Gene Summary

Gene:CD79A; CD79a molecule
Aliases: IGA, MB-1
Summary:The B lymphocyte antigen receptor is a multimeric complex that includes the antigen-specific component, surface immunoglobulin (Ig). Surface Ig non-covalently associates with two other proteins, Ig-alpha and Ig-beta, which are necessary for expression and function of the B-cell antigen receptor. This gene encodes the Ig-alpha protein of the B-cell antigen component. Alternatively spliced transcript variants encoding different isoforms have been described. [provided by RefSeq, Jul 2008]
Databases:OMIM, HGNC, Ensembl, GeneCard, Gene
Protein:B-cell antigen receptor complex-associated protein alpha chain
Source:NCBIAccessed: 30 August, 2019


What does this gene/protein do?
Show (11)
Pathways:What pathways are this gene/protein implicaed in?
Show (4)

Cancer Overview

Research Indicators

Publications Per Year (1994-2019)
Graph generated 30 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.

Tag cloud generated 30 August, 2019 using data from PubMed, MeSH and CancerIndex

Specific Cancers (7)

Data table showing topics related to specific cancers and associated disorders. Scope includes mutations and abnormal protein expression.

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

Latest Publications: CD79A (cancer-related)

Morishita T, Hishida A, Okugawa Y, et al.
Polymorphisms in folic acid metabolism genes do not associate with cancer cachexia in Japanese gastrointestinal patients.
Nagoya J Med Sci. 2018; 80(4):529-539 [PubMed] Free Access to Full Article Related Publications
We used clinical data from Iga General Hospital to examine the association between polymorphisms in

Meiss F, Technau-Hafsi K, Kern JS, May AM
Eosinophilic dermatosis of hematologic malignancy: Correlation of molecular characteristics of skin lesions and extracutaneous manifestations of hematologic malignancy.
J Cutan Pathol. 2019; 46(3):175-181 [PubMed] Related Publications
BACKGROUND: Skin diseases are frequent in patients with chronic lymphocytic leukemia (CLL) and other hematological neoplasias. Eosinophilic dermatosis (ED) of hematologic malignancy has long been considered a nonspecific cutaneous reaction pattern. Recently neoplastic cells have been shown to be present in ED, thus challenging the classification as a nonspecific dermatosis.
METHODS: We report five patients with ED in association with CLL. We further investigated the presence of neoplastic B-cells in the skin infiltrate by immunohistochemistry and immunoglobulin heavy chain rearrangement and compared these to extracutaneous manifestations of CLL.
RESULTS: The phenotype of the lymphocytic infiltrate was predominately CD3+ (range: 60%-90%). CD20+ and CD79a+ lymphocytes were less frequent, accounting for up to 15% (range: absent - 15%). CD23+ lymphocytes represented up to 20% (range: absent - 20%) of the infiltrate. The analysis of the immunoglobulin heavy chain rearrangement in the skin specimens showed clonal rearrangements in 4/5 patients and in three of these four patients clones were identical to extracutaneous CLL manifestations.
CONCLUSION: Our data show that neoplastic B-cells are very frequently found in ED when systematically evaluated. This findings support the hypothesis that leukemic cells play a pathogenetic role in ED of hematologic malignancy.

Sekiguchi N, Nomoto J, Nagata A, et al.
Gene Expression Profile Signature of Aggressive Waldenström Macroglobulinemia with Chromosome 6q Deletion.
Biomed Res Int. 2018; 2018:6728128 [PubMed] Free Access to Full Article Related Publications
Background: Waldenström macroglobulinemia (WM) is a rare, indolent B-cell lymphoma. Clinically, chromosome 6q deletion (6q del) including loss of the B lymphocyte-induced maturation protein 1 gene (BLIMP-1) is reported to be associated with poor prognosis. However, it remains unclear how the underlying biological mechanism contributes to the aggressiveness of WM with 6q del.
Methods: Here, we conducted oligonucleotide microarray analysis to clarify the differences in gene expression between WM with and without 6q del. Gene ontology (GO) analysis was performed to identify the main pathways underlying differences in gene expression. Eight bone marrow formalin-fixed paraffin-embedded samples of WM were processed for interphase fluorescence in situ hybridization analysis, and three were shown to have 6q del.
Results: GO analysis revealed significant terms including "lymphocyte activation" (corrected p value=6.68E-11), which included 31 probes. Moreover,
Conclusion: The present study suggested that the BCR signaling pathway and

Yonese I, Takase H, Yoshimori M, et al.
CD79B mutations in primary vitreoretinal lymphoma: Diagnostic and prognostic potential.
Eur J Haematol. 2019; 102(2):191-196 [PubMed] Related Publications
OBJECTIVE: Primary vitreoretinal lymphoma (PVRL) is a rare type of lymphoma wherein the lesions are limited to the eyes. PVRL is difficult to diagnose because of the challenges related to obtaining sufficient samples for biopsy. Moreover, PVRL has poor outcomes and often leads to the development of central nervous system (CNS) lesions during its course. Two studies recently reported that approximately 70%-80% of patients with vitreoretinal lymphoma have MYD88
METHOD: By using direct sequencing and allele-specific polymerase chain reaction, we examined the mutation of CD79B
RESULTS: Among the included patients, six patients (35%) were found with CD79B

