG-1, HMSNL, RIT42, TARG1, PROXY1 -NDRG1 and Lung Cancer
9
CRP 1q23.2 PTX1 -CRP and Lung Cancer
9
TNFRSF11A 18q22.1 FEO, OFE, ODFR, OSTS, PDB2, RANK, CD265, OPTB7, TRANCER, LOH18CR1 -TNFRSF11A and Lung Cancer
9
XRCC5 2q35 KU80, KUB2, Ku86, NFIV, KARP1, KARP-1 -XRCC5 and Lung Cancer
9
HYAL2 3p21.3 LUCA2 -HYAL2 and Lung Cancer
9
CXCL5 4q13.3 SCYB5, ENA-78 -CXCL5 and Lung Cancer
9
AVPR1B 1q32 AVPR3 -AVPR1B and Lung Cancer
9
FEN1 11q12.2 MF1, RAD2, FEN-1 -FEN1 and Lung Cancer
9
ETS2 21q22.2 ETS2IT1 -ETS2 and Lung Cancer
9
EP300 22q13.2 p300, KAT3B, RSTS2 -EP300 and Lung Cancer
9
TP53BP1 15q15-q21 p202, 53BP1 -TP53BP1 and Lung Cancer
9
TIMP1 Xp11.3-p11.23 EPA, EPO, HCI, CLGI, TIMP Prognostic
-TIMP1 and Non Small Cell Lung Cancer
9
MTDH 8q22.1 3D3, AEG1, AEG-1, LYRIC, LYRIC/3D3 -MTDH and Lung Cancer
9
RAG2 11p12 RAG-2 -RAG2 and Lung Cancer
9
SLIT2 4p15.2 SLIL3, Slit-2 -SLIT2 and Lung Cancer
9
CD274 9p24 B7-H, B7H1, PDL1, PD-L1, PDCD1L1, PDCD1LG1 -CD274 and Lung Cancer
9
PTPRD 9p23-p24.3 HPTP, PTPD, HPTPD, HPTPDELTA, RPTPDELTA -PTPRD and Lung Cancer
9
CYP24A1 20q13 CP24, HCAI, CYP24, P450-CC24 -CYP24A1 and Lung Cancer
9
ING1 13q34 p33, p47, p33ING1, p24ING1c, p33ING1b, p47ING1a -ING1 and Lung Cancer
8
SPRY2 13q31.1 hSPRY2 -SPRY2 and Lung Cancer
8
EPB41L3 18p11.32 4.1B, DAL1, DAL-1 -EPB41L3 and Lung Cancer
8
ALDH3A1 17p11.2 ALDH3, ALDHIII -ALDH3A1 and Lung Cancer
8
TBK1 12q14.1 NAK, T2K -TBK1 and Lung Cancer
8
ARNT 1q21 HIF1B, TANGO, bHLHe2, HIF1BETA, HIF-1beta, HIF1-beta, HIF-1-beta -ARNT and Lung Cancer
8
LPP 3q28 -LPP and Lung Cancer
8
FOXA2 20p11 HNF3B, TCF3B -FOXA2 and Lung Cancer
8
MDC1 6p21.3 NFBD1 -MDC1 and Lung Cancer
8
DUSP1 5q34 HVH1, MKP1, CL100, MKP-1, PTPN10 -DUSP1 and Lung Cancer
8
CCDC6 10q21 H4, PTC, TPC, TST1, D10S170 -CCDC6 and Lung Cancer
8
HSPB1 7q11.23 CMT2F, HMN2B, HSP27, HSP28, Hsp25, SRP27, HS.76067, HEL-S-102 -HSPB1 and Lung Cancer
8
HOXA5 7p15.2 HOX1, HOX1C, HOX1.3 -HOXA5 and Lung Cancer
8
HOXA1 7p15.3 BSAS, HOX1, HOX1F -HOXA1 and Lung Cancer
8
MCM2 3q21 BM28, CCNL1, CDCL1, cdc19, D3S3194, MITOTIN -MCM2 and Lung Cancer
8
MTAP 9p21 BDMF, MSAP, DMSFH, LGMBF, DMSMFH, c86fus, HEL-249 -MTAP and Lung Cancer
8
EREG 4q13.3 ER, Ep, EPR -EREG and Lung Cancer
8
AKR1B10 7q33 HIS, HSI, ARL1, ARL-1, ALDRLn, AKR1B11, AKR1B12 -AKR1B10 and Lung Cancer
8
CCNB2 15q22.2 HsT17299 -CCNB2 and Lung Cancer
8
TNFRSF10A 8p21 DR4, APO2, CD261, TRAILR1, TRAILR-1 -TNFRSF10A and Lung Cancer
8
CXCL10 4q21 C7, IFI10, INP10, IP-10, crg-2, mob-1, SCYB10, gIP-10 -CXCL10 and Lung Cancer
8
CYR61 1p22.3 CCN1, GIG1, IGFBP10 -CYR61 and Lung Cancer
8
HOTAIR 12q13.13 HOXAS, HOXC-AS4, HOXC11-AS1, NCRNA00072 -HOTAIR and Lung Cancer
8
CRTC1 19p13.11 MECT1, TORC1, TORC-1, WAMTP1 -CRTC1 and Lung Cancer
8
MBD2 18q21 DMTase, NY-CO-41 -MBD2 and Lung Cancer
8
SMARCA2 9p22.3 BRM, SNF2, SWI2, hBRM, NCBRS, Sth1p, BAF190, SNF2L2, SNF2LA, hSNF2a -SMARCA2 and Lung Cancer
8
MIRLET7G 3p21.1 LET7G, let-7g, MIRNLET7G, hsa-let-7g -MicroRNA let-7g and Lung Cancer
8
NFKB1 4q24 p50, KBF1, p105, EBP-1, NF-kB1, NFKB-p50, NFkappaB, NF-kappaB, NFKB-p105, NF-kappa-B -NFKB1 and Lung Cancer
8
CYP2C19 10q24 CPCJ, CYP2C, P450C2C, CYPIIC17, CYPIIC19, P450IIC19 -CYP2C19 and Lung Cancer
8
TPX2 20q11.2 DIL2, p100, DIL-2, HCTP4, FLS353, HCA519, REPP86, C20orf1, C20orf2, GD:C20orf1 -TPX2 and Lung Cancer
8
CLMP 11q24.1 ACAM, ASAM, CSBM, CSBS -CLMP and Lung Cancer
8
HYAL1 3p21.31 MPS9, NAT6, LUCA1, HYAL-1 -HYAL1 and Lung Cancer
8
ATG5 6q21 ASP, APG5, APG5L, hAPG5, APG5-LIKE -ATG5 and Lung Cancer
8
LATS2 13q12.11 KPM -LATS2 and Lung Cancer
8
AIDA 1q41 C1orf80 -AIDA and Lung Cancer
8
DDR1 6p21.3 CAK, DDR, NEP, HGK2, PTK3, RTK6, TRKE, CD167, EDDR1, MCK10, NTRK4, PTK3A -DDR1 and Lung Cancer
7
XRCC2 7q36.1 -XRCC2 and Lung Cancer
7
PWAR1 15q11.2 PAR1, PAR-1, D15S227E -PAR1 and Lung Cancer
7
MIRLET7B 22q13.31 LET7B, let-7b, MIRNLET7B, hsa-let-7b -MicroRNA let-7b and Lung Cancer
7
AMFR 16q21 GP78, RNF45 -AMFR and Lung Cancer
7
ABCC2 10q24 DJS, MRP2, cMRP, ABC30, CMOAT -ABCC2 and Lung Cancer
7
CALCA 11p15.2 CT, KC, PCT, CGRP, CALC1, CGRP1, CGRP-I -CALCA and Lung Cancer
7
UCHL1 4p14 NDGOA, PARK5, PGP95, PGP9.5, Uch-L1, HEL-117, PGP 9.5 -UCHL1 and Lung Cancer
7
ING4 12p13.31 my036, p29ING4 -ING4 and Lung Cancer
7
ADAM9 8p11.22 MCMP, MDC9, CORD9, Mltng -ADAM9 and Lung Cancer
7
MVP 16p11.2 LRP, VAULT1 -MVP and Lung Cancer
7
DNAJB4 1p31.1 DjB4, HLJ1, DNAJW -DNAJB4 and Lung Cancer
7
SEMA3F 3p21.3 SEMA4, SEMAK, SEMA-IV -SEMA3F and Lung Cancer
7
PPP2R1B 11q23.1 PR65B, PP2A-Abeta -PPP2R1B and Lung Cancer
7
BCHE 3q26.1-q26.2 E1, CHE1, CHE2 -BCHE and Lung Cancer
7
MAPK8 10q11.22 JNK, JNK1, PRKM8, SAPK1, JNK-46, JNK1A2, SAPK1c, JNK21B1/2 -MAPK8 and Lung Cancer
7
KL 13q12 -KL and Lung Cancer
7
EIF3E 8q22-q23 INT6, EIF3S6, EIF3-P48, eIF3-p46 -EIF3E and Lung Cancer
7
MBD1 18q21 RFT, PCM1, CXXC3 -MBD1 and Lung Cancer
7
SNAI2 8q11 SLUG, WS2D, SLUGH1, SNAIL2 -SNAI2 and Lung Cancer
7
RASSF5 1q32.1 RAPL, Maxp1, NORE1, NORE1A, NORE1B, RASSF3 -RASSF5 and Lung Cancer
7
CHGA 14q32 CGA -CHGA and Lung Cancer
7
ID2 2p25 GIG8, ID2A, ID2H, bHLHb26 Prognostic
-ID2 Expression in Lung Cancer
7
DMBT1 10q26.13 GP340, muclin -DMBT1 and Lung Cancer
7
SHC1 1q21 SHC, SHCA -SHC1 and Lung Cancer
7
PRB2 12p13.2 Ps, cP7, IB-9, PRPPRB1 -PRB2 and Lung Cancer
7
WNT3A 1q42 -WNT3A and Lung Cancer
7
XRCC4 5q14.2 -XRCC4 and Lung Cancer
7
ZMYND10 3p21.3 BLU, FLU, CILD22 -ZMYND10 and Lung Cancer
7
LYN 8q13 JTK8, p53Lyn, p56Lyn -LYN and Lung Cancer
7
EXO1 1q43 HEX1, hExoI -EXO1 and Lung Cancer
7
CYP2A13 19q13.2 CPAD, CYP2A, CYPIIA13 -CYP2A13 and Lung Cancer
7
SPRR1B 1q21-q22 SPRR1, GADD33, CORNIFIN -SPRR1B and Lung Cancer
7
DDB2 11p11.2 XPE, DDBB, UV-DDB2 -DDB2 and Lung Cancer
7
CTNNA1 5q31.2 CAP102 -CTNNA1 and Lung Cancer
7
PRKCA 17q22-q23.2 AAG6, PKCA, PRKACA, PKC-alpha -PRKCA and Lung Cancer
7
MAP2K4 17p12 JNKK, MEK4, MKK4, SEK1, SKK1, JNKK1, SERK1, MAPKK4, PRKMK4, SAPKK1, SAPKK-1 -MAP2K4 and Lung Cancer
7
MSN Xq11.1 HEL70 -MSN and Lung Cancer
7
TRAF6 11p12 RNF85, MGC:3310 -TRAF6 and Lung Cancer
7
WNT7A 3p25 -WNT7A and Lung Cancer
7
RARS 5q35.1 HLD9, ArgRS, DALRD1 -RARS and Lung Cancer
7
CAST 5q15 BS-17, PLACK -CAST and Lung Cancer
7
SNAI1 20q13.2 SNA, SNAH, SNAIL, SLUGH2, SNAIL1, dJ710H13.1 -SNAI1 and Lung Cancer
6
SPRR1A 1q21-q22 SPRK -SPRR1A and Lung Cancer
6
FOSB 19q13.32 AP-1, G0S3, GOS3, GOSB -FOSB and Lung Cancer
6
SLC29A1 6p21.1 ENT1 -SLC29A1 and Lung Cancer
6
ROBO1 3p12 SAX3, DUTT1 -ROBO1 and Lung Cancer
6
DRD2 11q23.2 D2R, D2DR -DRD2 and Lung Cancer
6
ECT2 3q26.1-q26.2 ARHGEF31 -ECT2 and Lung Cancer
6
SPRR2B 1q21-q22 -SPRR2B and Lung Cancer
6
ENO1 1p36.2 NNE, PPH, MPB1, ENO1L1 -ENO1 and Lung Cancer
6
MMP10 11q22.2 SL-2, STMY2 -MMP10 and Lung Cancer
6
CDCP1 3p21.31 CD318, TRASK, SIMA135 -CDCP1 and Lung Cancer
6
REST 4q12 XBR, NRSF -REST and Lung Cancer
6
NUMB 14q24.3 S171, C14orf41, c14_5527 -NUMB and Lung Cancer
6
NOX4 11q14.3 KOX, KOX-1, RENOX -NOX4 and Lung Cancer
6
PTPRF 1p34 LAR, BNAH2 -PTPRF and Lung Cancer
6
HDGF 1q23.1 HMG1L2 -HDGF and Lung Cancer
6
AKR1C1 10p15-p14 C9, DD1, DDH, DDH1, H-37, HBAB, MBAB, HAKRC, DD1/DD2, 2-ALPHA-HSD, 20-ALPHA-HSD -AKR1C1 and Lung Cancer
6
ARHGDIB 12p12.3 D4, GDIA2, GDID4, LYGDI, Ly-GDI, RAP1GN1, RhoGDI2 -ARHGDIB and Lung Cancer
6
FOLR1 11q13.4 FBP, FOLR -FOLR1 and Lung Cancer
6
SPRR2C 1q21-q22 -SPRR2C and Lung Cancer
6
DLEC1 3p21.3 F56, DLC1, CFAP81 -DLEC1 and Lung Cancer
6
PTTG1 5q35.1 EAP1, PTTG, HPTTG, TUTR1 -PTTG1 and Lung Cancer
6
PDPN 1p36.21 T1A, GP36, GP40, Gp38, OTS8, T1A2, TI1A, T1A-2, AGGRUS, HT1A-1, PA2.26 -PDPN and Lung Cancer
6
DUSP6 12q22-q23 HH19, MKP3, PYST1 -DUSP6 and Lung Cancer
6
GATA5 20q13.33 GATAS, bB379O24.1 -GATA5 and Lung Cancer
6
MAX 14q23 bHLHd4 -MAX and Lung Cancer
6
PDCD1 2q37.3 PD1, PD-1, CD279, SLEB2, hPD-1, hPD-l, hSLE1 -PDCD1 and Lung Cancer
6
PITX1 5q31.1 BFT, CCF, POTX, PTX1, LBNBG -PITX1 and Lung Cancer
6
RAD52 12p13-p12.2 -RAD52 and Lung Cancer
6
CDK5 7q36 LIS7, PSSALRE -CDK5 and Lung Cancer
6
TTL 2q13 -TTL and Lung Cancer
6
GATA4 8p23.1-p22 TOF, ASD2, VSD1, TACHD -GATA4 and Lung Cancer
6
SPRR2A 1q21-q22 -SPRR2A and Lung Cancer
6
BTG2 1q32 PC3, TIS21 -BTG2 and Lung Cancer
6
CDC25B 20p13 -CDC25B and Lung Cancer
6
TFG 3q12.2 TF6, HMSNP, SPG57, TRKT3 -TFG and Lung Cancer
6
ITGB3 17q21.32 GT, CD61, GP3A, BDPLT2, GPIIIa, BDPLT16 -ITGB3 and Lung Cancer
6
DLX4 17q21.33 BP1, DLX7, DLX8, DLX9 -DLX4 and Lung Cancer
6
FEV 2q36 PET-1, HSRNAFEV -FEV and Lung Cancer
6
TGFBR3 1p33-p32 BGCAN, betaglycan -TGFBR3 and Lung Cancer
6
UBE2C 20q13.12 UBCH10, dJ447F3.2 -UBE2C and Lung Cancer
6
GAB1 4q31.21 -GAB1 and Lung Cancer
6
ACTA2 10q23.3 AAT6, ACTSA, MYMY5 -ACTA2 and Lung Cancer
6
NEUROD1 2q32 BETA2, BHF-1, MODY6, NEUROD, bHLHa3 -NEUROD1 and Lung Cancer
6
ACTN4 19q13 FSGS, FSGS1, ACTININ-4 -ACTN4 and Lung Cancer
5
TSG101 11p15.1 TSG10, VPS23 -TSG101 and Lung Cancer
5
PRDX1 1p34.1 PAG, PAGA, PAGB, PRX1, PRXI, MSP23, NKEFA, TDPX2, NKEF-A -PRDX1 and Lung Cancer
5
LEPR 1p31 OBR, OB-R, CD295, LEP-R, LEPRD -LEPR and Lung Cancer
5
AQP1 7p14 CO, CHIP28, AQP-CHIP -AQP1 and Lung Cancer
5
SEMA3A 7p12.1 HH16, SemD, COLL1, SEMA1, SEMAD, SEMAL, coll-1, Hsema-I, SEMAIII, Hsema-III -SEMA3A and Lung Cancer
5
ADAMTS1 21q21.2 C3-C5, METH1 -ADAMTS1 and Lung Cancer
5
PYCARD 16p11.2 ASC, TMS, TMS1, CARD5, TMS-1 -PYCARD and Lung Cancer
5
TP73 1p36.3 P73 -TP73 and Lung Cancer
5
RPA1 17p13.3 HSSB, RF-A, RP-A, REPA1, RPA70, MST075 -RPA1 and Lung Cancer
5
GAS6 13q34 AXSF, AXLLG -GAS6 and Lung Cancer
5
MINA 3q11.2 ROX, MDIG, NO52, MINA53 -MINA and Lung Cancer
5
ERCC6 10q11.23 CSB, CKN2, COFS, ARMD5, COFS1, RAD26, UVSS1 -ERCC6 and Lung Cancer
5
SQSTM1 5q35 p60, p62, A170, OSIL, PDB3, ZIP3, p62B -SQSTM1 and Lung Cancer
5
CTCFL 20q13.31 CT27, BORIS, CTCF-T, HMGB1L1, dJ579F20.2 -CTCFL and Lung Cancer
5
FPGS 9q34.1 -FPGS and Lung Cancer
5
TJP1 15q13 ZO-1 -TJP1 and Lung Cancer
5
CCL19 9p13 ELC, CKb11, MIP3B, MIP-3b, SCYA19 -CCL19 and Lung Cancer
5
MBD4 3q21.3 MED1 -MBD4 and Lung Cancer
5
ASPSCR1 17q25.3 TUG, ASPL, ASPS, RCC17, UBXD9, UBXN9, ASPCR1 -ASPSCR1 and Lung Cancer
