Gene Summary

Gene:FGF6; fibroblast growth factor 6
Aliases: HST2, HBGF-6
Summary:The protein encoded by this gene is a member of the fibroblast growth factor (FGF) family. FGF family members possess broad mitogenic and cell survival activities, and are involved in a variety of biological processes, including embryonic development, cell growth, morphogenesis, tissue repair, tumor growth and invasion. This gene displayed oncogenic transforming activity when transfected into mammalian cells. The mouse homolog of this gene exhibits a restricted expression profile predominantly in the myogenic lineage, which suggested a role in muscle regeneration or differentiation. [provided by RefSeq, Jul 2008]
Databases:OMIM, HGNC, Ensembl, GeneCard, Gene
Protein:fibroblast growth factor 6
Source:NCBIAccessed: 31 August, 2019


What does this gene/protein do?
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Pathways:What pathways are this gene/protein implicaed in?
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Cancer Overview

Research Indicators

Publications Per Year (1994-2019)
Graph generated 31 August 2019 using data from PubMed using criteria.

Literature Analysis

Mouse over the terms for more detail; many indicate links which you can click for dedicated pages about the topic.

  • Proto-Oncogene Proteins
  • Multigene Family
  • FGFR2
  • Childhood Cancer
  • DNA Methylation
  • Fibroblast Growth Factors
  • FISH
  • Molecular Sequence Data
  • DNA Sequence Analysis
  • Polymerase Chain Reaction
  • X Chromosome
  • Karyotyping
  • Temperature
  • Infant
  • snRNP Core Proteins
  • Translocation
  • Gene Amplification
  • Transcription
  • Base Sequence
  • Mesothelioma
  • Chromosome Banding
  • Chromosome 11
  • Single Nucleotide Polymorphism
  • Survival Rate
  • Chromosome 12
  • Hybrid Cells
  • RNA
  • Young Adult
  • Sequence Tagged Sites
  • Genes, Neoplasm
  • Biomarkers, Tumor
  • Cancer DNA
  • Cancer Gene Expression Regulation
  • Breast Cancer
  • Oligonucleotide Array Sequence Analysis
  • Genome, Human
  • Genetic Markers
  • Chromosome Mapping
Tag cloud generated 31 August, 2019 using data from PubMed, MeSH and CancerIndex

Latest Publications: FGF6 (cancer-related)

Singhi AD, George B, Greenbowe JR, et al.
Real-Time Targeted Genome Profile Analysis of Pancreatic Ductal Adenocarcinomas Identifies Genetic Alterations That Might Be Targeted With Existing Drugs or Used as Biomarkers.
Gastroenterology. 2019; 156(8):2242-2253.e4 [PubMed] Related Publications
BACKGROUND & AIMS: It has been a challenge to select treatment for patients with pancreatic ductal adenocarcinomas (PDACs) based on genome alterations. We performed targeted genomic profile analyses of a large number of PDACs to assess the full spectrum of actionable genomic alterations.
METHODS: We performed targeted genomic profile analyses of 3594 PDAC samples from an international cohort, including capture-based targeted genomic profiling of as many as 315 cancer-associated genes and intron regions of 28 genes that are rearranged in cancer cells. Tumor mutation burden (TMB) and microsatellite instability (MSI) status were also assessed. TMB was calculated across a 1.14-megabase region; TMB-high was defined as ≥20 mutations/megabase. MSI-high status was assigned based on analysis of 114 intron homopolymer loci.
RESULTS: KRAS, TP53, CDKN2A, and SMAD4 were the most frequently altered genes in PDAC. We found KRAS mutations in 88% of samples. Among PDACs without mutations in KRAS, we found alterations in genes whose products are in the mitogen-activated protein kinase signaling pathway and are candidate drug targets (actionable targets, n = 132; 4%), as well as gene fusions (n = 51), gene amplifications (n = 35), genes with missense mutations (n = 30), and genes that contain deletions (n = 16). Many of these encode proteins in receptor tyrosine kinase, RAS, or mitogen-activated protein kinase signaling pathways. Aside from TP53, alterations in genes encoding DNA damage repair proteins (BRCA and FANC) were detected in 14% of PDACs. Among PDACs evaluated for MSI (n = 2563) and TMB (n = 1021), MSI-high and/or TMB-high phenotypes were detected in 0.5% of samples. Alterations in FGF23, CCND2, PIK3CA, and FGF6 were more commonly detected in intraductal papillary mucinous neoplasm-associated PDACs.
CONCLUSIONS: In targeted genomic profile analyses of 3594 PDACs, we found 17% to contain genomic alterations that might make the tumor cells susceptible to currently used anticancer agents. We identified mutations in genes that could contribute to progression of intraductal papillary mucinous neoplasms into malignancies. These alterations might be used as biomarkers for early detection.