Hallas C, Preukschas M, Tiemann M
Immunohistochemical distinction of ABC and GCB in extranodal DLBCL is not reflected in mutation patterns.
Leuk Res. 2019; 76:107-111 [PubMed] Related Publications
Gene expression profiling (GEP) separated diffuse large B-cell lymphoma (DLBCL) in two different entities, i.e. activated B cell-like (ABC) and germinal center B cell-like (GCB) lymphomas with ABC lymphomas demonstrating a less favorable outcome. NF-kB pathway activating mutations in MYD88, CD79A/B and CARD11 are predominantly found in ABC type lymphomas. Targeted therapies affecting NF-kB pathways have shown therapeutic potential in this subtype. Immunohistochemistry algorithms have been developed as a tool for distinguishing these entities in routine clinical diagnostics. To test whether this immunohistochemistry classifier would detect the biological differences between the entities 147 DLBCLs were subtyped into ABC and GCB using the Visco-Young algorithm. Mutation analysis demonstrated mutations in MYD88 or CD79 A/B in 21% (10/47) of non-GCB type but only in 3% (1/31) of GCB lymphomas (p = 0.012) in nodal lymphomas. In primary extra nodal lymphomas, however, 17.5% (4/23) of GCB type and 37.5% (15/40) of non-GCB lymphomas carried mutations in MYD88 and CD79 A/B. While the Visco-Young algorithm was sufficient to detect biological differences (i.e. mutation patterns) in nodal DLBCL it did not distinguish GCB and non-GCB type lymphomas of primary extranodal sites. Here, the morphological sites of the lymphomas seem to be more important for their molecular pattern than their immunohistochemical status.

Zhou Y, Liu W, Xu Z, et al.
Analysis of Genomic Alteration in Primary Central Nervous System Lymphoma and the Expression of Some Related Genes.
Neoplasia. 2018; 20(10):1059-1069 [PubMed] Free Access to Full Article Related Publications
Primary central nervous system lymphoma (PCNSL) is a rare and special type of non-Hodgkin lymphoma. The treatment of PCNSL is comprehensive, combining surgery, radiotherapy, and chemotherapy. However, the outcome is poor because of its high invasiveness and rate of recurrence. We analyzed 22 cases of PCNSL using next-generation sequencing (NGS) to detect 64 candidate genes. We used immunohistochemical methods to analyze gene expression in 57 PCNSL samples. NGS showed that recurrent mutations in KMT2D and CD79B, components of the NF-κB pathway, accounted for 65% of total mutations in PCNSL samples. The most frequent mutated gene was PIM1 (77.27%, 17/22), followed by MYD88 (63.64%, 14/22), CD79B (69.09%, 13/22), and KMT2D (50.00%, 11/22). Mutations of the CD79B gene were associated with an inferior progression-free survival (PFS), and GNA13 gene mutations were associated with a shorter PFS and overall survival (OS) in PCNSL patients (P < .05). PIM1 and MYD88 were highly expressed in PCNSL patients and were related to their OS time. MYD88 overexpression might be an independent and poor prognostic predictor of OS time. In summary, we identified highly recurrent genetic lesions in CD79B and KMT2D, components of the NF-κB pathway, in PCNSL and validated the expression of PIM1 and MYD88 related to poor survival, thereby providing novel insights into the pathogenesis and precision medicine of PCNSL.

Yang Z, Tao Y, Xu X, et al.
Bufalin inhibits cell proliferation and migration of hepatocellular carcinoma cells via APOBEC3F induced intestinal immune network for IgA production signaling pathway.
Biochem Biophys Res Commun. 2018; 503(3):2124-2131 [PubMed] Related Publications
OBJECTIVE: This study aimed to evaluate functions of APOBEC3F gene in biological process of hepatocellular carcinoma (HCC) and anti-tumor mechanisms of bufalin.
METHODS: Effect of APOBEC3F and bufalin on cell proliferation and migration abilities were evaluated by CCK-8, wounding healing tests and transwell assays in SK-Hep1 and Bel-7404 cells. Bioinformatic analysis were also used to compare APOBEC3F expression levels, detect coexpressed genes and enrichment of pathways.
RESULTS: APOBEC3F was overexpressed in tumor tissues compared to adjacent tissues in HCC patients. And, APOBEC3F promotes cell proliferation and migration in SK-Hep1 and Bel-7404 cells. Bufalin inhibits cell proliferation and migration and reduces APOBEC3F expression. GO and KEGG enrichment of APOBEC3F-coexpressed genes revealed that APOBEC3F might active intestinal immune network for IgA production signaling pathway, leading to malignant biological behaviors of HCC cells. Additionally, siAPOBEC3F could decrease pIgR, CCR9, CCR10 and CXCR4 protein levels. And, bufalin inhibits the pIgR, CCR9, CCR10 and CXCR4 protein expressions.
CONCLUSIONS: Bufalin inhibits cell proliferation and migration of HCC cells via APOBEC3F induced intestinal immune network for IgA production signaling pathway.