5
IL1A 2q14 IL1, IL-1A, IL1F1, IL1-ALPHA -IL1A and Lung Cancer
5
PGLS 19p13.2 6PGL -PGLS and Lung Cancer
5
EFEMP1 2p16 DHRD, DRAD, FBNL, MLVT, MTLV, S1-5, FBLN3, FIBL-3 -EFEMP1 and Lung Cancer
5
CXCR3 Xq13 GPR9, MigR, CD182, CD183, Mig-R, CKR-L2, CMKAR3, IP10-R -CXCR3 and Lung Cancer
5
EPHB6 7q33-q35 HEP -EPHB6 and Lung Cancer
5
PYGM 11q13.1 -PYGM and Lung Cancer
5
IL15 4q31 IL-15 -IL15 and Lung Cancer
5
BMP7 20q13 OP-1 -BMP7 and Lung Cancer
5
CD46 1q32 MCP, TLX, AHUS2, MIC10, TRA2.10 -CD46 and Lung Cancer
5
LIG4 13q33-q34 LIG4S -LIG4 and Lung Cancer
5
CRTC2 1q21.3 TORC2, TORC-2 -CRTC2 and Lung Cancer
5
NOTO 2p13.2 -NOTO and Lung Cancer
5
IL2RG Xq13.1 P64, CIDX, IMD4, CD132, SCIDX, IL-2RG, SCIDX1 -IL2RG and Lung Cancer
5
ALCAM 3q13.1 MEMD, CD166 -ALCAM and Lung Cancer
5
TMEFF2 2q32.3 TR, HPP1, TPEF, TR-2, TENB2, CT120.2 -TMEFF2 and Lung Cancer
5
PTGER2 14q22 EP2 -PTGER2 and Lung Cancer
5
SULF2 20q13.12 HSULF-2 -SULF2 and Lung Cancer
5
SSTR1 14q13 SS1R, SS1-R, SRIF-2, SS-1-R -SSTR1 and Lung Cancer
5
CCNA1 13q12.3-q13 CT146 -CCNA1 and Lung Cancer
5
TAGLN 11q23.3 SM22, SMCC, TAGLN1, WS3-10 -TAGLN and Lung Cancer
5
CEACAM6 19q13.2 NCA, CEAL, CD66c -CEACAM6 and Lung Cancer
5
BRAP 12q24 IMP, BRAP2, RNF52 -BRAP and Lung Cancer
5
CYP2C9 10q24 CPC9, CYP2C, CYP2C10, CYPIIC9, P450IIC9 -CYP2C9 and Lung Cancer
5
SCGB3A1 5q35.3 HIN1, HIN-1, LU105, UGRP2, PnSP-2 -SCGB3A1 and Lung Cancer
5
HSPA1B 6p21.3 HSP70-2, HSP70.2, HSP70-1B -HSPA1B and Lung Cancer
5
EZR 6q25.3 CVL, CVIL, VIL2, HEL-S-105 -EZR and Lung Cancer
5
PDPK1 16p13.3 PDK1, PDPK2, PDPK2P, PRO0461 -PDPK1 and Lung Cancer
5
FURIN 15q26.1 FUR, PACE, SPC1, PCSK3 -FURIN and Lung Cancer
5
PPARD 6p21.2 FAAR, NUC1, NUCI, NR1C2, NUCII, PPARB -PPAR delta and Lung Cancer
5
RALBP1 18p11.3 RIP1, RLIP1, RLIP76 -RALBP1 and Lung Cancer
5
IGFBP5 2q35 IBP5 -IGFBP5 and Lung Cancer
5
MTA2 11q12.3 PID, MTA1L1 -MTA2 and Lung Cancer
5
HDAC4 2q37.3 HD4, AHO3, BDMR, HDACA, HA6116, HDAC-4, HDAC-A -HDAC4 and Lung Cancer
5
SUV39H1 Xp11.23 MG44, KMT1A, SUV39H, H3-K9-HMTase 1 -SUV39H1 and Lung Cancer
5
S100A9 1q21 MIF, NIF, P14, CAGB, CFAG, CGLB, L1AG, LIAG, MRP14, 60B8AG, MAC387 -S100A9 and Lung Cancer
5
WISP1 8q24.22 CCN4, WISP1c, WISP1i, WISP1tc -WISP1 and Lung Cancer
5
IGFBP4 17q21.2 BP-4, IBP4, IGFBP-4, HT29-IGFBP -IGFBP4 and Lung Cancer
4
DLL4 15q14 hdelta2 -DLL4 and Lung Cancer
4
SOS1 2p21 GF1, HGF, NS4, GGF1, GINGF -SOS1 and Lung Cancer
4
CCL3 17q12 MIP1A, SCYA3, G0S19-1, LD78ALPHA, MIP-1-alpha -CCL3 and Lung Cancer
4
RALA 7p15-p13 RAL -RALA and Lung Cancer
4
JAG2 14q32 HJ2, SER2 -JAG2 and Lung Cancer
4
TFPI 2q32 EPI, TFI, LACI, TFPI1 -TFPI and Lung Cancer
4
ZBTB7A 19p13.3 LRF, FBI1, FBI-1, ZBTB7, ZNF857A, pokemon -ZBTB7A and Lung Cancer
4
WHSC1L1 8p11.2 NSD3, pp14328 -WHSC1L1 and Lung Cancer
4
TANK 2q24.2 ITRAF, TRAF2, I-TRAF -TANK and Lung Cancer
4
HOXA11 7p15.2 HOX1, HOX1I -HOXA11 and Lung Cancer
4
SATB1 3p23 -SATB1 and Lung Cancer
4
MACC1 7p21.1 7A5, SH3BP4L -MACC1 and Lung Cancer
4
MIRLET7D 9q22.32 LET7D, let-7d, MIRNLET7D, hsa-let-7d -None and MicroRNA let-d Cancer
4
PDCD6 5p15.33 ALG2, ALG-2, PEF1B -PDCD6 and Lung Cancer
4
MAD1L1 7p22 MAD1, PIG9, TP53I9, TXBP181 -MAD1L1 and Lung Cancer
4
HTATIP2 11p15.1 CC3, TIP30, SDR44U1 -HTATIP2 and Lung Cancer
4
MAP3K8 10p11.23 COT, EST, ESTF, TPL2, AURA2, MEKK8, Tpl-2, c-COT -MAP3K8 and Lung Cancer
4
INHA 2q35 -INHA and Lung Cancer
4
SKP1 5q31 OCP2, p19A, EMC19, SKP1A, OCP-II, TCEB1L -SKP1 and Lung Cancer
4
ATG7 3p25.3 GSA7, APG7L, APG7-LIKE -ATG7 and Lung Cancer
4
FER 5q21 TYK3, PPP1R74, p94-Fer -FER and Lung Cancer
4
ARID2 12q12 p200, BAF200 -ARID2 and Lung Cancer
4
CDC6 17q21.3 CDC18L, HsCDC6, HsCDC18 -CDC6 and Lung Cancer
4
NRP2 2q33.3 NP2, NPN2, PRO2714, VEGF165R2 -NRP2 and Lung Cancer
4
ATF2 2q32 HB16, CREB2, TREB7, CREB-2, CRE-BP1 -ATF2 and Lung Cancer
4
POLK 5q13 DINP, POLQ, DINB1 -POLK and Lung Cancer
4
NRP1 10p12 NP1, NRP, BDCA4, CD304, VEGF165R -NRP1 and Lung Cancer
4
HPSE 4q21.3 HPA, HPA1, HPR1, HSE1, HPSE1 -HPSE and Lung Cancer
4
VCAN 5q14.3 WGN, ERVR, GHAP, PG-M, WGN1, CSPG2 -VCAN and Lung Cancer
4
HSP90AB1 6p12 HSP84, HSPC2, HSPCB, D6S182, HSP90B -HSP90AB1 and Lung Cancer
4
RPS6 9p21 S6 -RPS6 and Lung Cancer
4
RALGDS 9q34.3 RGF, RGDS, RalGEF -RALGDS and Lung Cancer
4
WNT2 7q31.2 IRP, INT1L1 -WNT2 and Lung Cancer
4
AQP3 9p13 GIL, AQP-3 -AQP3 and Lung Cancer
4
LOXL2 8p21.3 LOR2, WS9-14 -LOXL2 and Lung Cancer
4
CDK7 5q12.1 CAK1, HCAK, MO15, STK1, CDKN7, p39MO15 -CDK7 and Lung Cancer
4
NR0B1 Xp21.3 AHC, AHX, DSS, GTD, HHG, AHCH, DAX1, DAX-1, NROB1, SRXY2 -NR0B1 and Lung Cancer
4
LIN28B 6q21 CSDD2 -LIN28B and Lung Cancer
4
MIRLET7E 19q13.41 LET7E, let-7e, MIRNLET7E, hsa-let-7e -MicroRNA let-7e and Lung Cancer
4
AGO2 8q24 Q10, EIF2C2 -EIF2C2 and Lung Cancer
4
AKAP12 6q24-q25 SSeCKS, AKAP250 -AKAP12 and Lung Cancer
4
GUSB 7q21.11 BG, MPS7 -GUSB and Lung Cancer
4
PPM1D 17q23.2 WIP1, PP2C-DELTA -PPM1D and Lung Cancer
4
IKBKE 1q32.1 IKKE, IKKI, IKK-E, IKK-i -IKBKE and Lung Cancer
4
MALL 2q13 BENE -MALL and Lung Cancer
4
CCL20 2q36.3 CKb4, LARC, ST38, MIP3A, Exodus, MIP-3a, SCYA20, MIP-3-alpha -CCL20 and Lung Cancer
4
SMAD6 15q22.31 AOVD2, MADH6, MADH7, HsT17432 -SMAD6 and Lung Cancer
4
LRP1B 2q21.2 LRPDIT, LRP-DIT -LRP1B and Lung Cancer
4
SERPINB2 18q21.3 PAI, PAI2, PAI-2, PLANH2, HsT1201 -SERPINB2 and Lung Cancer
4
DOK2 8p21.3 p56DOK, p56dok-2 -DOK2 and Lung Cancer
4
FGF9 13q11-q12 GAF, FGF-9, SYNS3, HBFG-9, HBGF-9 -FGF9 and Lung Cancer
4
CXCR1 2q35 C-C, CD128, CD181, CKR-1, IL8R1, IL8RA, CMKAR1, IL8RBA, CDw128a, C-C-CKR-1 -CXCR1 and Lung Cancer
4
HOXA4 7p15.2 HOX1, HOX1D -HOXA4 and Lung Cancer
4
SOX18 20q13.33 HLTS, HLTRS -SOX18 and Lung Cancer
4
NEK2 1q32.3 NLK1, RP67, NEK2A, HsPK21, PPP1R111 -NEK2 and Lung Cancer
4
MAPK14 6p21.3-p21.2 RK, p38, CSBP, EXIP, Mxi2, CSBP1, CSBP2, CSPB1, PRKM14, PRKM15, SAPK2A, p38ALPHA -MAPK14 and Lung Cancer
4
FOXC2 16q24.1 LD, MFH1, MFH-1, FKHL14 -FOXC2 and Lung Cancer
4
TACC3 4p16.3 ERIC1, ERIC-1 -TACC3 and Lung Cancer
4
PLAU 10q22.2 ATF, QPD, UPA, URK, u-PA, BDPLT5 -PLAU and Lung Cancer
4
CASP6 4q25 MCH2 -CASP6 and Lung Cancer
4
BMP6 6p24-p23 VGR, VGR1 -BMP6 and Lung Cancer
4
SERPINA1 14q32.1 PI, A1A, AAT, PI1, A1AT, PRO2275, alpha1AT -SERPINA1 and Lung Cancer
4
NFKBIA 14q13 IKBA, MAD-3, NFKBI -NFKBIA and Lung Cancer
4
CD151 11p15.5 GP27, MER2, RAPH, SFA1, PETA-3, TSPAN24 -CD151 and Lung Cancer
4
CCL21 9p13 ECL, SLC, CKb9, TCA4, 6Ckine, SCYA21 -CCL21 and Lung Cancer
4
VIPR1 3p22 II, HVR1, RDC1, V1RG, VIPR, VIRG, VAPC1, VPAC1, VPAC1R, VIP-R-1, VPCAP1R, PACAP-R2, PACAP-R-2 -VIPR1 and Lung Cancer
4
CCR1 3p21 CKR1, CD191, CKR-1, HM145, CMKBR1, MIP1aR, SCYAR1 -CCR1 and Lung Cancer
4
TP53I3 2p23.3 PIG3 -TP53I3 and Lung Cancer
4
CDH3 16q22.1 CDHP, HJMD, PCAD -CDH3 and Lung Cancer
4
MAGEB2 Xp21.3 DAM6, CT3.2, MAGE-XP-2 -MAGEB2 and Lung Cancer
4
MUC5B 11p15.5 MG1, MUC5, MUC9, MUC-5B -MUC5B and Lung Cancer
4
MED1 17q12 PBP, CRSP1, RB18A, TRIP2, PPARBP, CRSP200, DRIP205, DRIP230, PPARGBP, TRAP220 -MED1 and Lung Cancer
4
KIAA1524 3q13.13 p90, CIP2A -KIAA1524 and Lung Cancer
4
ASH1L 1q22 ASH1, KMT2H, ASH1L1 -ASH1L and Lung Cancer
4
SPINK1 5q32 TCP, PCTT, PSTI, TATI, Spink3 -SPINK1 and Lung Cancer
4
MIRLET7I 12q14.1 LET7I, let-7i, MIRNLET7I, hsa-let-7i -MicroRNA let-7i and Lung Cancer
4
ROCK1 18q11.1 ROCK-I, P160ROCK -ROCK1 and Lung Cancer
4
KLK10 19q13 NES1, PRSSL1 -KLK10 and Non-Small Cell Lung Cancer
4
FGF19 11q13.3 -FGF19 and Lung Cancer
4
DEC1 9q32 CTS9 -DEC1 and Lung Cancer
4
SSTR5 16p13.3 SS-5-R -SSTR5 and Lung Cancer
4
CD81 11p15.5 S5.7, CVID6, TAPA1, TSPAN28 -CD81 and Lung Cancer
4
TFRC 3q29 T9, TR, TFR, p90, CD71, TFR1, TRFR -TFRC and Lung Cancer
4
MIR107 10q23.31 MIRN107, miR-107 -MIRN107 microRNA, human and Lung Cancer
4
BCL2L11 2q13 BAM, BIM, BOD -BCL2L11 and Lung Cancer
4
LAMC2 1q25-q31 B2T, CSF, EBR2, BM600, EBR2A, LAMB2T, LAMNB2 -LAMC2 and Lung Cancer
4
NNAT 20q11.2-q12 Peg5 -NNAT and Lung Cancer
3
ROCK2 2p24 ROCK-II -ROCK2 and Lung Cancer
3
TGFBI 5q31 CSD, CDB1, CDG2, CSD1, CSD2, CSD3, EBMD, LCD1, BIGH3, CDGG1 -TGFBI and Lung Cancer
3
PPARGC1A 4p15.1 LEM6, PGC1, PGC1A, PGC-1v, PPARGC1, PGC-1(alpha) -PPARGC1A and Lung Cancer
3
LGALS4 19q13.2 GAL4, L36LBP -LGALS4 and Lung Cancer
3
OPCML 11q25 OPCM, OBCAM, IGLON1 -OPCML and Lung Cancer
3
IQGAP1 15q26.1 SAR1, p195, HUMORFA01 -IQGAP1 and Lung Cancer
3
TLE1 9q21.32 ESG, ESG1, GRG1 -TLE1 and Lung Cancer
3
PVT1 8q24 LINC00079, NCRNA00079, onco-lncRNA-100 -PVT1 and Lung Cancer
3
BCL2L2 14q11.2-q12 BCLW, BCL-W, PPP1R51, BCL2-L-2 -BCL2L2 and Lung Cancer
3
BAGE 21p11.1 not on ref BAGE1, CT2.1 -BAGE and Lung Cancer
3
RAP1GDS1 4q23-q25 GDS1, SmgGDS -RAP1GDS1 and Lung Cancer
3
LARS 5q32 LRS, LEUS, LFIS, ILFS1, LARS1, LEURS, PIG44, RNTLS, HSPC192, hr025Cl -LARS and Lung Cancer
3
DAB2IP 9q33.1-q33.3 AIP1, AIP-1, AF9Q34, DIP1/2 -DAB2IP and Lung Cancer
3
MT1G 16q13 MT1, MT1K -MT1G and Lung Cancer
3
MCM4 8q11.2 NKCD, CDC21, CDC54, NKGCD, hCdc21, P1-CDC21 -MCM4 and Lung Cancer
3
PLA2G2A 1p35 MOM1, PLA2, PLA2B, PLA2L, PLA2S, PLAS1, sPLA2 -PLA2G2A and Lung Cancer
3
RAD23B 9q31.2 P58, HR23B, HHR23B -RAD23B and Lung Cancer
3
ROR2 9q22 BDB, BDB1, NTRKR2 -ROR2 and Lung Cancer
3
ING2 4q35.1 ING1L, p33ING2 -ING2 and Lung Cancer
3
MEST 7q32 PEG1 -MEST and Lung Cancer
3
REV1 2q11.1-q11.2 REV1L -REV1 and Lung Cancer
3
SOX1 13q34 -SOX1 and Lung Cancer
3
SMPD1 11p15.4 ASM, NPD, ASMASE -SMPD1 and Lung Cancer
3
HOXD10 2q31.1 HOX4, HOX4D, HOX4E, Hox-4.4 -HOXD10 and Lung Cancer
3
GPX2 14q24.1 GPRP, GPx-2, GI-GPx, GPRP-2, GPx-GI, GSHPx-2, GSHPX-GI -GPX2 and Lung Cancer
3
CDK9 9q34.1 TAK, C-2k, CTK1, CDC2L4, PITALRE -CDK9 and Lung Cancer
3
U2AF1 21q22.3 RN, FP793, U2AF35, U2AFBP, RNU2AF1 -U2AF1 and Lung Cancer
3
RALB 2q14.2 -RALB and Lung Cancer
3
TRA 14q11.2 IMD7, TCRA, TCRD, TRA@, TRAC -TRA and Lung Cancer
3
SNRPE 1q32 SME, Sm-E, B-raf, HYPT11 -SNRPE and Lung Cancer
3
FGF10 5p13-p12 -FGF10 and Lung Cancer
3
PEA15 1q21.1 PED, MAT1, HMAT1, MAT1H, PEA-15, HUMMAT1H -PEA15 and Lung Cancer
3
HOXB7 17q21.3 HOX2, HOX2C, HHO.C1, Hox-2.3 -HOXB7 and Lung Cancer