Mayol G, Martín-Subero JI, Ríos J, et al.
DNA hypomethylation affects cancer-related biological functions and genes relevant in neuroblastoma pathogenesis.
PLoS One. 2012; 7(11):e48401 [PubMed] Free Access to Full Article Related Publications
Neuroblastoma (NB) pathogenesis has been reported to be closely associated with numerous genetic alterations. However, underlying DNA methylation patterns have not been extensively studied in this developmental malignancy. Here, we generated microarray-based DNA methylation profiles of primary neuroblastic tumors. Stringent supervised differential methylation analyses allowed us to identify epigenetic changes characteristic for NB tumors as well as for clinical and biological subtypes of NB. We observed that gene-specific loss of DNA methylation is more prevalent than promoter hypermethylation. Remarkably, such hypomethylation affected cancer-related biological functions and genes relevant to NB pathogenesis such as CCND1, SPRR3, BTC, EGF and FGF6. In particular, differential methylation in CCND1 affected mostly an evolutionary conserved functionally relevant 3' untranslated region, suggesting that hypomethylation outside promoter regions may play a role in NB pathogenesis. Hypermethylation targeted genes involved in cell development and proliferation such as RASSF1A, POU2F2 or HOXD3, among others. The results derived from this study provide new candidate epigenetic biomarkers associated with NB as well as insights into the molecular pathogenesis of this tumor, which involves a marked gene-specific hypomethylation.

Herrmann A, Haake A, Ammerpohl O, et al.
Pipeline for large-scale microdroplet bisulfite PCR-based sequencing allows the tracking of hepitype evolution in tumors.
PLoS One. 2011; 6(7):e21332 [PubMed] Free Access to Full Article Related Publications
Cytosine methylation provides an epigenetic level of cellular plasticity that is important for development, differentiation and cancerogenesis. We adopted microdroplet PCR to bisulfite treated target DNA in combination with second generation sequencing to simultaneously assess DNA sequence and methylation. We show measurement of methylation status in a wide range of target sequences (total 34 kb) with an average coverage of 95% (median 100%) and good correlation to the opposite strand (rho = 0.96) and to pyrosequencing (rho = 0.87). Data from lymphoma and colorectal cancer samples for SNRPN (imprinted gene), FGF6 (demethylated in the cancer samples) and HS3ST2 (methylated in the cancer samples) serve as a proof of principle showing the integration of SNP data and phased DNA-methylation information into "hepitypes" and thus the analysis of DNA methylation phylogeny in the somatic evolution of cancer.