Königova N, Skoumalova I, Onderkova J, et al.
HLA-B gene somatic insertion/deletion mutations in patients with acute myelogenous leukaemia.
Int J Immunogenet. 2018; 45(6):323-328 [PubMed] Related Publications
Loss of heterozygosity is considered to be the most common type of tumour-specific somatic mutation of the human leucocyte antigens (HLA) genes in patients with haematological malignancies. Nevertheless, subtle DNA sequence changes, namely short insertions/deletions, may also abolish the expression of HLA molecules and interfere with routine HLA typing. Two male patients with acute myelogenous leukaemia (AML) were indicated for the search of a suitable donor for allogeneic haematopoietic stem cell transplantation (aHSCT). The patients and their relatives were initially HLA typed by serological and DNA techniques at a low-resolution level. The HLA high-resolution (HR) type was obtained by means of sequencing-based typing (SBT). In both cases, anomalous frameshifts in the sequence were observed in the HLA-B gene, namely in exon 3 (Case 1, heterozygous deletion of two bases) and exon 4 (Case 2, heterozygous insertion of two bases). In the second case, the insertion variant was associated with a loss of HLA-B8 expression. To reveal whether these sequence patterns may be caused by somatic mutations in the malignant cells, blood sample in remission (Case 1) and buccal swab sample (Case 2) were collected from the patients. In an important manner, the SBT in these germline samples revealed common HLA-B*07:02,*15:01 (Case 1) and HLA-B*08:01,*35:02 (Case 2) types with no evidence for the sequence alteration observed in the initial samples. In conclusion, the insertion/deletion sequence variants of the HLA-B gene in two patients were limited to the initial blood samples with a substantial proportion of AML cells and thus may be attributed to the somatic mutation in the malignant cells. HLA somatic mutations should be taken into account in patients with haematological malignancies to prevent HLA mistyping and inappropriate selection of an aHSCT donor.

Liang L, Zeng JH, Qin XG, et al.
Distinguishable Prognostic Signatures of Left- and Right-Sided Colon Cancer: a Study Based on Sequencing Data.
Cell Physiol Biochem. 2018; 48(2):475-490 [PubMed] Related Publications
BACKGROUND/AIMS: Left- and right-sided colon cancers are considered to be two different diseases and have altered outcomes. However, specific molecules to predict the prognosis of left- and right-sided colon cancers are currently lacking.
METHODS: Expression profiling of colon cancer were downloaded from The Cancer Genome Atlas (TCGA). Differentially expressed genes (DEGs) of left- and right-sided colon cancers were compared by DESeq analysis. The prognostic values of DEGs were assessed by univariate and multivariate Cox regression. Prognostic index models of two side colon cancers were conducted with prognostic values genes, respectively. Interaction of DEGs was then analyzed by the protein-protein interaction (PPI). Different biology function of two sides of colon cancer was assessed by Gene Set Enrichment Analysis (GSEA).
RESULTS: A total of 167 DEGs were identified between left- and right-sided colon cancers based on TCGA data. Using univariate COX regression analysis, five genes (PHACTR3, CKMT2, CYP2W1, ERFE, HOXC4) were related to overall survival in left-sided, and eight distinguishable genes (EREG, ERFE, HOXC6, SLC22A31, TFF1, GFI1, ZG16, RASL10B) in right-sided. Further, left-sided prognostic model was established with PHACTR3 and CKMT2 (HR=2.040; 95%CI=1.004-4.145; P=0.049). Distinguishable prognostic signature for right-sided colon cancer was established based on EREG, ERFE, GFI1, and RASL10B (HR=3.530; 95%CI: 1.934-6.444; P< 0.001) in multivariate analysis. PPI analysis of 167 DEGs showed that CCL5, GNG4, GNLY, GZMH, DRD2, and FASLG genes were at the core of interaction network. In GSEA function analysis, four pathways, including antigen processing and presentation, natural killer cell mediated cytotoxicity, intestinal immune network for Iga production, and type I diabetes mellitus, were significantly enriched in the DEGs of the right-sided colon cancer.
CONCLUSIONS: This study constructs a panel of potential prognostic model of left- and right-sided colon cancers, respectively. We also provide molecular biological alterations between left- and right-sided colon cancers.

Phelan JD, Young RM, Webster DE, et al.
A multiprotein supercomplex controlling oncogenic signalling in lymphoma.
Nature. 2018; 560(7718):387-391 [PubMed] Free Access to Full Article Related Publications
B cell receptor (BCR) signalling has emerged as a therapeutic target in B cell lymphomas, but inhibiting this pathway in diffuse large B cell lymphoma (DLBCL) has benefited only a subset of patients