3
PRDX6 1q25.1 PRX, p29, AOP2, 1-Cys, NSGPx, aiPLA2, HEL-S-128m -PRDX6 and Lung Cancer
3
PIAS3 1q21 ZMIZ5 -PIAS3 and Lung Cancer
3
KLK5 19q13.33 SCTE, KLKL2, KLK-L2 -KLK5 and Lung Cancer
3
CX3CR1 3p21.3 V28, CCRL1, GPR13, CMKDR1, GPRV28, CMKBRL1 -CX3CR1 and Lung Cancer
3
SKIL 3q26 SNO, SnoA, SnoI, SnoN -SKIL and Lung Cancer
3
CASP2 7q34-q35 ICH1, NEDD2, CASP-2, NEDD-2, PPP1R57 -CASP2 and Lung Cancer
3
LAPTM4B 8q22.1 LC27, LAPTM4beta -LAPTM4B and Lung Cancer
3
KLK14 19q13.3-q13.4 KLK-L6 -KLK14 and Lung Cancer
3
ROR1 1p31.3 NTRKR1, dJ537F10.1 -ROR1 and Lung Cancer
3
CTSD 11p15.5 CPSD, CLN10, HEL-S-130P -CTSD and Lung Cancer
3
CCNE2 8q22.1 CYCE2 -CCNE2 and Lung Cancer
3
UGT2B17 4q13 BMND12, UDPGT2B17 -UGT2B17 and Lung Cancer
3
CMBL 5p15.2 JS-1 -CMBL and Lung Cancer
3
SSTR3 22q13.1 SS3R, SS3-R, SS-3-R, SSR-28 -SSTR3 and Lung Cancer
3
SIRT3 11p15.5 SIR2L3 -SIRT3 and Lung Cancer
3
PGK1 Xq13.3 PGKA, MIG10, HEL-S-68p -PGK1 and Lung Cancer
3
DUSP4 8p12-p11 TYP, HVH2, MKP2, MKP-2 -DUSP4 and Lung Cancer
3
CLDN3 7q11.23 RVP1, HRVP1, C7orf1, CPE-R2, CPETR2 -CLDN3 and Lung Cancer
3
MYH9 22q13.1 MHA, FTNS, EPSTS, BDPLT6, DFNA17, NMMHCA, NMHC-II-A, NMMHC-IIA -MYH9 and Lung Cancer
3
TNFRSF1B 1p36.22 p75, TBPII, TNFBR, TNFR2, CD120b, TNFR1B, TNFR80, TNF-R75, p75TNFR, TNF-R-II -TNFRSF1B and Lung Cancer
3
POLB 8p11.2 -POLB and Lung Cancer
3
CLDN7 17p13.1 CLDN-7, CEPTRL2, CPETRL2, Hs.84359, claudin-1 -CLDN7 and Lung Cancer
3
HIP1 7q11.23 SHON, HIP-I, ILWEQ, SHONbeta, SHONgamma -HIP1 and Lung Cancer
3
PRKCDBP 11p15.4 SRBC, HSRBC, CAVIN3, cavin-3 -PRKCDBP and Lung Cancer
3
PBRM1 3p21 PB1, BAF180 -PBRM1 and Lung Cancer
3
TNFRSF10D 8p21 DCR2, CD264, TRUNDD, TRAILR4, TRAIL-R4 -TNFRSF10D and Lung Cancer
3
CASP5 11q22.3 ICH-3, ICEREL-III, ICE(rel)III -CASP5 and Lung Cancer
3
CUL4A 13q34 -CUL4A and Lung Cancer
3
TBX21 17q21.32 TBET, T-PET, T-bet, TBLYM -TBX21 and Lung Cancer
3
PRC1 15q26.1 ASE1 -PRC1 and Lung Cancer
3
CCL22 16q13 MDC, ABCD-1, SCYA22, STCP-1, DC/B-CK, A-152E5.1 -CCL22 and Lung Cancer
3
PTK7 6p21.1-p12.2 CCK4, CCK-4 -PTK7 and Lung Cancer
3
MTSS1 8p22 MIM, MIMA, MIMB -MTSS1 and Lung Cancer
3
BOLL 2q33 BOULE -BOLL and Lung Cancer
3
CCR6 6q27 BN-1, DCR2, DRY6, CCR-6, CD196, CKRL3, GPR29, CKR-L3, CMKBR6, GPRCY4, STRL22, CC-CKR-6, C-C CKR-6 -CCR6 and Lung Cancer
3
MAPKAPK2 1q32 MK2, MK-2, MAPKAP-K2 -MAPKAPK2 and Lung Cancer
3
IRF7 11p15.5 IMD39, IRF7A, IRF7B, IRF7C, IRF7H, IRF-7H -IRF7 and Lung Cancer
3
LZTS1 8p22 F37, FEZ1 -LZTS1 and Lung Cancer
3
SPDEF 6p21.3 PDEF, bA375E1.3 -SPDEF and Lung Cancer
3
GREM1 15q13.3 DRM, HMPS, MPSH, PIG2, CRAC1, CRCS4, DAND2, HMPS1, IHG-2, DUP15q, C15DUPq, GREMLIN, CKTSF1B1 -GREM1 and Lung Cancer
3
TNKS 8p23.1 TIN1, ARTD5, PARPL, TINF1, TNKS1, pART5, PARP5A, PARP-5a -TNKS and Lung Cancer
3
CXCL14 5q31 KEC, KS1, BMAC, BRAK, NJAC, MIP2G, MIP-2g, SCYB14 -CXCL14 and Lung Cancer
3
BAG3 10q25.2-q26.2 BIS, MFM6, BAG-3, CAIR-1 -BAG3 and Lung Cancer
3
MARS 12q13.3 MRS, ILLD, CMT2U, ILFS2, METRS, MTRNS, SPG70 -MARS and Lung Cancer
3
SLC7A5 16q24.3 E16, CD98, LAT1, 4F2LC, MPE16, hLAT1, D16S469E -SLC7A5 and Lung Cancer
3
TNFSF13 17p13.1 APRIL, CD256, TALL2, ZTNF2, TALL-2, TRDL-1, UNQ383/PRO715 -TNFSF13 and Lung Cancer
3
CAV2 7q31.1 CAV -CAV2 and Lung Cancer
3
S100A11 1q21 MLN70, S100C, HEL-S-43 -S100A11 and Lung Cancer
3
GJA1 6q22.31 HSS, CMDR, CX43, EKVP, GJAL, ODDD, AVSD3, HLHS1 -GJA1 and Lung Cancer
3
TLR7 Xp22.3 TLR7-like -TLR7 and Lung Cancer
2
GRASP 12q13.13 TAMALIN -GRASP and Lung Cancer
2
LIMK1 7q11.23 LIMK, LIMK-1 -LIMK1 and Lung Cancer
2
NR3C2 4q31.1 MR, MCR, MLR, NR3C2VIT -NR3C2 and Lung Cancer
2
FRAT1 10q24.1 -FRAT1 and Lung Cancer
2
S100A10 1q21 42C, P11, p10, GP11, ANX2L, CAL1L, CLP11, Ca[1], ANX2LG -S100A10 and Lung Cancer
2
SLC22A18 11p15.4 HET, ITM, BWR1A, IMPT1, TSSC5, ORCTL2, BWSCR1A, SLC22A1L, p45-BWR1A -SLC22A18 and Lung Cancer
2
DKC1 Xq28 DKC, CBF5, DKCX, NAP57, NOLA4, XAP101 -DKC1 and Lung Cancer
2
ADGRB1 8q24.3 BAI1, GDAIF -BAI1 and Lung Cancer
2
OCLN 5q13.1 BLCPMG, PPP1R115 -OCLN and Lung Cancer
2
LAMB3 1q32 AI1A, LAM5, LAMNB1, BM600-125KDA -LAMB3 and Lung Cancer
2
MIR1258 2q31.3 MIRN1258, mir-1258, hsa-mir-1258 -MicroRNA miR-1258 and Lung Cancer
2
GOPC 6q21 CAL, FIG, PIST, GOPC1, dJ94G16.2 -GOPC and Lung Cancer
2
RARRES3 11q12.3 RIG1, TIG3, HRSL4, HRASLS4, PLA1/2-3 -RARRES3 and Lung Cancer
2
AGTR2 Xq22-q23 AT2, ATGR2, MRX88 -AGTR2 and Lung Cancer
2
KLF5 13q22.1 CKLF, IKLF, BTEB2 -KLF5 and Lung Cancer
2
RAD17 5q13 CCYC, R24L, RAD24, HRAD17, RAD17SP -RAD17 and Lung Cancer
2
STC1 8p21.2 STC -STC1 and Lung Cancer
2
CD276 15q23-q24 B7H3, B7-H3, B7RP-2, 4Ig-B7-H3 -CD276 and Lung Cancer
2
LRP1 12q13.3 APR, LRP, A2MR, CD91, APOER, LRP1A, TGFBR5, IGFBP3R -LRP1 and Lung Cancer
2
HHIP 4q28-q32 HIP -HHIP and Lung Cancer
2
TXNRD1 12q23-q24.1 TR, TR1, TXNR, TRXR1, GRIM-12 -TXNRD1 and Lung Cancer
2
ATIC 2q35 PURH, AICAR, AICARFT, IMPCHASE, HEL-S-70p -ATIC and Lung Cancer
2
ARL11 13q14.2 ARLTS1 -ARL11 and Lung Cancer
2
DACH1 13q22 DACH -DACH1 and Lung Cancer
2
KPNA2 17q24.2 QIP2, RCH1, IPOA1, SRP1alpha -KPNA2 and Lung Cancer
2
GFRA1 10q26.11 GDNFR, RET1L, RETL1, TRNR1, GDNFRA, GFR-ALPHA-1 -GFRA1 and Lung Cancer
2
HTRA1 10q26.3 L56, HtrA, ARMD7, ORF480, PRSS11, CARASIL -HTRA1 and Lung Cancer
2
XRCC6 22q13.2 ML8, KU70, TLAA, CTC75, CTCBF, G22P1 -XRCC6 and Lung Cancer
2
EPHB3 3q27.1 ETK2, HEK2, TYRO6 -EPHB3 and Lung Cancer
2
KISS1R 19p13.3 HH8, CPPB1, GPR54, AXOR12, KISS-1R, HOT7T175 -KISS1R and Lung Cancer
2
ATP7A Xq21.1 MK, MNK, DSMAX, SMAX3 -ATP7A and Lung Cancer
2
SRPX Xp21.1 DRS, ETX1, SRPX1, HEL-S-83p -SRPX and Lung Cancer
2
LMO4 1p22.3 -LMO4 and Lung Cancer
2
PTGER4 5p13.1 EP4, EP4R -PTGER4 and Lung Cancer
2
GAGE1 Xp11.23 CT4.1, GAGE-1 -GAGE1 and Lung Cancer
2
NEFL 8p21 NFL, NF-L, NF68, CMT1F, CMT2E, PPP1R110 -NEFL and Lung Cancer
2
CDH17 8q22.1 HPT1, CDH16, HPT-1 -CDH17 and Lung Cancer
2
AKAP9 7q21-q22 LQT11, PRKA9, AKAP-9, CG-NAP, YOTIAO, AKAP350, AKAP450, PPP1R45, HYPERION, MU-RMS-40.16A -AKAP9 and Lung Cancer
2
POLI 18q21.1 RAD30B, RAD3OB -POLI and Lung Cancer
2
RRM2B 8q23.1 P53R2, MTDPS8A, MTDPS8B -RRM2B and Lung Cancer
2
SLPI 20q12 ALP, MPI, ALK1, BLPI, HUSI, WAP4, WFDC4, HUSI-I -SLPI and Lung Cancer
2
MYCL 1p34.2 LMYC, L-Myc, MYCL1, bHLHe38 -MYCL and Lung Cancer
2
PLAT 8p12 TPA, T-PA -PLAT and Lung Cancer
2
TPM4 19p13.12-p13.11 HEL-S-108 -TPM4 and Lung Cancer
2
CD3D 11q23.3 T3D, IMD19, CD3-DELTA -CD3D and Lung Cancer
2
LIMD1 3p21.3 -LIMD1 and Lung Cancer
2
RIN1 11q13.2 -RIN1 and Lung Cancer
2
SACS 13q12 SPAX6, ARSACS, DNAJC29, PPP1R138 -SACS and Lung Cancer
2
TPM1 15q22.1 CMH3, TMSA, CMD1Y, LVNC9, C15orf13, HTM-alpha -TPM1 and Lung Cancer
2
MAFG 17q25.3 hMAF -MAFG and Lung Cancer
2
CLTC 17q23.1 Hc, CHC, CHC17, CLH-17, CLTCL2 -CLTC and Lung Cancer
2
NOX1 Xq22 MOX1, NOH1, NOH-1, GP91-2 -NOX1 and Lung Cancer
2
KDM5A 12p11 RBP2, RBBP2, RBBP-2 -KDM5A and Lung Cancer
2
MMP8 11q22.2 HNC, CLG1, MMP-8, PMNL-CL -MMP8 and Lung Cancer
2
CCL17 16q13 TARC, ABCD-2, SCYA17, A-152E5.3 -CCL17 and Lung Cancer
2
IL24 1q32 C49A, FISP, MDA7, MOB5, ST16, IL10B -IL24 and Lung Cancer
2
MUC7 4q13.3 MG2 -MUC7 and Lung Cancer
2
STK4 20q11.2-q13.2 KRS2, MST1, YSK3, TIIAC -STK4 and Lung Cancer
2
ST5 11p15.4 HTS1, p126, DENND2B -ST5 and Lung Cancer
2
PPP1R3A 7q31.1 GM, PP1G, PPP1R3 -PPP1R3A and Lung Cancer
2
ALOX5 10q11.2 5-LO, 5LPG, LOG5, 5-LOX -ALOX5 and Lung Cancer
2
IL23R 1p31.3 -IL23R and Lung Cancer
2
HOXB3 17q21.3 HOX2, HOX2G, Hox-2.7 -HOXB3 and Lung Cancer
2
RCVRN 17p13.1 RCV1 -RCVRN and Lung Cancer
2
NEMF 14q22 NY-CO-1, SDCCAG1 -NEMF and Lung Cancer
2
ASAH1 8p22 AC, PHP, ASAH, PHP32, ACDase, SMAPME -ASAH1 and Lung Cancer
2
CBLB 3q13.11 Cbl-b, RNF56, Nbla00127 -CBLB and Lung Cancer
2
CXCL11 4q21.2 IP9, H174, IP-9, b-R1, I-TAC, SCYB11, SCYB9B -CXCL11 and Lung Cancer
2
PATZ1 22q12.2 ZSG, MAZR, PATZ, RIAZ, ZBTB19, ZNF278, dJ400N23 -PATZ1 and Lung Cancer
1
C2orf44 2p23.3 WDCP, PP384 -C2orf44 and Lung Cancer
1
PCSK7 11q23.3 LPC, PC7, PC8, SPC7 -PCSK7 and Lung Cancer
1
NTRK1 1q21-q22 MTC, TRK, TRK1, TRKA, Trk-A, p140-TrkA Translocation
-CD74-NTRK1 fusion in Lung Cancer
1
KMT2A 11q23.3 HRX, MLL, MLL1, TRX1, ALL-1, CXXC7, HTRX1, MLL1A, WDSTS -KMT2A and Lung Cancer
1
HERPUD1 16q13 SUP, HERP, Mif1 -HERPUD1 and Lung Cancer
1
GPHN 14q23.3 GPH, GEPH, HKPX1, GPHRYN, MOCODC -GPHN and Lung Cancer
1
IDO1 8p12-p11 IDO, INDO, IDO-1 -IDO1 and Lung Cancer
1
RXRG 1q22-q23 RXRC, NR2B3 -RXRG and Lung Cancer
1
VIPR2 7q36.3 VPAC2, VPAC2R, VIP-R-2, VPCAP2R, PACAP-R3, DUP7q36.3, PACAP-R-3, C16DUPq36.3 -VIPR2 and Lung Cancer
1
MIR1297 13 MIRN1297, mir-1297, hsa-mir-1297 -MicroRNA miR-1297 and Lung Cancer
1
MIR10B 2q31.1 MIRN10B, mir-10b, miRNA10B, hsa-mir-10b -MIR10B and Lung Cancer
1
CBLC 19q13.2 CBL-3, RNF57, CBL-SL -CBLC and Lung Cancer
1
CHCHD7 8q12.1 COX23 -CHCHD7 and Lung Cancer
1
ZNRF3 22q12.1 RNF203, BK747E2.3 -ZNRF3 and Lung Cancer
1
TNFRSF6B 20q13.3 M68, TR6, DCR3, M68E, DJ583P15.1.1 -TNFRSF6B Amplification in Lung Cancer
1
CEACAM3 19q13.2 CEA, CGM1, W264, W282, CD66D -CEACAM3 and Lung Cancer
1
BANP 16q24 BEND1, SMAR1, SMARBP1 -BANP and Lung Cancer
1
PLCD1 3p22-p21.3 NDNC3, PLC-III -PLCD1 and Lung Cancer
1
MIR1301 2 MIRN1301, mir-1301, hsa-mir-1301 -MicroRNA miR-1301 and Lung Cancer
1
ENDOU 12q13.1 P11, PP11, PRSS26 -ENDOU and Lung Cancer
1
TRD 14q11.2 TCRD, TRD@, TCRDV1 -TRD and Lung Cancer
1
CTNND1 11q12.1 CAS, p120, CTNND, P120CAS, P120CTN, p120(CAS), p120(CTN) -CTNND1 and Lung Cancer
1
ARHGAP26 5q31 GRAF, GRAF1, OPHN1L, OPHN1L1 -ARHGAP26 and Lung Cancer
1
GJB2 13q11-q12 HID, KID, PPK, CX26, DFNA3, DFNB1, NSRD1, DFNA3A, DFNB1A -GJB2 and Lung Cancer
1
MIR1271 5q35 MIRN1271, hsa-mir-1271 -MIRN1271 microRNA, human and Lung Cancer
1
MIR125A 19q13.41 MIRN125A, miRNA125A -MIR125A and Lung Cancer
1
PRIM1 12q13 p49 -PRIM1 and Lung Cancer
1
RXRB 6p21.3 NR2B2, DAUDI6, RCoR-1, H-2RIIBP -RXRB and Lung Cancer
1
LINC00632 Xq27.1 -RP1-177G6.2 and Lung Cancer
FRS2 12q15 SNT, SNT1, FRS2A, SNT-1, FRS2alpha -FRS2 and Lung Cancer
TUBE1 6q21 TUBE, dJ142L7.2 -TUBE1 and Lung Cancer