Sheffer M, Bacolod MD, Zuk O, et al.
Association of survival and disease progression with chromosomal instability: a genomic exploration of colorectal cancer.
Proc Natl Acad Sci U S A. 2009; 106(17):7131-6 [PubMed] Free Access to Full Article Related Publications
During disease progression the cells that comprise solid malignancies undergo significant changes in gene copy number and chromosome structure. Colorectal cancer provides an excellent model to study this process. To indentify and characterize chromosomal abnormalities in colorectal cancer, we performed a statistical analysis of 299 expression and 130 SNP arrays profiled at different stages of the disease, including normal tissue, adenoma, stages 1-4 adenocarcinoma, and metastasis. We identified broad (> 1/2 chromosomal arm) and focal (< 1/2 chromosomal arm) events. Broad amplifications were noted on chromosomes 7, 8q, 13q, 20, and X and broad deletions on chromosomes 4, 8p, 14q, 15q, 17p, 18, 20p, and 22q. Focal events (gains or losses) were identified in regions containing known cancer pathway genes, such as VEGFA, MYC, MET, FGF6, FGF23, LYN, MMP9, MYBL2, AURKA, UBE2C, and PTEN. Other focal events encompassed potential new candidate tumor suppressors (losses) and oncogenes (gains), including CCDC68, CSMD1, POLR1D, and PMEPA1. From the expression data, we identified genes whose expression levels reflected their copy number changes and used this relationship to impute copy number changes to samples without accompanying SNP data. This analysis provided the statistical power to show that deletions of 8p, 4p, and 15q are associated with survival and disease progression, and that samples with simultaneous deletions in 18q, 8p, 4p, and 15q have a particularly poor prognosis. Annotation analysis reveals that the oxidative phosphorylation pathway shows a strong tendency for decreased expression in the samples characterized by poor prognosis.

Katoh M
Cancer genomics and genetics of FGFR2 (Review).
Int J Oncol. 2008; 33(2):233-7 [PubMed] Related Publications
FGFR2 gene encodes FGFR2b in epithelial cells, and FGFR2c in mesenchymal cells. FGFR2b is a high affinity receptor for FGF1, FGF3, FGF7, FGF10 and FGF22, while FGFR2c for FGF1, FGF2, FGF4, FGF6, FGF9, FGF16 and FGF20. Here genomics and genetics of FGFR2, and therapeutics targeted to FGFR2 will be reviewed. Single nucleotide polymorphisms (SNPs) of FGFR2 are associated with increased risk of breast cancer. Gene amplification or missense mutation of FGFR2 occurs in gastric cancer, lung cancer, breast cancer, ovarian cancer, and endometrial cancer. Genetic alterations of FGFR2 induce aberrant FGFR2 signaling activation due to release of FGFR2 from autoinhibition, or creation of FGF signaling autocrine loop. Class switch of FGFR2b to FGFR2c is associated with more malignant phenotype. FGF and canonical WNT signals synergize during mammary carcinogenesis, but counteract during osteogenesis and adipogenesis. Among PD173074, SU5402, and AZD2171 functioning as FGFR inhibitors, AZD2171 is the most promising anti-cancer drug. Cancer genomics and genetics are utilized to predict cancer-driving pathway for therapeutic optimization. FGFR2ome is defined as a complete data set of SNP, copy number variation (CNV), missense mutation, gene amplification, and predominant isoform of FGFR2. FGFR2ome analyses in patients with several tumor types among various populations should be carried out to establish integrative database of FGFR2 for the rational clinical application of FGFR2-targeted cancer therapy.

Katoh M
WNT and FGF gene clusters (review).
Int J Oncol. 2002; 21(6):1269-73 [PubMed] Related Publications
Mouse mammary tumor virus (MMTV) is a retrovirus, activating Wnt genes (Wnt1/int-1, Wnt3/int-4, Wnt10b), Fgf genes (Fgf3/int-2, Fgf4, Fgf8) and other genes (Notch4/int-3, Eif3s6/int-6) due to proviral integration. Among 19 WNT genes, WNT3 and WNT14B genes are clustered in human chromosome 17q21, WNT3A and WNT14 in human chromosome 1q42, WNT10A and WNT6 in human chromosome 2q35, and WNT10B and WNT1 in human chromosome 12q13. Among 22 FGF genes, FGF19, FGF4 and FGF3 genes are clustered in human chromosome 11q13, while FGF23 and FGF6 in human chromosome 12p13. WNT and FGF gene clusters are conserved between the human genome and the mouse genome. Activation of mouse Wnt or Fgf genes due to proviral integration of MMTV occurs in 5 out of 13 clustered genes, and in 1 out of 28 solitary genes (p=0.0033), which clearly indicates that mouse Wnt or Fgf gene clusters are recombination hot spots associated with carcinogenesis. Recombination results in retroviral integration as well as in chromosomal translocation, gene amplification and deletion during carcinogenesis. The CCND1-FGF19-FGF4-FGF3 gene cluster in human chromosome 11q13 is amplified in breast cancer, squamous cell carcinoma of head and neck, and bladder tumors, and is also translocated in parathyroid tumors and B-cell lymphoma. WNT gene clusters on human chromosome 1q42, 2q35, 12q13, and 17q21 as well as FGF gene cluster on human chromosome 12p13 might be amplified or translocated in human cancer just like FGF gene cluster on human chromosome 11q13.