Xue N, Lin JH, Xing S, et al.
Plasma Macrophage Migration Inhibitory Factor and CCL3 as Potential Biomarkers for Distinguishing Patients with Nasopharyngeal Carcinoma from High-Risk Individuals Who Have Positive Epstein-Barr Virus Capsid Antigen-Specific IgA.
Cancer Res Treat. 2019; 51(1):378-390 [PubMed] Free Access to Full Article Related Publications
PURPOSE: The purpose of this study was to identify novel plasma biomarkers for distinguishing nasopharyngeal carcinoma (NPC) patients from healthy individuals who have positive Epstein-Barr virus (EBV) viral capsid antigen (VCA-IgA).
Materials and Methods: One hundred seventy-four plasma cytokines were analyzed by a Cytokine Array in eight healthy individuals with positive EBV VCA-IgA and eight patients with NPC. Real-time polymerase chain reaction, Western blotting, enzyme-linked immunosorbent assay (ELISA), and immunohistochemistry were employed to detect the expression levels of macrophage migration inhibitory factor (MIF) and CC chemokine ligand 3 (CCL3) in NPC cell lines and tumor tissues. Plasma MIF and CCL3 were measured by ELISA in 138 NPC patients, 127 EBV VCA-IgA negative (VN) and 100 EBV VCA-IgA positive healthy donors (VP). Plasma EBV VCA-IgA was determined by immunoenzymatic techniques.
RESULTS: Thirty-four of the 174 cytokines varied significantly between the VP and NPC group. Plasma MIF and CCL3 were significantly elevated in NPC patients compared with VN and VP. Combination of MIF and CCL3 could be used for the differential diagnosis of NPC from VN cohort (area under the curve [AUC], 0.913; sensitivity, 90.00%; specificity, 80.30%), and combination of MIF, CCL3, and VCA-IgA could be used for the differential diagnosis of NPC from VP cohort (AUC, 0.920; sensitivity, 90.00%; specificity, 84.00%), from (VN+VP) cohort (AUC, 0.961; sensitivity, 90.00%; specificity, 92.00%). Overexpressions of MIF and CCL3 were observed in NPC plasma, NPC cell lines and NPC tissues.
CONCLUSION: Plasma MIF, CCL3, and VCA-IgA combination significantly improves the diagnostic specificity of NPC in high-risk individuals.

Okugawa Y, Toiyama Y, Ichikawa T, et al.
Colony-stimulating factor-1 and colony-stimulating factor-1 receptor co-expression is associated with disease progression in gastric cancer.
Int J Oncol. 2018; 53(2):737-749 [PubMed] Related Publications
Colony‑stimulating‑factor‑1 (CSF‑1) is a hematopoietic growth factor that exerts its effects through the c‑fms/CSF‑1 receptor (CSF‑1R). The CSF‑1/CSF‑1R axis is thought to be involved in the development of several types of cancer. This study aimed to clarify the clinical and biological significance of the CSF‑1/CSF‑1R axis in gastric cancer (GC). For this purpose, we evaluated CSF‑1 and CSF‑1R expression in GC tissues from 148 patients by RT‑qPCR and immunohistochemistry. The biological roles of the CSF‑1/CSF‑1R axis were investigated by measuring the cell proliferation and migration, and anoikis resistance in a human GC cell line following treatment with recombinant human CSF‑1 and/or CSF‑1R inhibitor. The results revealed that an elevated expression of CSF‑1 or CSF‑1R significantly correlated with disease progression and with a poor overall survival (OS, P=0.037 and 0.016, respectively) and disease‑free survival (DFS, P<0.001 and <0.001, respectively) of patients with GC. Furthermore, a high co‑expression of CSF‑1 and CSF‑1R was an independent prognostic factor for OS (HR, 1.38; 95% CI, 1.02‑1.88; P=0.038) and DFS (HR, 1.79; 95% CI, 1.21‑2.67; P=0.004), and an independent risk factor for lymph node and peritoneal metastasis. Immunohistochemical analysis revealed an intense CSF‑1/CSF‑1R expression in the cytoplasm of cancer cells in primary GC tissues. CSF‑1 or CSF‑1R expression positively correlated with vascular endothelial growth factor A (VEGFA) or Fms related tyrosine kinase 1 (FLT1) expression in GC tissues. Treatment with recombinant human CSF‑1 promoted proliferation, migration and anoikis resistance in a GC cell line. These effects were generally blocked by CSF‑1R inhibition. On the whole, the findings of this study indicate that the CSF‑1/CSF‑1R axis may be a clinically useful prognostic and predictive biomarker for lymph node and peritoneal metastasis and a potential therapeutic target in GC.

He X, Kläsener K, Iype JM, et al.
Continuous signaling of CD79b and CD19 is required for the fitness of Burkitt lymphoma B cells.
EMBO J. 2018; 37(11) [PubMed] Free Access to Full Article Related Publications
Expression of the B-cell antigen receptor (BCR) is essential not only for the development but also for the maintenance of mature B cells. Similarly, many B-cell lymphomas, including Burkitt lymphoma (BL), require continuous BCR signaling for their tumor growth. This growth is driven by immunoreceptor tyrosine-based activation motif (ITAM) and PI3 kinase (PI3K) signaling. Here, we employ CRISPR/Cas9 to delete BCR and B-cell co-receptor genes in the human BL cell line Ramos. We find that Ramos B cells require the expression of the BCR signaling component Igβ (CD79b), and the co-receptor CD19, for their fitness and competitive growth in culture. Furthermore, we show that in the absence of any other BCR component, Igβ can be expressed on the B-cell surface, where it is found in close proximity to CD19 and signals in an ITAM-dependent manner. These data suggest that Igβ and CD19 are part of an alternative B-cell signaling module that use continuous ITAM/PI3K signaling to promote the survival of B lymphoma and normal B cells.