Note: list is not exhaustive. Number of papers are based on searches of PubMed (click on topic title for arbitrary criteria used).

Latest Publications

Deben C, Van den Bossche J, Van Der Steen N, et al.
Deep sequencing of the TP53 gene reveals a potential risk allele for non-small cell lung cancer and supports the negative prognostic value of TP53 variants.
Tumour Biol. 2017; 39(2):1010428317694327 [PubMed] Related Publications
The TP53 gene remains the most frequently altered gene in human cancer, of which variants are associated with cancer risk, therapy resistance, and poor prognosis in several tumor types. To determine the true prognostic value of TP53 variants in non-small cell lung cancer, this study conducted further research, particularly focusing on subtype and tumor stage. Therefore, we determined the TP53 status of 97 non-small cell lung cancer adenocarcinoma patients using next generation deep sequencing technology and defined the prognostic value of frequently occurring single nucleotide polymorphisms and mutations in the TP53 gene. Inactivating TP53 mutations acted as a predictor for both worse overall and progression-free survival in stage II-IV patients and patients treated with DNA-damaging (neo)adjuvant therapy. In stage I tumors, the Pro-allele of the TP53 R72P polymorphism acted as a predictor for worse overall survival. In addition, we detected the rare R213R (rs1800372, minor allele frequency: 0.0054) polymorphism in 7.2% of the patients and are the first to show the significant association with TP53 mutations in non-small cell lung cancer adenocarcinoma patients (p = 0.003). In conclusion, Our findings show an important role for TP53 variants as negative predictors for the outcome of non-small cell lung cancer adenocarcinoma patients, especially for TP53 inactivating mutations in advanced stage tumors treated with DNA-damaging agents, and provide the first evidence of the R213R G-allele as possible risk factor for non-small cell lung cancer.