Niini T, Vettenranta K, Hollmén J, et al.
Expression of myeloid-specific genes in childhood acute lymphoblastic leukemia - a cDNA array study.
Leukemia. 2002; 16(11):2213-21 [PubMed] Related Publications
Several specific cytogenetic changes are known to be associated with childhood acute lymphoblastic leukemia (ALL), and many of them are important prognostic factors for the disease. Little is known, however, about the changes in gene expression in ALL. Recently, the development of cDNA array technology has enabled the study of expression of hundreds to thousands of genes in a single experiment. We used the cDNA array method to study the gene expression profiles of 17 children with precursor-B ALL. Normal B cells from adenoids were used as reference material. We discuss the 25 genes that were most over-expressed compared to the reference. These included four genes that are normally expressed only in the myeloid lineages of the hematopoietic cells: RNASE2, GCSFR, PRTN3 and CLC. We also detected over-expression of S100A12, expressed in nerve cells but also in myeloid cells. In addition to the myeloid-specific genes, other over-expressed genes included AML1, LCP2 and FGF6. In conclusion, our study revealed novel information about gene expression in childhood ALL. The data obtained may contribute to further studies of the pathogenesis and prognosis of childhood ALL.

Le Coniat M, Della Valle V, Marynen P, Berger R
A new breakpoint, telomeric to TEL/ETV6, on the short arm of chromosome 12 in T cell acute lymphoblastic leukemia.
Leukemia. 1997; 11(8):1360-3 [PubMed] Related Publications
Abnormalities of the short arm of chromosome 12 frequently involve the TEL/ETV6 gene in acute leukemias. In two cases of T cell acute lymphoblastic leukemia with translocation t(12;14)(p13;q11) and t(7;12)(q35;p13), respectively, the breakpoints were located telomeric to the TEL/ETV6 locus. Further fluorescence in situ hybridization (FISH) studies showed that the breakpoint was located between two markers, FGF6 (centromeric) and D12S983 (telomeric) on 12p in both patients. This result suggests that a new chromosomal breakpoint can nonrandomly involve rearrangements in T cell malignancies. The breakpoint on chromosome 14 was localized centromeric to the TRCA/D locus.

Ikeda H, Sato N, Matsuura A, et al.
Clonal dominance of human autologous cytotoxic T lymphocytes against gastric carcinoma: molecular stability of the CDR3 structure of the TCR alphabeta gene.
Int Immunol. 1996; 8(1):75-82 [PubMed] Related Publications
In our previous study, RT-PCR suggested that cytotoxic T lymphocyte (CTL) clones may specifically recognize human autologous gastric signet ring cell tumor (HST2) by using TCR products of Valpha7 and Vbeta20 subfamilies. In this report, we first determined the TCR nucleotide sequences of one such CTL from patient's peripheral blood lymphocytes (PBL), the PBL were newly stimulated with a mixed lymphocyte-autologus tumor cell (HST2) culture (MLTC) and cytotoxic T cell lines, such as HPBL3x, were obtained. RT-PCR and the nucleotide sequence data indicated that HPBL3x also showed TCR Valpha7 and Vbeta transcripts, and that HPBL3x TCR was composed of the exact same CDR3 gene structures as those of the TcHLT2 clone. T cells with same TCR structures were also detected in patient's non-treated peripheral blood, although they were infrequent. These data indicated that functional cytotoxic T cells with these distinct CDR3 equivalent structures were the dominant effector cells against HST2 autologous tumor cells. Moreover, the highly dominant and reproducible clonal expansion of T cells bearing heterodimeric TCR with identical variable, N diversity and constant region structures suggest that the molecular nature of governing antigenic peptide to TcHDT2 may be stable and perhaps immunologically dominant in the interaction between CTL and HST2 autologous tumor cells.