Dang YW, Lin P, Liu LM, et al.
In silico analysis of the potential mechanism of telocinobufagin on breast cancer MCF-7 cells.
Pathol Res Pract. 2018; 214(5):631-643 [PubMed] Related Publications
BACKGROUNDS AND AIMS: The extractives from a ChanSu, traditional Chinese medicine, have been discovered to possess anti-inflammatory and tumor-suppressing abilities. However, the molecular mechanism of telocinobufagin, a compound extracted from ChanSu, on breast cancer cells has not been clarified. The aim of this study is to investigate the underlying mechanism of telocinobufagin on breast cancer cells.
METHODS AND MATERIALS: The differentially expressed genes after telocinobufagin treatment on breast cancer cells were searched and downloaded from Gene Expression Omnibus (GEO), ArrayExpress and literatures. Bioinformatics tools were applied to further explore the potential mechanism of telocinobufagin in breast cancer using the Kyoto Encyclopedia of genes and genomes (KEGG) pathway, Gene ontology (GO) enrichment, panther, and protein-protein interaction analyses. To better comprehend the role of telocinobufagin in breast cancer, we also queried the Connectivity Map using the gene expression profiles of telocinobufagin treatment.
RESULTS: One GEO accession (GSE85871) provided 1251 differentially expressed genes after telocinobufagin treatment on MCF-7 cells. The pathway of neuroactive ligand-receptor interaction, cell adhesion molecules (CAMs), intestinal immune network for IgA production, hematopoietic cell lineage and calcium signaling pathway were the key pathways from KEGG analysis. IGF1 and KSR1, owning to higher protein levels in breast cancer tissues, IGF1 and KSR1 could be the hub genes related to telocinobufagin treatment. It was indicated that the molecular mechanism of telocinobufagin resembled that of fenspiride.
CONCLUSIONS: Telocinobufagin might regulate neuroactive ligand-receptor interaction pathway to exert its influences in breast cancer MCF-7 cells, and its molecular mechanism might share some similarities with fenspiride. This study only presented a comprehensive picture of the role of telocinobufagin in breast cancer MCF-7 cells using big data. However, more thorough and deeper researches are required to add to the validity of this study.

Kuo PY, Jatiani SS, Rahman AH, et al.
SOX11 augments BCR signaling to drive MCL-like tumor development.
Blood. 2018; 131(20):2247-2255 [PubMed] Free Access to Full Article Related Publications
Mantle cell lymphoma (MCL) is characterized by increased B-cell receptor (BCR) signaling, and BTK inhibition is an effective therapeutic intervention in MCL patients. The mechanisms leading to increased BCR signaling in MCL are poorly understood, as mutations in upstream regulators of BCR signaling such as CD79A, commonly observed in other lymphomas, are rare in MCL. The transcription factor SOX11 is overexpressed in the majority (78% to 93%) of MCL patients and is considered an MCL-specific oncogene. So far, attempts to understand SOX11 function in vivo have been hampered by the lack of appropriate animal models, because germline deletion of SOX11 is embryonically lethal. We have developed a transgenic mouse model (Eμ-SOX11-EGFP) in the C57BL/6 background expressing murine SOX11 and EGFP under the control of a B-cell-specific IgH-Eμ enhancer. The overexpression of SOX11 exclusively in B cells exhibits oligoclonal B-cell hyperplasia in the spleen, bone marrow, and peripheral blood, with an immunophenotype (CD5

Yeo SG, Won YS, Kim SH, Park DC
Differences in C-type lectin receptors and their adaptor molecules in the peritoneal fluid of patients with endometriosis and gynecologic cancers.
Int J Med Sci. 2018; 15(4):411-416 [PubMed] Free Access to Full Article Related Publications
Endometriosis, although not malignant, has clinically demonstrated properties of invasiveness and metastasis. The pathogenesis of endometriosis, however, has not yet been elucidated. The immunological differences between endometriosis and malignant gynecologic tumors were analyzed by assessing C-type lectin receptors, which are associated with innate immunity, and immunoglobulin secretion, which is associated with B cell adaptive immunity, in the peritoneal fluid of these patients. Peritoneal fluid samples were obtained from 42 patients with benign masses (control group), 38 with endometriosis, and 43 with gynecologic (ovarian, uterine, and cervical) cancers. The levels of expression in these samples of mRNAs encoding the C-type lectin receptors Dectin-1, MR1, MR2, DC-SIGN, Syk, Card 9, Bcl 10, Malt 1, src, Dec 205, Galectin, Tim 3, Trem 1, and DAP 12, were measured by real-time reverse transcription polymerase chain reaction, and the concentrations of IgG, IgA and IgM were measured by enzyme-linked immunosorbent assays (ELISA). Findings in the three groups were compared. The level of galectin mRNA was significantly lower, and the levels of MR2 and DAP 12 mRNAs significantly higher, in the endometriosis than in the control group (p<0.05 each). Compared with the gynecologic cancer group, the level of Bcl 10 mRNA was significantly lower, and the levels of MR1, MR2, Syk, Card 9, Malt 1, Dec 205, Tim 3, and DAP 12 mRNAs significantly higher, in the endometriosis group (p<0.05 each). The levels of MR2 and DAP 12 mRNAs were significantly higher in the endometriosis than in the control group (p<0.05 each), whereas the level of galectin mRNA was similar in the endometriosis and gynecologic cancer groups. IgA and IgG concentrations in peritoneal fluid were significantly lower in the gynecologic cancer than in the control group (p<0.05 each). However, concentrations of all three immunoglobulins in the endometriosis group did not differ from those in the other two groups (p>0.05). C-type lectin receptors and immunoglobulins act cooperatively and are closely associated in the pathogenesis of endometriosis. The decreased expression of galectin mRNA in the peritoneal fluid of the endometriosis group suggests that endometriosis and gynecologic cancers have similar immunologic characteristics.