Shi J, Yuan M, Wang ZD, et al.
Comprehensive profiling and quantitation of oncogenic mutations in non-small cell lung carcinoma using single-molecule amplification and re-sequencing technology.
Tumour Biol. 2017; 39(2):1010428317691413 [PubMed] Related Publications
The carcinogenesis of non-small cell lung carcinoma has been found to associate with activating and resistant mutations in the tyrosine kinase domain of specific oncogenes. Here, we assessed the type, frequency, and abundance of epithelial growth factor receptor, KRAS, BRAF, and ALK mutations in 154 non-small cell lung carcinoma specimens using single-molecule amplification and re-sequencing technology. We found that epithelial growth factor receptor mutations were the most prevalent (44.2%), followed by KRAS (18.8%), ALK (7.8%), and BRAF (5.8%) mutations. The type and abundance of the mutations in tumor specimens appeared to be heterogeneous. Thus, we conclude that identification of clinically significant oncogenic mutations may improve the classification of patients and provide valuable information for determination of the therapeutic strategies.

Okada T, Kurabayashi A, Akimitsu N, Furihata M
Expression of Cadherin-17 Promotes Metastasis in a Highly Bone Marrow Metastatic Murine Breast Cancer Model.
Biomed Res Int. 2017; 2017:8494286 [PubMed] Free Access to Full Article Related Publications
We previously established 4T1E/M3 highly bone marrow metastatic mouse breast cancer cells through in vivo selection of 4T1 cells. But while the incidence of bone marrow metastasis of 4T1E/M3 cells was high (~80%) when injected intravenously to mice, it was rather low (~20%) when injected subcutaneously. Therefore, using 4T1E/M3 cells, we carried out further in vitro and in vivo selection steps to establish FP10SC2 cells, which show a very high incidence of metastasis to lungs (100%) and spines (85%) after subcutaneous injection into mice. qRT-PCR and western bolt analysis revealed that cadherin-17 gene and protein expression were higher in FP10SC2 cells than in parental 4T1E/M3 cells. In addition, immunostaining revealed the presence of cadherin-17 at sites of bone marrow and lung metastasis after subcutaneous injection of FP10SC2 cells into mice. Suppressing cadherin-17 expression in FP10SC2 cells using RNAi dramatically decreased the cells' anchorage-independent growth and migration in vitro and their metastasis to lung and bone marrow in vivo. These findings suggest that cadherin-17 plays a crucial role in mediating breast cancer metastasis to bone marrow.

Takeda K, Yamasaki A, Igishi T, et al.
Frequency of Epidermal Growth Factor Receptor Mutation in Smokers with Lung Cancer Without Pulmonary Emphysema.
Anticancer Res. 2017; 37(2):765-771 [PubMed] Related Publications
BACKGROUND: Chronic obstructive pulmonary disease is a smoking-related disease, and is categorized into the emphysema and airway dominant phenotypes. We examined the relationship between emphysematous changes and epidermal growth factor receptor (EGFR) mutation status in patients with lung adenocarcinoma.
PATIENTS AND METHODS: The medical records for 250 patients with lung adenocarcinoma were retrospectively reviewed. All patients were categorized into the emphysema or non-emphysema group.
RESULTS: Wild-type EGFR was detected in 136 (54%) and mutant EGFR in 48 (19%). Emphysematous changes were observed in 87 (36%) patients. EGFR mutation was highly frequent in the non-emphysema group (p=0.0014). Multivariate logistic regression analysis showed that emphysema was an independent risk factor for reduced frequency of EGFR mutation (Odds Ratio=3.47, p=0.005).
CONCLUSION: Our data showed a relationship between emphysematous changes and EGFR mutation status. There might be mutually exclusive genetic risk factors for carcinogenesis and development of emphysematous changes.

Naykoo NA, Dil-Afroze, Rasool R, et al.
Single nucleotide polymorphisms, haplotype association and tumour expression of the vascular endothelial growth factor (VEGF) gene with lung carcinoma.
Gene. 2017; 608:95-102 [PubMed] Related Publications
VEGF contains several polymorphic sites known to influence its expression. We examined the possible association between+405(-634)C>G,+936C>T,-2578C>A and lung cancer in 199 Kashmiri patients and 401 healthy controls. VEGF+405CG,+936CT+TT and-2578CA genotypes were significantly associated with lung cancer risk compared to VEGF+405CC,+936CC and-2578AA+CC genotypes [OR=0.07 (0.04-0.13), P<0.0001, OR=0.36 (0.25-0.52), P<0.0001 and 0.08 (0.05-0.13), P<0.0001]. Haplotype analysis revealed that CGA and TGA haplotypes of VEGF gene conveys the risk for lung cancer [OR=0.18 (0.10-0.33), P<0.0001 and 0.07 (0.03-0.13), P<0.0001]. VEGF expression revealed non-significant association with the genotypes of the three SNPs. In conclusion, the SNPs examined appear to influence lung cancer susceptibility while as genotypes of the SNPs don't appear to have significant association with VEGF mRNA expression in lung tumours.

Hao Y, Yang X, Zhang D, et al.
Long noncoding RNA LINC01186, regulated by TGF-β/SMAD3, inhibits migration and invasion through Epithelial-Mesenchymal-Transition in lung cancer.
Gene. 2017; 608:1-12 [PubMed] Related Publications
Accumulating evidence suggests that long noncoding RNAs (lncRNAs) are crucial regulators of the Epithelial-Mesenchymal-Transition (EMT). TGF-β signaling is a major inducer of EMT and can facilitate lung cancer metastasis. However, the role of lncRNAs in this process remains largely unknown. Here, we have identified 291 lncRNAs which were differentially expressed in lung cancer tissues compared with adjacent normal tissues. Of these, the gene body or vicinity of 19 transcripts were also bound by SMAD3. The expression of LINC01186 was significantly decreased in A549 cells treated with TGF-β1. Furthermore, LINC01186 was stably down-regulated in lung cancer tissues compared with normal tissues in TCGA data sets and another published lung cancer data sets. The bioinformatics analysis suggested that LINC01186 was associated with TGF-β and might participate in EMT process. Moreover, knocking-down LINC01186 promoted cell migration and invasion, whereas, LINC01186 overexpression prevented cell metastasis. Importantly, LINC01186 expression was regulated by SMAD3. And LINC01186 affected several EMT markers expression. These findings suggest that LINC01186, a mediator of TGF-β signaling, can play a significant role in the regulation of EMT and lung cancer cell migration and invasion.

Matikas A, Mistriotis D, Georgoulias V, Kotsakis A
Targeting KRAS mutated non-small cell lung cancer: A history of failures and a future of hope for a diverse entity.
Crit Rev Oncol Hematol. 2017; 110:1-12 [PubMed] Related Publications
Lung cancer remains the leading cause of cancer-related deaths in both men and women. However, the discovery of several oncogenic driver mutations and the development of immune checkpoint inhibitors resulted in improved clinical outcomes for most patients. Although activating KRAS mutations are the most common recurring molecular events in lung adenocarcinoma, little progress has been made during the past decades with no new agents being approved for this indication. The elucidation of the underlying biology of this diverse patient subgroup offers great potential and renewed hope regarding the rational development, rigorous evaluation and subsequent approval of novel targeted agents and combinations which will effectively suppress compensatory escape routes and the emergence of resistance, issues that have plagued previous attempts. Here, we review in a structured manner all aspects of KRAS positive non-small cell lung cancer, including the molecular biology, clinicopathologic characteristics, the prognostic and predictive value of KRAS mutations, as well as previous and contemporary approaches towards the treatment of this elusive target.

Zhao Z, Wang J, Wang S, et al.
LncRNA CCAT2 promotes tumorigenesis by over-expressed Pokemon in non-small cell lung cancer.
Biomed Pharmacother. 2017; 87:692-697 [PubMed] Related Publications
BACKGROUND: Non-small cell lung cancer (NSCLC) remains one of the most important death-related diseases, with poor effective diagnosis and less therapeutic biomarkers. LncRNA colon cancer-associated transcript 2 (CCAT2) was identified as an oncogenic lncRNA and over-expressed in many tumor cells. The aims of this study were to detect the correlation between CCAT2 and its regulatory genes and then explore the potential mechanism between them in NSCLC.
METHODS: In this study, qRT-PCR was used to detect CCAT2, Pokemon and p21 expression. Western-blot was used to detect protein levels of Pokemon and p21. CCK-8 assay and Transwell chambers were used to assess cell viability and invasion.
RESULTS: CCAT2 and Pokemon were over-expressed in NSCLC tissue and cells. In NSCLC cells, CCAT2 knockdown significantly decreased cell viability and invasion as well as Pokemon expression, but increased the expression of p21; then CCAT2 overexpression revealed an opposite result. In addition, over-expressed Pokemon reversed the results that induced by si-CCAT2, while down-regulation of Pokemon significantly reversed the results that induced by CCAT2 overexpression.
CONCLUSION: The results indicated that CCAT2 promotes tumorigenesis by over-expression of Pokemon, and the potential mechanism might relate to the Pokemon related gene p21.

Ma P, Zhang M, Nie F, et al.
Transcriptome analysis of EGFR tyrosine kinase inhibitors resistance associated long noncoding RNA in non-small cell lung cancer.
Biomed Pharmacother. 2017; 87:20-26 [PubMed] Related Publications
The non-small cell lung cancer (NSCLC) patients harbor mutations in the epidermal growth factor receptor (EGFR) can be therapeutically targeted by EGFR tyrosine kinase inhibitors (EGFR-TKI), such as gefitinib, and show improved progression-free survival. However, most of the patients who are initially responsive to EGFR TKIs with activating EGFR mutations eventually develop acquired resistance after long-term therapy, and are followed by disease progression. Recently, diverse mechanisms of acquired EGFR TKI resistance have been reported, but little is known about the role of long noncoding RNAs in EGFR TKIs resistance. To gain insight into the expression pattern and potential function of lncRNAs in NSCLC cells EGFR-TKI resistance, we analyzed expression patterns in EGFR-TKIs-resistant cell lines and compared it with their parental sensitive cell line by using gene profiling datasets from Gene Expression Omnibus (GEO). Then, the expression levels of five chose lncRNAs were validated in PC9-gefitinib resistant cells (PC9G) and sensitive cells by using real-time quantitative PCR (qPCR). Among of these five lncRNAs, CASC9 expression was upregulated in PC9G and knockdown of its expression could increase the sensitivity of PC9G cells to gefitinib, while EWAST1 (LINC00227) is downregulated in PC9G cells and overexpressed EWAST1 also lead to increased sensitivity of PC9G cells to gefitinib. As indicated by GO analysis, the CASC9 and EWAST1 co-expressed genes are involved in several important pathways including regulation of cell growth, regulation of cell apoptosis and Chromatin assembly. Taken together, dysregulated lncRNAs play critical roles in EGFR-TKIs resistant NSCLC cells and might be used as novel potential targets to reverse EGFR-TKI resistance for NSCLC patients.

Herpel E, Rieker RJ, Dienemann H, et al.
SMARCA4 and SMARCA2 deficiency in non-small cell lung cancer: immunohistochemical survey of 316 consecutive specimens.
Ann Diagn Pathol. 2017; 26:47-51 [PubMed] Related Publications
The chromatin remodeling switch sucrose nonfermentable (SWI/SNF) complex has been increasingly implicated in the pathogenesis and dedifferentiation of neoplasms from several organs with prognostic and potential therapeutic implications. We herein investigated the expression of the SWI/SNF complex catalytic subunits SMARCA4 (BRG1) and SMARCA2 (BRM) in 316 consecutive non-small cell lung cancer (NSCLC) specimens on tissue microarrays (171 adenocarcinomas [ADCAs], 130 squamous cell carcinomas [SCCs], 9 adenosquamous carcinomas, and 6 large cell carcinomas) excluding undifferentiated/giant cell or rhabdoid carcinomas. Complete loss of SMARCA4 was observed in 8 (5.5%) of 146 evaluable pulmonary ADCAs and 6 (5.2%) of 115 evaluable pulmonary SCCs, whereas 9 (6.4%) of 140 ADCAs and 2 (1.7%) of 117 SCCs showed SMARCA2 loss. Two of 6 large cell carcinomas were SMARCA2 deficient. Concurrent loss of both markers was observed in 4 cases (2 ADCAs and 2 SCCs). Of 15 ADCAs with loss of either or both markers, 12 (80%) were TTF1 negative. In conclusion, SMARCA4 and SMARCA2 deficiency is observed in 5.1% and 4.8% of NSCLC, respectively. SMARCB1 expression was intact in all cases. The presence of differentiated histology (glandular or squamous) is a novel aspect among SWI/SNF-deficient carcinomas which in other organs generally are associated with undifferentiated/rhabdoid morphology. The predominance of TTF1 negativity among SWI/SNF-deficient pulmonary ADCA (80%) underlines the need to include these 2 markers in the evaluation of TTF1-negative ADCA of putative pulmonary origin. Given the recently documented potential of SMARCA4 loss as a predictor of chemosensitivity to platinum-based chemotherapy in NSCLC, recognition of the clinicopathological features of SMARCA4-deficient NSCLC in routine surgical pathology practice is recommended.

Liu Y, Wang F, Xu P
miR-590 accelerates lung adenocarcinoma migration and invasion through directly suppressing functional target OLFM4.
Biomed Pharmacother. 2017; 86:466-474 [PubMed] Related Publications
MicroRNA-590 (miR-590) shows oncogenic functions in various tumor types, but little is known about biological functions of miR-590 in lung adenocarcinoma. In this study, we observe that miR-590 is not only overexpressed in lung adenocarcinoma tissues and metastatic lymph nodes, but also significantly increased in lung adenocarcinoma cell lines. Moreover, gain-of-function and loss-of-function studies show miR-590 serve as a tumor suppressor regulating lung adenocarcinoma cells migration and invasion. Furthermore, OLFM4 is proved to as a functional target for miR-590 to regulate lung adenocarcinoma cells migration and invasion. In conclusion, miR-590 regulates lung adenocarcinoma metastasis through directly modulating functional target OLFM4.