Penault-Llorca F, Bertucci F, Adélaïde J, et al.
Expression of FGF and FGF receptor genes in human breast cancer.
Int J Cancer. 1995; 61(2):170-6 [PubMed] Related Publications
The family of FGF growth factors is involved in several biological processes and might play an important role in tumorigenesis. We have studied the respective expression of 8 of the 9 characterized FGF genes, and of the 4 known FGF receptor genes, in a panel of 10 tumor-cell lines and 103 breast-tumor samples, using RT-PCR and Northern-blot analyses. FGF1 and FGF2 were expressed in almost all samples, while expression of FGF5, FGF6, FGF7, and FGF9 was more restricted. FGFR1, FGFR2 and FGFR4 were expressed at high levels in respectively 22%, 4% and 32% of tumors. FGFR3 expression was not detected. The transcript encoding an FGFR1 isoform with 2 immunoglobulin-like domains was the most prevalent.

Aerssens J, Guo C, Vermeesch J, et al.
A physical map of the region spanning the chromosome 12 translocation breakpoint in a mesothelioma with a t(X;12)(q22;p13).
Cytogenet Cell Genet. 1995; 71(3):268-75 [PubMed] Related Publications
We have constructed a physical map of a 4.6-cM region of human chromosome band 12p13.3 that contains a translocation breakpoint from a mesothelioma with a t(X;12)(q22;p13). The map contains a contig of 22 yeast artificial chromosomes (YACs), onto which we have placed 18 sequence tagged site (STS) markers, including seven genes: D12S370, FGF6, KCAN1, KCNA5, KCNA6, NTF3, and VWF. A second YAC contig, comprised of 22 YAC clones, was located distal to the mesothelioma breakpoint and contained 12 STS markers, including four genes (CACNL1A1, D12S380E, D12S381E, and D12S382E). Based on STS content and fluorescence in situ hybridization experiments, two stable, nonchimeric YAC clones were found that span the mesothelioma breakpoint. A long-range restriction map of an 800-kb region was constructed and used to refine the mesothelioma breakpoint to a region of approximately 100 kb, flanked by the potassium channel genes KCNA1 and KCNA5. The latter was confirmed by direct visual hybridization (DIRVISH) experiments, using cosmids isolated for markers flanking the breakpoint as probes.

Iida S, Katoh O, Tokunaga A, Terada M
Expression of fibroblast growth factor gene family and its receptor gene family in the human upper gastrointestinal tract.
Biochem Biophys Res Commun. 1994; 199(3):1113-9 [PubMed] Related Publications
All of 13 human esophageal cancer cell lines contained mRNAs for both basic fibroblast growth factor (bFGF) and its receptor, FGFR1/N-sam protein, while they did not have mRNAs for keratinocyte growth factor (KGF) despite the presence of mRNAs for the KGF receptor gene, K-sam. The results indicate that in human esophageal cancer, bFGF plays roles in an autocrine manner, while KGF acts as a paracrine mediator. In contrast, only one of seven human gastric cancer cell lines contained bFGF mRNAs, while three out of the seven had mRNAs for FGFR1/N-sam protein. The KGF gene was not expressed in any of the gastric cancer cell lines, while K-sam mRNAs were detected in six out of the seven. The results demonstrate that in most human gastric cancers, bFGF does not act as an autocrine mediator, while KGF acts as a paracrine factor. The mRNAs for the other four members of the fibroblast growth factor (FGF) family, including acidic FGF, int-2 protein, hst-1 protein, FGF5 protein and FGF6/hst-2 protein could not be detected in the esophageal and gastric cancer cell lines.