Okugawa Y, Yao L, Toiyama Y, et al.
Prognostic impact of sarcopenia and its correlation with circulating miR-21 in colorectal cancer patients.
Oncol Rep. 2018; 39(4):1555-1564 [PubMed] Related Publications
Severe malnutrition accompanied by sarcopenia and cachexia, is strongly associated with the surgical and oncological outcomes in cancer patients. The aim of the present study was to clarify the clinical significance of sarcopenia and its correlation with sarcopenia-associated miRNA in colorectal cancer (CRC). A total of 167 CRC patients were enrolled in the present study. We evaluated psoas muscle mass index (PMI) and intramuscular adipose tissue content (IMAC). The expression of miR-21 in CRC tissues and preoperative serum was evaluated using quantitative PCR. Despite the lack of significant correlation between IMAC and disease-correlated factors, decreased PMI was significantly associated with well-established clinicopathological factors for disease progression. Decreased PMI was an independent prognostic factor for both overall survival and disease-free survival and was an independent risk factor for various types of metastasis. In contrast to the expression of tissue miR-21, the expression of serum miR-21 was significantly increased in CRC patients with low PMI. Furthermore, postoperative PMI was drastically improved compared with preoperative PMI in CRC patients with potentially curative resections. In conclusion, skeletal muscle mass may be a prognostic and predictive biomarker for distant metastasis in CRC patients and quantification of serum miR-21 expression could help clinicians make decisions regarding nutrition intervention strategies in CRC patients.

Li L, Ma Y, Xu Y, Maerkeya K
TIM-3 expression identifies a distinctive PD-1
Int Immunopharmacol. 2018; 57:139-146 [PubMed] Related Publications
Follicular helper T (Tfh) cells are critical regulators of immune responses in several human malignancies. Their characteristics in ovarian cancer (OC) patients remain unclear. In this study, the circulating CD4

Wu J, Zhang H, Wang W, et al.
Plasma microRNA signature of patients with IgA nephropathy.
Gene. 2018; 649:80-86 [PubMed] Related Publications
We looked for differentially expressed MicroRNAs (miRNAs) in Immunoglobulin A nephropathy (IgAN). Forty-eight miRNAs were identified through the initial screening phase (2 IgAN pools vs. 1 normal control (NC) pool) using quantitative reverse transcription polymerase chain reaction (qRT-PCR) based Exiqon panel (miRCURY-Ready-to-Use-PCR-Human-panel-I + II-V

Zhuang Q, Cheng K, Ming Y
CX3CL1/CX3CR1 Axis, as the Therapeutic Potential in Renal Diseases: Friend or Foe?
Curr Gene Ther. 2017; 17(6):442-452 [PubMed] Free Access to Full Article Related Publications
The fractalkine receptor chemokine (C-X3-C motif) receptor 1 (CX3CR1) and its highly selective ligand CX3CL1 mediate chemotaxis and adhesion of immune cells, which are involved in the pathogenesis and progression of numerous inflammatory disorders and malignancies. The CX3CL1/CX3CR1 axis has recently drawn attention as a potential therapeutic target because it is involved in the ontogeny, homeostatic migration, or colonization of renal phagocytes. We performed a Medline/PubMed search to detect recently published studies that explored the relationship between the CX3CL1/CX3CR1 axis and renal diseases and disorders, including diabetic nephropathy, renal allograft rejection, infectious renal diseases, IgA nephropathy, fibrotic kidney disease, lupus nephritis and glomerulonephritis, acute kidney injury and renal carcinoma. Most studies demonstrated its role in promoting renal pathopoiesis; however, several recent studies showed that the CX3CL1/CX3CR1 axis could also reduce renal pathopoiesis. Thus, the CX3CL1/CX3CR1 axis is now considered to be a double-edged sword that could provide novel perspectives into the pathogenesis and treatment of renal diseases and disorders.