Balestro E, Baraldo S, Piloni D, Stella GM
Lung tumors, COPD and immune response: is epigenetics the bottom line?
Minerva Med. 2016; 107(6 Suppl 1):1-8 [PubMed] Related Publications
NSCLC is a heterogeneous disorder consisting of distinct molecular subtypes which can be treated by using specific drugs targeted to distinct genetic lesions. It is well known that NSCLS incidence is higher in chronic obstructive pulmonary disease (COPD) patients because they share a common risk factor (cigarette smoking) and it is believed that the typical inflammatory microenvironment observed in COPD may influence the molecular mechanisms responsible of carcinogenesis. In the last years, the role of epigenetic processes in cell biology and tissue pathology has been extensively studied both in COPD and NSCLC. The recent paper by Wauters et al. showed a specific pattern of driver mutations and molecular features in NSCLC raising in the context of COPD. All these findings have shown for the first time that lung tumors found in COPD patients differ from those observed in patient without COPD due to the presence of a specific tumor microenvironment which is characterized by reduced CD4+ Treg cells. On this basis, the present work aims at discussing and analyzing the context-specific mechanisms of clonal selection and evolution mainly focusing on the epigenetic alterations and at pointing out the potential therapeutic implications.

Chen T, Ren H, Thakur A, et al.
miR-382 inhibits tumor progression by targeting SETD8 in non-small cell lung cancer.
Biomed Pharmacother. 2017; 86:248-253 [PubMed] Related Publications
Previous studies showed that miR-382 plays important roles in several types of cancers. Nevertheless, its expression and function in non-small cell lung cancer (NSCLC) remains largely unknown. In this study, we found that miR-382 expression was evidently downregulated in NSCLC tissue and cell lines in comparison with the adjacent normal tissues and human bronchial epithelial cell line (16HBE). Moreover, the expression levels of miR-382 were significantly associated with last-stage and tumor metastasis in NSCLC patients. In addition, exogenous miR-382 evidently inhibited NSCLC cell proliferation, migration and invasion in vitro. We also revealed SETD8 as a direct target of miR-382 in NSCLC, and restored SETD8 partially reversed the negative effects miR-382 on NSCLC cells. In total, our study demonstrated that miR-382 dysregulated in NSCLC and involved in NSCLC tumorigenesis and metastasis by suppressing SETD8 expression, which may help to identify effective therapies for NSCLC treatment.

Gan WY, Li HM, Zhang YG, et al.
Association between IL18-607C/A and -137G/C polymorphisms and susceptibility to non-small cell lung cancer in a Chinese population.
Genet Mol Res. 2016; 15(4) [PubMed] Related Publications
Lung cancer is one of the main causes of cancer-related mortality in males and females worldwide. A pleiotropic effect has been observed in the interleukin 18 gene (IL18); its effects include the activation of natural killer cell cytotoxicity and the promotion of the Th1 immune response through the alteration of the expression of interferon-γ and TNF-α in humans. IL18 is therefore involved in the elimination of tumor cells in the human body. We recruited 357 patients with non-small cell lung cancer (NSCLC) and 414 controls to evaluate the correlation between two genetic variations (IL18-607C/A and IL18-137G/C) and the pathogenesis of NSCLC. We used polymerase chain reaction-restriction fragment length polymorphism to genotype IL18-607C/A and IL18-137G/C. Statistical analysis revealed that individuals harboring the AA genotype of IL18-607C/A had an increased risk of NSCLC compared to those harboring the CC genotype (OR = 2.20, 95%CI = 1.30-3.74). Individuals expressing the A allele of IL18-607C/A had an elevated risk of developing NSCLC compared to those expressing the C allele (OR = 1.31, 95%CI = 1.06-1.62). In summary, our analysis shows that the IL18-607C/A genetic variation is related to the risk of NSCLC, whereas the IL18-137G/C variation is not. Therefore, the IL18-607C/A variation is related to the pathogenesis of NSCLC in the Chinese population studied.

Zheng Y, Li X, Jiang Y, et al.
Promoter hypermethylation of Wnt inhibitory factor-1 in patients with lung cancer: A systematic meta-analysis.
Medicine (Baltimore). 2016; 95(49):e5433 [PubMed] Free Access to Full Article Related Publications
BACKGROUND: Promoter hypermethylation of Wnt inhibitory factor-1 (WIF-1)-a tumor suppressor gene-has been detected in several types of human tumors. However, the association between WIF-1 promoter hypermethylation and lung cancer remains to be elucidated. Therefore, we conducted this study to evaluate the clinical significance of WIF-1 promoter hypermethylation in lung cancer.
METHODS: A comprehensive literature search was conducted to obtain eligible studies. The combined odds ratios (ORs) or hazard ratios and 95% confidence intervals were used to estimate the strength of associations.
RESULTS: A total of 8 eligible publications with 626 cases and 512 controls were included in our study. The combined ORs revealed that WIF-1 promoter hypermethylation was significantly higher in lung cancer than in controls (OR 10.53, P < 0.001). Moreover, WIF-1 promoter hypermethylation was significantly associated with smoking behavior (OR 1.88, P = 0.002). No significant correlation was found between WIF-1 promoter hypermethylation and sex status, age status, tumor stage, and pathological types in cancer. Multivariate analysis results indicated the absence of correlation between WIF-1 promoter hypermethylation and with relapse-free survival and overall survival. Subgroup analysis by sample type demonstrated that promoter hypermethylation of WIF-1 was significantly associated with an increased risk of lung cancer in the tissue (OR 7.89, P < 0.001), blood (OR 21.83, P = 0.034), and pleural effusion subgroups (OR 157.43, P = 0.001).
CONCLUSIONS: Promoter hypermethylation of WIF-1 may play a crucial role in lung cancer carcinogenesis. It may be a noninvasive biomarker using blood or pleural effusion detection. WIF-1 promoter hypermethylation is correlated with smoking behavior, but not with sex status, age status, tumor stage, pathological types, and the prognosis of lung cancer patients in terms of relapse-free survival and overall survival. More investigations, including a larger number of subjects, are required to further confirm the findings of our analysis.

Isla D, Felip E, Viñolas N, et al.
Lung Cancer in Women with a Family History of Cancer: The Spanish Female-specific Database WORLD07.
Anticancer Res. 2016; 36(12):6647-6653 [PubMed] Related Publications
BACKGROUND: The WORLD07 project is a female-specific database to prospectively analyze the characteristics of Spanish women with lung cancer.
PATIENTS AND METHODS: We analyzed and compared lung cancer features in women with and without a family history of cancer/lung cancer.
RESULTS: Two thousand and sixty women were included: 876 had a family history of cancer (lung cancer, 34%) and 886 did not, with no significant differences between groups, except for smoking status (p=0.036). We found statistically significant correlations between epidermal growth factor receptor (EGFR) mutation and smoking status in patients with a family history of cancer (r=-0.211; p<0.001) and lung cancer (r=-0.176; p<0.001). Longer median overall survival was observed in women with a family history of cancer and lung cancer.
CONCLUSION: Among Spanish women with lung cancer, a greater proportion were current smokers in those with a family history of cancer/lung cancer. There was a significant correlation between the presence of EGFR mutation and smoking.

Ozbayer C, Degirmenci I, Ustuner D, et al.
miRSNPs of miR1274 and miR3202 Genes that Target MeCP2 and DNMT3b Are Associated with Lung Cancer Risk: A Study Conducted on MassARRAY Genotyping.
J Environ Pathol Toxicol Oncol. 2016; 35(3):223-236 [PubMed] Related Publications
Genetic variants of miRNAs that target DNMTs and MBDs involved in DNA methylation were scanned with current databases, and 35 miRSNPs in 22 miRNA genes were identified. The aim of the study was to determine the association between these variants of miRNA genes and lung cancer (LC). DNA samples were isolated from blood samples and genotyped using a Sequenom MassARRAY System. An association between the rs188912830 gene variant of miR3202 that targets the MeCP2 protein and LC was indicated in both subtypes. The presence of the C-allele in patients with LC and its subtypes was significantly lower, and the absence of the C-allele was determined to increase the risk of LC by 7,429-times compared to the presence (p=0,010). The rs318039 gene variant of miR1274 that targets DNMT3b was found to be associated with LC subtypes. When allele distributions were compared, the numbers of individuals with the C-allele were significantly lower in the NSCLC and SCLC groups. No significant associations were found for the rs72563729 variant of the miR200b gene that targets DNMT3a or for the rs145416750 variant of the miR513c gene that targets TRDMT1. The other 33 variants were found to be ancestral genotypes. Consequently, rs188912830 and rs318039 variations were associated with LC subtypes. Importantly, this study is the first to indicate the functional characterisation of miRSNPs of genes that target DNA methylation.

Vanni I, Coco S, Bonfiglio S, et al.
Whole exome sequencing of independent lung adenocarcinoma, lung squamous cell carcinoma, and malignant peritoneal mesothelioma: A case report.
Medicine (Baltimore). 2016; 95(48):e5447 [PubMed] Free Access to Full Article Related Publications
The presence of multiple primary tumors (MPT) in a single patient has been identified with an increasing frequency. A critical issue is to establish if the second tumor represents an independent primary cancer or a metastasis. Therefore, the assessment of MPT clonal origin might help understand the disease behavior and improve the management/prognosis of the patient.Herein, we report a 73-year-old male smoker who developed 2 primary lung cancers (adenocarcinoma and squamous cell carcinoma) and a malignant peritoneal mesothelioma (PM).Whole exome sequencing (WES) of the 3 tumors and of germline DNA was performed to determine the clonal origin and identify genetic cancer susceptibility.Both lung cancers were characterized by a high mutational rate with distinct mutational profiles and activation of tumor-specific pathways. Conversely, the PM harbored a relative low number of genetic variants and a novel mutation in the WT1 gene that might be involved in the carcinogenesis of nonasbestos-related mesothelioma. Finally, WES of the germinal DNA displayed several single nucleotide polymorphisms in DNA repair genes likely conferring higher cancer susceptibility.Overall, WES did not disclose any somatic genetic variant shared across the 3 tumors, suggesting their clonal independency; however, the carcinogenic effect of smoke combined with a deficiency in DNA repair genes and the patient advanced age might have been responsible for the MPT development. This case highlights the WES importance to define the clonal origin of MPT and susceptibility to cancer.

Yoshida K, Kono T
[Lung Cancer].
Gan To Kagaku Ryoho. 2016; 43(11):1321-1325 [PubMed] Related Publications
Personalized lung cancer therapy has progressed by targeting several oncogenic aberrations that drive lung carcinogenesis. Recent advances in gene analysis technologies, including next-generation sequencing that yields large amounts of genomic data, have greatly contributed to this progress. In addition, immune checkpoint blockade therapy has become available in Japan, and extensive searches for biomarkers predictive of therapeutic response have been carried out. "Clinical sequencing" which analyzes aberrations in a set of therapy-related genes in patient cancer specimens, has been actively conducted in Japan and other countries. This will help to establish more efficient and effective precision cancer medicine based on gene information. Herein, we summarize the recent progress in personalized lung cancer therapy research, including clinical sequencing.

Liu Y, Xing Z, Zhan P, et al.
Is it feasible to detect epidermal growth factor receptor mutations in circulating tumor cells in nonsmall cell lung cancer?: A meta-analysis.
Medicine (Baltimore). 2016; 95(47):e5115 [PubMed] Free Access to Full Article Related Publications
BACKGROUND: The value of circulating tumor cells (CTCs) in detecting epidermal growth factor receptor (EGFR) mutations in patients with nonsmall cell lung cancer (NSCLC) is controversial. We performed a meta-analysis to investigate the diagnostic significance of CTCs with tumor tissues as the standard control.
METHODS: A systematic literature search, including papers published until November 26, 2015, was performed using PubMed, Medline, Embase, Web of Science, and the China National Knowledge Infrastructure, and the references of retrieved articles were screened. The pooled sensitivity, specificity, and diagnostic odds ratio (DOR) were calculated according to the data selection from the included studies. The evaluation indexes of the diagnostic performance were the summary receiver operating characteristic curve (SROC) and area under the SROC (AUSROC).
RESULTS: Eight eligible articles with a total of 170 participants were identified in our meta-analysis. The pooled sensitivity and specificity were 0.91 [95% CI: 0.55-0.99] and 0.99 [95% CI: 0.59-1.00]. The positive likelihood ratio and negative likelihood ratio were 68 [95% CI: 1.4-3364] and 0.09 [95% CI: 0.01-0.64], respectively. The DOR was 788 [95% CI: 9-71884]. The high diagnostic performance of CTCs in detecting EGFR mutations was indicated by the AUSROC of 0.99 [95% CI: 0.98-1.00].
CONCLUSIONS: CTCs are a feasible and highly specific biomarker for detecting the EGFR mutation status in NSCLC patients.

Wang ZH, Li Z, Hu M, et al.
Ovol2 gene inhibits the Epithelial-to-Mesenchymal Transition in lung adenocarcinoma by transcriptionally repressing Twist1.
Gene. 2017; 600:1-8 [PubMed] Related Publications
BACKGROUND: Associated with recent achievements in therapy for advanced lung adenocarcinoma, there will still be an unmet medical need for effective treatment of stage IIIb/IV, and the prognosis of lung cancer is not optimistic till now.
OBJECTIVE: In order to obtain some essential evidences for a potential targeted therapy in lung adenocarcinoma, the effects of Ovol2 gene on Epithelial-to-Mesenchymal Transition (EMT) was observed and the probable mechanisms were analyzed.
METHODS: Ovol2 expression was previously evaluated by immunochemistry in lung adenocarcinoma tissue, and Ovol2 was overexpressed by lentivirus infection in A549 cells. Subsequently, the migration and invasion ability of A549 cells was tested by Transwell and Wound healing experiments. The mRNA level of genes correlated to EMT was detected by Real-time PCR, and the expression of reasonable makers was probed by Western Blot. Finally, rescue experiment, Luciferase assay, and chromatin immunoprecipitation assay were performed to explore the probable mechanisms.
RESULTS: After treated with Ovol2 overexpression, the expression level of E-cadherin was increased, while the expression level of Vimentin and Twist1 was declined not only in the mRNA level but also in the protein level. Moreover, we found that Ovol2 represses transcription of Twist1 by binding to its promoter directly. Wound healing and Transwell assays indicate that the migration and invasion ability were downregulated by Ovol2 in A549 cells.
CONCLUSION: Ovol2 can suppress migration and invasion ability of A549 cells, and prevent EMT by inhibition of Twist1 transcription directly.