Ikeda H, Sato N, Matsuura A, Kikuchi K
Analysis of T-cell receptor V region gene usage of cytotoxic T-lymphocytes and tumor-infiltrating lymphocytes derived from human autologous gastric signet ring cell carcinomas.
Cancer Res. 1993; 53(13):3078-84 [PubMed] Related Publications
To determine the T-cell receptor (TCR) V alpha/V beta gene usage of the human autologous gastric tumor-specific cytotoxic T-lymphocytes (CTLs), we first established two pairs of tumor cell lines, HST2 and SSTW, from the malignant peritoneal effusions of signet ring cell carcinomas and their peripheral blood lymphocyte-derived tumor-specific CD8-positive CTL lines, TcHST2 and TcSSTW. TCR V alpha/V beta gene usage from these CTL was examined using the reversely transcribed-polymerase chain reaction method, demonstrating that the V alpha 7, V alpha 12, and V beta 20 transcripts were commonly detected. The fact that repeated antigenic stimulation by mixed lymphocyte-autologous tumor cell cultures brought about the specific cytolysis and the restricted TCR usage of TCR V alpha 7, V alpha 12, and V beta 20 strongly suggests that these TCR V region products participated in T-cell-cancer interaction. This restricted TCR V gene usage in the gastric signet ring cell carcinomas led us to examine further the frequency of TCR V alpha/V beta usage in 11 cases of in vivo tumor-infiltrating lymphocytes with this particular type of tumor. The data showed that V alpha 7, V alpha 12, V beta 6, and V beta 20 were also predominantly expressed among these tumor-infiltrating lymphocytes in vivo. However, it seemed that T-cells with these TCR V region products are not specific for the gastric signet ring cell carcinomas, since they also frequently infiltrate into noncancerous lesions, such as peptic ulcers. These data may suggest that T-cells with certain TCR V alpha/V beta products could preferentially infiltrate into the stomach tissue, while some of these T-cells may be cytotoxic to the neoplastic autologous tumor cells.

Iida S, Yoshida T, Naito K, et al.
Human hst-2 (FGF-6) oncogene: cDNA cloning and characterization.
Oncogene. 1992; 7(2):303-9 [PubMed] Related Publications
The hst-2 gene was previously identified by its close homology to the hst-1 gene. Cosmid clones containing the hst-2 gene were cloned from a normal human genomic library. Focus-forming activity was observed for the hst-2 cosmids when NIH3T3 transfection assay was performed in a serum-free medium, whereas induction of morphological transformation was difficult to detect in an ordinary serum-supplemented medium. The hst-2 cDNA was cloned from the NIH3T3 transformant. Nucleotide sequence analysis of the cDNA indicates that the hst-2 gene encodes a 198 amino acid transforming protein containing a signal peptide with the characteristics of a heparin-binding growth factor. The coding sequence was almost identical to the published portion of the exon sequence of the FGF-6 gene, indicating that hst-2 is identical to FGF-6. The hst-2 cDNA fragment, when inserted into an expression vector, was able to transform NIH3T3 cells effectively, and the resulting transformant formed a well-vascularized tumor in nude mice, thus suggesting an angiogenic property similar to some other members of the family. RNA blot analysis revealed the expression of the hst-2 gene in human leukemia cell lines with platelet/megakaryocytic differentiation potential.

Hagemeijer A, Lafage M, Mattei MG, et al.
Localization of the HST/FGFK gene with regard to 11q13 chromosomal breakpoint and fragile site.
Genes Chromosomes Cancer. 1991; 3(3):210-4 [PubMed] Related Publications
The HST/FGFK gene, a member of the fibroblast growth factor gene family and a protooncogene, is localized on chromosomal band 11q13. Genes in this region are frequently involved in hematopoietic and solid tumors. Here we show that the HST gene lies telomeric to the BCL1 gene, the t(11;14)(q13;q32) breakpoint, and the FRA11A rare fragile site.

de Lapeyriere O, Rosnet O, Benharroch D, et al.
Structure, chromosome mapping and expression of the murine Fgf-6 gene.
Oncogene. 1990; 5(6):823-31 [PubMed] Related Publications
The sixth member of the fibroblast growth factor gene family was cloned and analysed in the mouse. It is composed of three coding exons and encodes a putative growth protein of 198 amino acids, possessing a potential signal peptide, and presenting 79% and 93.5% sequence similarity with the mouse Hst/K-fgf and human FGF-6 genes products, respectively. The murine Fgf-6 gene is located in a region distinct from the Int-41 locus and belongs to a linkage group conserved between chromosome 12 in man and chromosome 6 in mouse. It presents an intrinsic oncogenic capacity since it is able to transform cultured fibroblasts. Fgf-6 mRNA levels are developmentally regulated with a peak of expression in the developing fetus at day 15.5 of gestation, moderate levels during late gestation and in the neonate. In the adult, Fgf-6 mRNA can be detected in testis, heart and skeletal muscle.