Goedert JJ, Hua X, Bielecka A, et al.
Postmenopausal breast cancer and oestrogen associations with the IgA-coated and IgA-noncoated faecal microbiota.
Br J Cancer. 2018; 118(4):471-479 [PubMed] Free Access to Full Article Related Publications
BACKGROUND: The diversity and composition of the gut microbiota may affect breast cancer risk by modulating systemic levels of oestrogens and inflammation. The current investigation tested this hypothesis in postmenopausal women by identifying breast cancer associations with an inflammation marker, oestrogen levels, and faecal microbes that were or were not coated with mucosal immunoglobulin A (IgA).
METHODS: In this population-based study, we compared 48 postmenopausal breast cancer cases (75% stage 0-1, 88% oestrogen-receptor positive) to 48 contemporaneous, postmenopausal, normal-mammogram, age-matched controls. Microbiota metrics employed 16S rRNA gene amplicon sequencing from IgA-coated and -noncoated faecal microbes. High-performance liquid chromatography/mass spectrometry (HPLC/MS) and radioimmunoassay were used to quantify urine prostaglandin E metabolite (PGE-M), a possible marker of inflammation; urine oestrogens and oestrogen metabolites were quantified by HPLC/MS-MS.
RESULTS: Women with pre-treatment breast cancer had non-significantly elevated oestrogen levels; controls' (but not cases') oestrogens were directly correlated with their IgA-negative microbiota alpha diversity (P=0.012). Prostaglandin E metabolite levels were not associated with case status, oestrogen levels, or alpha diversity. Adjusted for oestrogens and other variables, cases had significantly reduced alpha diversity and altered composition of both their IgA-positive and IgA-negative faecal microbiota. Cases' faecal microbial IgA-positive imputed Immune System Diseases metabolic pathway genes were increased; also, cases' IgA-positive and IgA-negative imputed Genetic Information Processing pathway genes were decreased (P⩽0.01).
CONCLUSIONS: Compared to controls, breast cancer cases had significant oestrogen-independent associations with the IgA-positive and IgA-negative gut microbiota. These suggest that the gut microbiota may influence breast cancer risk by altered metabolism, oestrogen recycling, and immune pressure.

Ius T, Ciani Y, Ruaro ME, et al.
An NF-κB signature predicts low-grade glioma prognosis: a precision medicine approach based on patient-derived stem cells.
Neuro Oncol. 2018; 20(6):776-787 [PubMed] Free Access to Full Article Related Publications
Background: While recent genome-wide association studies have suggested novel low-grade glioma (LGG) stratification models based on a molecular classification, we explored the potential clinical utility of patient-derived cells. Specifically, we assayed glioma-associated stem cells (GASC) that are patient-derived and representative of the glioma microenvironment.
Methods: By next-generation sequencing, we analyzed the transcriptional profile of GASC derived from patients who underwent anaplastic transformation either within 48 months (GASC-BAD) or ≥7 years (GASC-GOOD) after surgery. Gene set enrichment and pathway enrichment analyses were applied. The prognostic role of a nuclear factor-kappaB (NF-κB) signature derived from GASC-BAD was tested in 530 newly diagnosed diffuse LGG patients comprised within The Cancer Genome Atlas (TCGA) database. The prognostic value of the GASC upstream regulator p65 NF-κB was assessed, by univariate and multivariate Cox analyses, in a single center case study, including 146 grade II LGGs.
Results: The key elements differentiating the transcriptome of GASC isolated from LGG with different prognoses were mostly related to hallmarks of cancer (eg, inflammatory/immune process, NF-κB activation). Consistently, the NF-κB signature extrapolated from the GASC study was prognostic in the dataset of TCGA. Finally, the nuclear expression of the NF-kB-p65 protein, assessed using an inexpensive immunohistochemical method, was an independent predictor of both overall survival and malignant progression-free survival in 146 grade II LGGs.
Conclusion: This study demonstrates for the first time the independent prognostic role of NF-kB activation in LGG and outlines the role of patient-based stem cell models as a tool for precision medicine approaches.

Shalapour S, Lin XJ, Bastian IN, et al.
Inflammation-induced IgA+ cells dismantle anti-liver cancer immunity.
Nature. 2017; 551(7680):340-345 [PubMed] Free Access to Full Article Related Publications
The role of adaptive immunity in early cancer development is controversial. Here we show that chronic inflammation and fibrosis in humans and mice with non-alcoholic fatty liver disease is accompanied by accumulation of liver-resident immunoglobulin-A-producing (IgA

Gladkikh AA, Potashnikova DM, Tatarskiy V, et al.
Comparison of the mRNA expression profile of B-cell receptor components in normal CD5-high B-lymphocytes and chronic lymphocytic leukemia: a key role of ZAP70.
Cancer Med. 2017; 6(12):2984-2997 [PubMed] Free Access to Full Article Related Publications
The B-cell receptor (BCR) signaling pathway is of great importance for B-cell survival and proliferation. The BCR expressed on malignant B-CLL cells contributes to the disease pathogenesis, and its signaling pathway is currently the target of several therapeutic strategies. Although various BCR alterations have been described in B-CLL at the protein level, the mRNA expression levels of tyrosine kinases in B-CLL compared to that in normal CD5-high and CD5-low B-lymphocytes remain unknown. In the current study, we measured the mRNA expression levels of CD79A, CD79B, LYN, SYK, SHP1, and ZAP70 in purified populations of CD5-high B-CLL cells, CD5-low B-cells from the peripheral blood of healthy donors, and CD5-high B-cells from human tonsils. Here, we report a clear separation in the B-CLL dataset between the ZAP70-high and ZAP70-low subgroups. Each subgroup has a unique expression profile of BCR signaling components that might reflect the functional status of the BCR signaling pathway. Moreover, the ZAP70-low subgroup does not resemble either CD5-high B-lymphocytes from the tonsils or CD5-low lymphocytes from PBMC (P < 0.05). We also show that ZAP70 is the only gene that is differentially expressed in CD5-high and CD5-low normal B-lymphocytes, confirming the key role of Zap-70 tyrosine kinase in BCR signaling alterations in B-CLL.