Chang H, Sung JH, Moon SU, et al.
EGF Induced RET Inhibitor Resistance in CCDC6-RET Lung Cancer Cells.
Yonsei Med J. 2017; 58(1):9-18 [PubMed] Free Access to Full Article Related Publications
PURPOSE: Rearrangement of the proto-oncogene rearranged during transfection (RET) has been newly identified potential driver mutation in lung adenocarcinoma. Clinically available tyrosine kinase inhibitors (TKIs) target RET kinase activity, which suggests that patients with RET fusion genes may be treatable with a kinase inhibitor. Nevertheless, the mechanisms of resistance to these agents remain largely unknown. Thus, the present study aimed to determine whether epidermal growth factor (EGF) and hepatocyte growth factor (HGF) trigger RET inhibitor resistance in LC-2/ad cells with CCDC6-RET fusion genes.
MATERIALS AND METHODS: The effects of EGF and HGF on the susceptibility of a CCDC6-RET lung cancer cell line to RET inhibitors (sunitinib, E7080, vandetanib, and sorafenib) were examined.
RESULTS: CCDC6-RET lung cancer cells were highly sensitive to RET inhibitors. EGF activated epidermal growth factor receptor (EGFR) and triggered resistance to sunitinib, E7080, vandetanib, and sorafenib by transducing bypass survival signaling through ERK and AKT. Reversible EGFR-TKI (gefitinib) resensitized cancer cells to RET inhibitors, even in the presence of EGF. Endothelial cells, which are known to produce EGF, decreased the sensitivity of CCDC6-RET lung cancer cells to RET inhibitors, an effect that was inhibited by EGFR small interfering RNA (siRNA), anti-EGFR antibody (cetuximab), and EGFR-TKI (Iressa). HGF had relatively little effect on the sensitivity to RET inhibitors.
CONCLUSION: EGF could trigger resistance to RET inhibition in CCDC6-RET lung cancer cells, and endothelial cells may confer resistance to RET inhibitors by EGF. E7080 and other RET inhibitors may provide therapeutic benefits in the treatment of RET-positive lung cancer patients.

Luo Y, Tong L, Meng H, et al.
MiR-335 regulates the chemo-radioresistance of small cell lung cancer cells by targeting PARP-1.
Gene. 2017; 600:9-15 [PubMed] Related Publications
The role of miR-335 in the regulation of chemosensitivity and radiosensitivity of small cell lung cancer (SCLC) was investigated. miR-335 was significantly downregulated in multi-drug-resistant SCLC H69AR and H446DDP cells compared with parental cells as detected by qRT-PCR. Then, we demonstrated the negative correlation between miR-335 expression and the chemo-radiosensitivity of SCLC cells, including cell proliferation, cell clonality and cell apoptosis. In addition, miR-335 overexpression inhibited cell migration in vitro and tumor growth in vivo, whereas inhibition of miR-335 promoted cell migration and tumor growth. The underlying mechanism was further studied. Poly [ADP-ribose] polymerase 1 (PARP-1) was identified as a direct target gene of miR-335 in SCLC by bioinformatics analysis and validated via luciferase reporter assay. Overexpression of miR-335 decreased the expression of PARP-1 mRNA and protein, and NF-κB protein levels were correspondingly downregulated, thus regulating the chemo-radiosensitivity of SCLC. Taken together, these findings indicate that miR-335 may serve as a critical regulator of chemo-radiotherapy resistance in SCLC and a new potential therapeutic target.

Volckmar AL, Endris V, Bozorgmehr F, et al.
Next-generation sequencing facilitates detection of the classic E13-A20 EML4-ALK fusion in an ALK-FISH/IHC inconclusive biopsy of a stage IV lung cancer patient: a case report.
Diagn Pathol. 2016; 11(1):133 [PubMed] Free Access to Full Article Related Publications
BACKGROUND: Inhibition of the oncogenic fusion-gene EML4-ALK is a current first-line approach for patients with stage IV non-small cell lung cancer. While FISH was established as the gold standard for identifying these patients, there is accumulating evidence that other methods of detection, i.e., immunohistochemistry and next-generation sequencing (NGS), exist that may be equally successful. However, the concordance of these methods is under investigation.
CASE PRESENTATION: Adding to the current literature, we here report a 56 year old female never-smoker with stage IV lung adenocarcinoma whose biopsy was IHC and FISH inconclusive but positive in NGS. Retroactive profiling of the resection specimen corroborated fusion reads obtained by NGS, FISH-positivity and showed weak ALK-positivity by IHC. Consequently, we diagnosed the case as ALK-positive rendering the patient eligible to crizotinib treatment.
CONCLUSIONS: With IHC on biopsy material only, this case would have been overlooked withholding effective therapy.

Ma H, Liu B, Wang S, Liu J
MicroRNA-383 is a tumor suppressor in human lung cancer by targeting endothelial PAS domain-containing protein 1.
Cell Biochem Funct. 2016; 34(8):613-619 [PubMed] Related Publications
Lung cancer is the deadliest of all human cancers worldwide. The role of microRNA (miR)-383 has been controversial in the initiation and progression of different cancers. We aimed to investigate the function of miR-383 in human lung cancer both in vitro and in vivo. MicroRNA-383 levels were analyzed in noncancerous versus cancerous human lung tissues and in normal versus lung cancer cell lines. Effect of miR-383 on cell migration and invasion was examined in vitro and on tumor growth by using a xenograft mouse model in vivo. Potential mRNA target of miR-383 was predicted, and underlying mechanism was explored as well. MicroRNA-383 was downregulated in lung cancer tissue and cell lines. Expression of miR-383 inhibited migration and invasion of human lung cancer cell lines in vitro and tumorigenesis of lung cancer xenografts in vivo. MicroRNA-383 directly targeted 3' untranslated region of endothelial PAS domain-containing protein 1 (EPAS1) messenger RNA and inhibited both its mRNA and protein expressions. Reintroduction of EPAS1 could bypass the inhibition by miR-383 on tumorigenesis of human lung cancer cell lines. MicroRNA-383 is a tumor suppressor in human lung cancer by inhibiting EPAS1, both of which could serve as potential therapeutic targets in the treatment of lung cancer.
SIGNIFICANCE OF THE STUDY: MicroRNA-383 is a tumor suppressor in human lung cancer, which functions to inhibit tumorigenesis of lung cancer cells both in vitro and in vivo. This inhibitory effect is mediated by direct targeting of EPAS1 mRNA and subsequent repressing of its expression. Both microRNA-383 and EPAS1 could serve as potential therapeutic targets in the treatment of lung cancer.

Lee SY, Jung DK, Choi JE, et al.
Functional polymorphisms in PD-L1 gene are associated with the prognosis of patients with early stage non-small cell lung cancer.
Gene. 2017; 599:28-35 [PubMed] Related Publications
INTRODUCTION: This study was conducted to investigate whether polymorphisms of genes involved in immune checkpoints can predict the prognosis of patients with early stage non-small cell lung cancer (NSCLC) after surgical resection.
MATERIALS AND METHODS: Twelve single nucleotide polymorphisms (SNPs) of PD-1, PD-L1, and CTLA-4 genes were selected and genotyped. A total of 354 patients with early stage NSCLC who underwent curative surgical resection were enrolled. The association of the SNPs with overall survival (OS) was analyzed.
RESULTS: Among the 12 SNPs investigated, PD-L1 rs4143815C>G, rs822336G>C, and rs822337T>A were significantly associated with worse survival outcomes in multivariate analyses. When the three SNPs were combined, OS decreased in a dose-dependent manner as the number of bad genotypes increased (Ptrend=0.0003). In the luciferase assay, rs4143815 G allele exhibited a decreased transcription activity compared with C allele (P=0.001), and the rs822336C-rs822337A haplotype had a decreased promoter activity compared with the rs822336G-rs822337T haplotype (P=0.004). Patients with higher expression of PD-L1 mRNA had a better survival compared with lower expression (P=0.03).
CONCLUSIONS: PD-L1 polymorphisms may be useful for the prediction of prognosis in patients with surgically resected NSCLC. Further studies are needed to confirm our findings and to understand the role of PD-L1 in the antitumor immunity and prognosis in NSCLC.

Wang F, Liu Y, Chen Y
Pituitary tumor transforming gene-1 in non-small cell lung cancer: Clinicopathological and immunohistochemical analysis.
Biomed Pharmacother. 2016; 84:1595-1600 [PubMed] Related Publications
Pituitary tumor transforming gene-1 (PTTG1) is a novel oncogene and overexpressed in a wide variety of human cancers. However, the clinical and prognostic significance of PTTG1 in non-small cell lung cancer (NSCLC) is still unknown. The expression status of PTTG1 in NSCLC at the publicly available GEO databases (GSE19804) was observed. The mRNA and protein expression of PTTG1 in NSCLC tissues and cell lines was detected by qRT-PCR and Western blot, and the association between PTTG1 expression and clinicopathological factors was analyzed by immunohistochemistry. In our Results, PTTG1 was one of genes overexpressed in NCSLC samples compared with paired adjacent normal lung samples in microarray data (GSE19804). PTTG1 mRNA and protein expressions were increased in NSCLC tissues and cell lines. PTTG1 protein expression was correlated with malignant status and poor prognosis of NSCLC patients. In conclusion, PTTG1 is correlated with NSCLC progression and as an independent poor prognostic factor in NSCLC patients.

Liu HX, Li J, Ye BG
Correlation between gene polymorphisms of CYP1A1, GSTP1, ERCC2, XRCC1, and XRCC3 and susceptibility to lung cancer.
Genet Mol Res. 2016; 15(4) [PubMed] Related Publications
Lung cancer is a common malignant tumor that is characterized by high morbidity and poor prognosis. Studies suggest that an individual's genetic background affects the risk of developing lung cancer. Therefore, we investigated the relationship between gene polymorphisms and susceptibility to lung cancer. We recruited 308 primary lung cancer patients as subjects and 253 healthy adults as controls. After extraction of DNA from blood samples, gene polymorphisms in CYP1A1, GSTP1, ERCC2, XRCC1, and XRCC3 were investigated by polymerase chain reaction and restriction fragment length polymorphism. The frequencies of the genotypes in both groups were investigated to obtain odds ratios and 95% confidence intervals, and correlation analysis was carried out. The analysis results showed that the following polymorphisms were correlated with susceptibility to lung cancer: rs4646903 in CYP1A1 (P < 0.001), rs1048943 in CYP1A1 (P < 0.001), rs1695 in GSTP1 (P < 0.05), rs13181 in ERCC2 (P < 0.001), and rs25487 in XRCC1 (P < 0.05); no such correlation existed in rs861539 in XRCC3 (P > 0.05). The study revealed that the more high-risk gene polymorphisms a patient carries, the greater the risk of developing lung cancer. Carriers of rs4646903 in CYP1A1, rs1048943 in CYP1A1, rs1695 in GSTP1, rs13181 in ERCC2, and rs25487 in XRCC1 are more likely to develop lung cancer.

Zheng L, Qi YX, Liu S, et al.
miR-129b suppresses cell proliferation in the human lung cancer cell lines A549 and H1299.
Genet Mol Res. 2016; 15(4) [PubMed] Related Publications
Lung cancer is one of the most prevalent malignant tumors, and is one of the primary causes of cancer-associated deaths. In 2002, an estimated 1.18 million lung cancer-associated deaths were recorded, accounting for 18% of cancer-related deaths and 2% of total mortality. Despite the great progress that has been made in lung cancer therapies, the mechanisms underlying lung cancer formation and development remain largely unknown. Meanwhile, the microRNA miR-129 has been shown to be involved in the formation of many types of cancer. Therefore, this study aims to investigate whether miR129b could suppress proliferation of lung cancer cell lines. NSCLC tissue samples were collected from the Department of Respiratory Medicine between April 2013 and December 2015. Ten normal health individuals were recruited as controls. Lung cancer cell lines A549 and H1299 were used to examine the suppressive effects of miR129b. Quantitative real-time PCR was used to detect miR129b expression. The MTT assay was used to analyze cell proliferation. Results indicated that miR-129b is down-regulated in lung cancer cell lines and NSCLC tissues. Furthermore, overexpression of miR-129b inhibited proliferation of lung cancer cells. In conclusion, miR-129b suppresses lung cancer cell proliferation, and can be a potential therapeutic target for treatment of lung cancers.

Zhang Y, Sun Z, Zhang Y, et al.
The microRNA-635 suppresses tumorigenesis in non-small cell lung cancer.
Biomed Pharmacother. 2016; 84:1274-1281 [PubMed] Related Publications
The microRNAs represent a class of noncoding RNAs with short length and play diverse roles in many biological processes. Despite tremendous effects have been devoted, the role of miR-635 in non-small cell lung cancer (NSCLC) remains elusive. Here we report a potential tumor suppressive function of miR-635 in NSCLC. By microRNA screening based on invasion assays, we identified series of functional miRNAs. The miR-635 was then identified as a potent inhibitor of cell invasion and differentially expressed in normal and cancerous tissues. We further confirmed that Ying Yang 1 (YY1) may be the direct target of miR-635 as miR-635 transfection can significantly decrease endogenous YY1 expression which can mimic the effect of siRNA-mediated YY1 knockdown. Meanwhile, both miR-635 transfection and YY1 silencing can attenuate NSCLC cell invasion. In addition, miR-635 transfection can also significantly inhibit the growth of xenograft tumors. Taken together, our results have suggested a novel tumor suppressive role for miR-635 in NSCLC.