Sugimura T, Yoshida T, Sakamoto H, et al.
Molecular biology of the hst-1 gene.
Ciba Found Symp. 1990; 150:79-89; discussion 89-98 [PubMed] Related Publications
The hst-1 gene (or HSTF1 by human gene nomenclature) was originally identified in our laboratory by an NIH/3T3 focus formation assay using DNA from a human gastric cancer. Sequence analysis predicted the hst-1 product to be a novel growth factor with 30-50% homology with six other heparin-binding growth factors: basic and acidic fibroblast growth factors (FGFs), the int-2 protein, FGF5, the hst-2/FGF6 protein and keratinocyte growth factor (KGF). A recombinant hst-1 protein was synthesized in silkworm cells and found to be a potent heparin-binding mitogen for murine fibroblasts and human vascular endothelial cells. Although hst-1 expression cannot be detected in most cancer cells, including gastric cancers, it is expressed in mouse embryos and in some germ cell tumours. Both hst-1 and int-2 are located on band q13.3 of human chromosome 11 within a distance of 35 kbp; in the mouse genome these two genes are separated by less than 20 kbp. They are differentially transcribed in the F9 mouse teratocarcinoma cell line; hst-1 is expressed in undifferentiated stem cells and int-2 in differentiated endodermal cells. The hst-1 and int-2 genes were coamplified in a variety of cancer cells, most notably in more than 50% of oesophageal cancers.

Theillet C, Le Roy X, De Lapeyrière O, et al.
Amplification of FGF-related genes in human tumors: possible involvement of HST in breast carcinomas.
Oncogene. 1989; 4(7):915-22 [PubMed] Related Publications
In order to document a possible involvement of structural alterations of FGF (Fibroblast Growth Factor)-like genes in human oncogenesis, we have screened a large series of human tumors for amplification of five FGF-related genes (Basic-FGF, INT2, HST, FGF5 and FGF6). None of 37 hematopoietic neoplasms, one out of 13 melanomas (8%), three out of 43 bladder tumors (7%) and 41 out of 238 breast carcinomas (17%) contained amplified FGF-related sequences, namely HST and INT2. Only these two genes, both located on band q13 of chromosome 11 have been found amplified. In all cases they were co-amplified and in only one instance did amplification extend to the ETS1 locus at position 11q23. INT2 and HST RNA could be evidenced by RNA/RNA in situ hybridization in breast carcinomas. Our results indicate a correlation between RNA expression and gene amplification in the case of HST but not of INT2. Although evaluation of the clinical significance of HST amplification and expression must await long-term follow-up of the patients, we suggest that HST gene product could play a role in development and/or progression of human breast cancer.

Marics I, Adelaide J, Raybaud F, et al.
Characterization of the HST-related FGF.6 gene, a new member of the fibroblast growth factor gene family.
Oncogene. 1989; 4(3):335-40 [PubMed] Related Publications
By screening a mouse cosmid library with a human HST probe under reduced conditions of stringency, we isolated several positive clones. One of them was identified as a new member of the fibroblast growth factor gene family, and called FGF.6. The human FGF.6 gene was subsequently isolated and sequenced. The deduced amino-acid sequence exhibited 70% identity with the HST gene product over the C-terminal two-thirds of the putative protein. FGF.6 was mapped to chromosome 12 at band p13 by in situ hybridization. The cloned normal human gene was able to transform mouse NIH3T3 fibroblasts using both focus- and tumorigenicity-assays.

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Cite this page: Cotterill SJ. FGF6, Cancer Genetics Web: http://www.cancer-genetics.org/FGF6.htm Accessed:

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