Recurrent Structural Abnormalities

Selected list of common recurrent structural abnormalities

This is a highly selective list aiming to capture structural abnormalies which are frequesnt and/or significant in relation to diagnosis, prognosis, and/or characterising specific cancers. For a much more extensive list see the Mitelman Database of Chromosome Aberrations and Gene Fusions in Cancer.

del(3p) in Lung Cancer

Hung J, Kishimoto Y, Sugio K, et al.
Allele-specific chromosome 3p deletions occur at an early stage in the pathogenesis of lung carcinoma.
JAMA. 1995; 273(7):558-63 [PubMed] Related Publications
BACKGROUND: Deletions in the short arm of chromosome 3 (3p) are present in most lung carcinomas.
OBJECTIVE: To investigate the role of these chromosome 3p deletions in the pathogenesis of non-small cell lung carcinomas.
DESIGN: Seven archival, paraffin-embedded, surgically resected lung cancer specimens were studied. Fifty precisely identified malignant and preneoplastic lesions present in bronchi, bronchioles, and alveoli were microdissected from stained slides and analyzed for allele loss using polymerase chain reaction-based assays for dinucleotide repeat polymorphisms at three chromosome 3p loci (3p14, 3p21.3, and 3p25).
SETTING: University-based medical center and affiliated hospitals.
SUBJECTS: Samples were analyzed from seven patients who underwent surgical resection with curative intent for non-small cell lung cancer and whose specimens included extensive multifocal areas of preneoplastic lesions (hyperplasia, metaplasia, dysplasia, or noninvasive cancer).
RESULTS: Lymphocytes from all seven cases were heterozygous (ie, informative) for all three microsatellites analyzed. Six (86%) of seven invasive cancers had loss of heterozygosity at one or more chromosome 3p sites. In the accompanying preneoplastic lesions, loss of heterozygosity was detected in none of two normal bronchioles, 13 (76%) of 17 hyperplasias, six (86%) of seven dysplasias, and four (100%) of four noninvasive cancers. Loss of heterozygosity was detected throughout the respiratory tract, in bronchi, bronchioles, and alveoli. In 18 (78%) of 23 preneoplastic lesions, the specific alleles lost were identical to those lost in the corresponding carcinomas. The probability of this happening by chance is 5.3 x 10(-3).
CONCLUSIONS: Deletions in the short arm of chromosome 3 occur at the earliest stage (hyperplasia) in the pathogenesis of lung cancer and involve all regions of the respiratory tract. Allele loss is highly specific, but its mechanism remains unknown. Our findings may be of considerable biologic, prognostic, and clinical significance.

Hosoe S, Shigedo Y, Ueno K, et al.
Detailed deletion mapping of the short arm of chromosome 3 in small cell and non-small cell carcinoma of the lung.
Lung Cancer. 1994; 10(5-6):297-305 [PubMed] Related Publications
We constructed a detailed deletion map of the short arm of chromosome 3 (3p) for 55 lung cancer cases by using 17 restriction fragment length polymorphism (RFLP) probes. Initially, we examined 40 small cell lung cancer (SCLC) cases and found three regions of deletion at 3p25-26, 3p21.3 and 3p14-cen, suggesting the possibility of at least three different tumor-suppressor genes on 3p. In order to obtain more detailed deletion area, and to compare the pattern of 3p deletion, we also examined 15 non-small cell lung cancer (NSCLC) cases. Compared to NSCLC cases, most of SCLC cases have widespread deletion on 3p, suggesting multiple tumor-suppressor genes on 3p may be inactivated in this type of cancer. In 3p21.3 area, minimum overlapping area of deletion lays between two probes which are close to each other. These data will be useful to isolate the putative tumor-suppressor genes located on the chromosome 3p.

Kohno H, Hiroshima K, Toyozaki T, et al.
p53 mutation and allelic loss of chromosome 3p, 9p of preneoplastic lesions in patients with nonsmall cell lung carcinoma.
Cancer. 1999; 85(2):341-7 [PubMed] Related Publications
BACKGROUND: An accumulation of mutations can result in carcinogenesis. Comparing genetic alterations in preneoplastic lesions with those seen in cancer in the same patient may be helpful in the early diagnosis of lung carcinoma or preneoplastic lesions.
METHODS: To identify genetic alterations that may play a role in the development of nonsmall cell lung carcinoma (NSCLC), the authors examined the p53 gene and microsatellite markers on chromosome 3p (D3S643, D3S1317), 9p (D9S171, IFNA) in 35 bronchial metaplastic lesions and 28 alveolar hyperplastic lesions from 61 patients.
RESULTS: A total of 8 metaplastic lesions (1 squamous metaplasia and 7 dysplasias) and 3 alveolar hyperplastic lesions (with atypia) showed genetic alterations, including loss of heterozygosity (LOH) of 3p, 9p and mutations of the p53 gene. In an analysis of microsatellite markers, 5 of 35 cases of squamous cell carcinoma (SCC) and 3 of 26 cases of adenocarcinoma (Ad) showed LOH in both preneoplastic lesions and synchronous cancers. Nine patients (25.7%) with SCC and 6 patients (23.1%) with Ad were shown to have mutations of the p53 gene by single-strand conformation polymorphism. In 2 of these 9 patients with SCC, the same mutation was observed in both dysplasia and SCC.
CONCLUSIONS: These findings suggest that several genetic alterations may occur in preneoplastic lesions or the early stage of SCC of the lung, whereas the genetic alterations examined appeared to occur relatively late in the pathogenesis of pulmonary adenocarcinoma.

del(9p) in Lung Cancer

Kishimoto Y, Sugio K, Hung JY, et al.
Allele-specific loss in chromosome 9p loci in preneoplastic lesions accompanying non-small-cell lung cancers.
J Natl Cancer Inst. 1995; 87(16):1224-9 [PubMed] Related Publications
BACKGROUND: Carcinogenesis is a multistep process, which may begin as a consequence of chromosomal changes. Deletions in the short arm of chromosome 9 (9p) have been observed in lung carcinomas. In addition, morphologically recognizable preneoplastic lesions, frequently multiple in number, precede onset of invasive carcinomas.
PURPOSE: We tested for deletions and loss of heterozygosity (LOH) at 9p loci in preneoplastic and neoplastic foci in lungs of patients with non-small-cell lung carcinomas (NSCLCs).
METHODS: Seven archival, paraffin-embedded, surgically resected NSCLC specimens were selected. They were predominantly from patients with adenocarcinomas and contained multiple preneoplastic lesions, including hyperplasia, metaplasia, dysplasia, and carcinoma in situ (CIS). Fifty-three histologically identified preneoplastic and malignant lesions present in bronchi, bronchioles, and alveoli were precisely microdissected from stained tissue sections with a micromanipulator. Stromal lymphocytes were used to determine constitutional heterozygosity. The specimens were analyzed for LOH using polymerase chain reaction-based assays for polymorphism in dinucleotide repeats (microsatellite markers) in interferon alfa (IFNA) and D9S171 loci on 9p.
RESULTS: All seven cases were constitutionally heterozygous for one or both microsatellite markers. Five of seven cases had LOH at one or both 9p loci in the invasive primary cancers (doubly informative cases). Four of these five cases also revealed LOH in preneoplastic foci. In the doubly informative cases, LOH was detected in five (38%) of 13 foci of hyperplasia, four (80%) of five foci of dysplasia, and three (100%) of three CIS lesions. LOH was detected in preneoplastic lesions from all regions of the respiratory tract, including bronchi, bronchioles, and alveoli, and involved five different cell types. The identical allele was lost from both the preneoplastic lesions and the corresponding tumors (12 of 12 lesions, 17 of 17 comparisons), a phenomenon we have referred to as "allele-specific mutation." Statistical analyses employing a cumulative binomial test demonstrated that the probabilities of such findings occurring by chance are 2.4 x 10(-4) and 7.6 x 10(-6), respectively. From comparisons with the previously published data on other chromosomal abnormalities in the same tissue specimens, it appears that LOH at 3p and 9p loci occurred early in the hyperplasia stage, but the ras gene point mutations were relatively late, at the CIS stage.
CONCLUSIONS: LOH at 9p loci occurs at the earliest stage in the pathogenesis of lung cancer and involves all regions of the respiratory tract. LOH in NSCLC is not random but targets a specific allele in individuals. Studying preneoplastic lesions may help identify intermediate markers for risk assessment and chemoprevention.

Kohno H, Hiroshima K, Toyozaki T, et al.
p53 mutation and allelic loss of chromosome 3p, 9p of preneoplastic lesions in patients with nonsmall cell lung carcinoma.
Cancer. 1999; 85(2):341-7 [PubMed] Related Publications
BACKGROUND: An accumulation of mutations can result in carcinogenesis. Comparing genetic alterations in preneoplastic lesions with those seen in cancer in the same patient may be helpful in the early diagnosis of lung carcinoma or preneoplastic lesions.
METHODS: To identify genetic alterations that may play a role in the development of nonsmall cell lung carcinoma (NSCLC), the authors examined the p53 gene and microsatellite markers on chromosome 3p (D3S643, D3S1317), 9p (D9S171, IFNA) in 35 bronchial metaplastic lesions and 28 alveolar hyperplastic lesions from 61 patients.
RESULTS: A total of 8 metaplastic lesions (1 squamous metaplasia and 7 dysplasias) and 3 alveolar hyperplastic lesions (with atypia) showed genetic alterations, including loss of heterozygosity (LOH) of 3p, 9p and mutations of the p53 gene. In an analysis of microsatellite markers, 5 of 35 cases of squamous cell carcinoma (SCC) and 3 of 26 cases of adenocarcinoma (Ad) showed LOH in both preneoplastic lesions and synchronous cancers. Nine patients (25.7%) with SCC and 6 patients (23.1%) with Ad were shown to have mutations of the p53 gene by single-strand conformation polymorphism. In 2 of these 9 patients with SCC, the same mutation was observed in both dysplasia and SCC.
CONCLUSIONS: These findings suggest that several genetic alterations may occur in preneoplastic lesions or the early stage of SCC of the lung, whereas the genetic alterations examined appeared to occur relatively late in the pathogenesis of pulmonary adenocarcinoma.

del(1p36) in Lung Cancer

Nomoto S, Haruki N, Tatematsu Y, et al.
Frequent allelic imbalance suggests involvement of a tumor suppressor gene at 1p36 in the pathogenesis of human lung cancers.
Genes Chromosomes Cancer. 2000; 28(3):342-6 [PubMed] Related Publications
The short arm of chromosome 1 is among the most frequently affected regions in various types of common adult cancers as well as in neuroblastoma. In a previous study of ours, frequent allelic imbalance at the TP73 locus at 1p36 was noted in lung cancer despite the absence of TP73 mutations. This suggested the possible existence of an as yet unidentified tumor suppressor gene on 1p. Our initial attempt using the candidate gene approach did not yield any somatic mutations in the 14-3-3sigma gene (official gene symbol, SFN), a mediator of G2 arrest by TP53. Detailed deletion mapping of the telomeric region of 1p was thus carried out as an initial step toward positional cloning. We used seven polymorphic markers in addition to TP73 to examine 61 primary lung cancers. Allelic imbalance at one or more loci of 1p36 was observed in 30 of the 61 cases, whereas D1S508 at 1p36.2 exhibited the highest frequency (45%) of allelic imbalance among the 1p36 markers examined. In contrast, two proximal markers at 1p32-34 showed significantly less frequent (11-14%) allelic imbalance. Consequently, the present study identified the shortest region of overlap between D1S507 and TP73, which included the most frequently affected marker, D1S508. In addition, several cases exhibited allelic imbalance confined to a subtelomeric region distal to D1S2845 at 1p36.3. The present findings warrant future studies to identify the putative tumor suppressor gene(s) at 1p36 to gain a better understanding of the molecular pathogenesis of lung cancer. Genes Chromosomes Cancer 28:342-346, 2000.

Yanada M, Yaoi T, Shimada J, et al.
Frequent hemizygous deletion at 1p36 and hypermethylation downregulate RUNX3 expression in human lung cancer cell lines.
Oncol Rep. 2005; 14(4):817-22 [PubMed] Related Publications
Runt-related transcription factor 3 (RUNX3) has been recognized as a tumor suppressor gene in gastric cancer because its expression level was reduced or disappeared due to epigenetic changes. To evaluate the usefulness of the RUNX3 gene as a biomarker of lung cancer, we have analyzed the expression of the RUNX3 gene in 15 lung cancer cell lines by real-time reverse transcription-polymerase chain reaction (RT-PCR), and demonstrated that RUNX3 gene expression was reduced or disappeared in all cell lines examined (100%). In addition, we have attempted to classify all the cell lines into three groups according to the expression level; less than 10% (group I), 10-30% (group II) and approximately 50% (group III). We further investigated methylation status of the CpG sites in the exon 1 region of RUNX3 by methylation specific PCR (MSP), and studied the correlation between the expression level and hemizygous deletion as revealed by bicolor fluorescence in situ hybridization (FISH). The CpG sites were hypermethylated in 8 cell lines (53%) and the RUNX3 loci were hemizygously deleted in another 8 cell lines (53%). Furthermore group I, II, and III corresponded well to methylation-positive cell lines, cell lines showing hemizygous deletion, and the rest of cell lines without methylation or hemizygous deletion, respectively. These results suggest that a comprehensive study on RUNX3 using real-time RT-PCR, MSP, and FISH could be beneficial in understanding the pathogenetic mechanisms of human lung cancer at the molecular level.

Shibukawa K, Miyokawa N, Tokusashi Y, et al.
High incidence of chromosomal abnormalities at 1p36 and 9p21 in early-stage central type squamous cell carcinoma and squamous dysplasia of bronchus detected by autofluorescence bronchoscopy.
Oncol Rep. 2009; 22(1):81-7 [PubMed] Related Publications
Heavy smokers with central type squamous cell carcinoma (SCC) frequently have multiple cancerous lesions in the bronchus. Autofluorescence bronchoscopy (AFB) is useful in the detection of early bronchogenic cancer and dysplastic lesions. We investigated the loss of heterozygosity (LOH) and microsatellite instability (MSI) and expression of four proteins in 13 early stage SCC (early SCC) and 9 squamous dysplasia detected by AFB and 19 cases of surgically resected invasive SCC (invasive SCC). In early SCC and squamous dysplasia, LOH/MSI of chromosome 1p36 was found in 62 and 33%, respectively, and of 9p21 in 54 and 63%, respectively. TAp73 expression of early SCC and squamous dysplasia was lower than that of normal bronchial epithelium, and p16 expression was not detectable in these lesions. These results suggested that the genetic abnormalities had already developed in the early stage of carcinogenesis of SCC, including squamous dysplasia. The AFB system was able to reveal abnormal autofluorescence in these precancerous lesions, including squamous dysplasia.

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