Liu R, Lu Z, Gu J, et al.
MicroRNAs 15A and 16-1 Activate Signaling Pathways That Mediate Chemotaxis of Immune Regulatory B cells to Colorectal Tumors.
Gastroenterology. 2018; 154(3):637-651.e7 [PubMed] Related Publications
BACKGROUND & AIMS: B cells infiltrate tumors, but little is known about how they affect tumor growth and progression. microRNA15A (MIR15A or miRNA15A) and microRNA16-1 (MIR16-1 or miRNA16-1) regulate cell proliferation, apoptosis, and drug resistance. We investigated their involvement in B-cell-mediated immune suppression by colorectal tumors.
METHODS: Mice with disruptions of the gene cluster that encodes MIR15A and MIR16-1 (knockout mice), and control (C57BL/B6) mice were given azoxymethane with dextran sodium sulfate (AD) to induce formation of colorectal tumors. Mice were given anti-CD20 to delete B cells, or injections of agomir to increase MIR15A and MIR16-1. Proliferation of CD8
RESULTS: Tumors that developed in knockout mice following administration of AD were larger and contained greater numbers of B cells than tumors that grew in control mice. Most of the B cells in the tumors were positive for immunoglobulin A (IgA
CONCLUSIONS: We found increased levels of MIR15A and MIR16-1 to reduce numbers of IgA

Walters DK, Arendt BK, Tschumper RC, et al.
Characterization and use of the novel human multiple myeloma cell line MC-B11/14 to study biological consequences of CRISPR-mediated loss of immunoglobulin A heavy chain.
Exp Hematol. 2018; 57:42-49.e1 [PubMed] Free Access to Full Article Related Publications
The genetic abnormalities underlying multiple myeloma (MM) are notoriously complex and intraclonal heterogeneity is a common disease feature. In the current study, we describe the establishment of a monoclonal immunoglobulin A (IgA) kappa (κ) MM cell line designated MC-B11/14. Cytogenetic and fluorescence in situ hybridization analyses of the original and relapse patient samples revealed that the MM clone was nonhyperdiploid and possessed an 11;14 chromosomal translocation. The MC-B11/14 cell line, established from the relapse sample, is tetraploid and houses the t(11;14) abnormality. Given our long-standing interest in Ig function and secretion, we next used CRISPR technology to knock out IgA heavy-chain expression in the MC-B11/14 cells to assess the biological consequences of converting this cell line to one only expressing κ light chains. As expected, secretion of intact IgA was undetectable from MC-B11/14

Ohata Y, Tatsuzawa A, Ohyama Y, et al.
A distinctive subgroup of oral EBV+ B-cell neoplasm with polymorphous features is potentially identical to EBV+ mucocutaneous ulcer.
Hum Pathol. 2017; 69:129-139 [PubMed] Related Publications
Epstein-Barr virus-positive mucocutaneous ulcer (EBVMCU) is a newly recognized provisional entity included in mature B-cell neoplasm in the latest 2016 World Health Organization Classification. It has a self-limited growth potential with a high predilection for oral cavities and occurs in age-related or iatrogenic immunodeficiency with indolent clinical courses. However, it shares histological features with EBV-positive diffuse large B-cell lymphoma (DLBCL), and this often leads to diagnostic challenges and controversies in patients with an oral EBV-positive B-cell neoplasm. The aim of this study was to better characterize and comprehend the pathophysiology of DLBCL and EBVMCU in the oral cavity. We conducted clinicopathologic and recurrent gene mutation analysis of 49 cases (14 EBV positive, 35 EBV negative), including cases diagnosed as DLBCL or B-cell lymphoproliferative disorders with high-grade morphology in the oral cavity. All EBV-positive cases matched the criteria of EBVMCU, with significantly earlier clinical stages than the EBV-negative group (P=.0006). Besides, histological analysis showed that all EBV-positive cases presented polymorphous features, whereas 91.4% (32/35) of the EBV-negative cases showed diffuse and monotonous proliferation (P<.0001). Furthermore, EBV-positive cases presented favorable clinical outcomes without disease-related death or recurrence. Gene mutation analysis (MYD88, CD79A, CD79B, CARD11, and EZH2) revealed that 33.3% (9/27) of EBV-negative cases harbored at least 1 gene mutation, whereas no gene mutation was observed in the EBV-positive group (0/11). These results suggest that oral EBV-positive B-cell lymphoid proliferation with polymorphous features often fulfill the criteria for EBVMCU, with clinicopathologically and genetically distinctive properties.

Antoniali G, Serra F, Lirussi L, et al.
Mammalian APE1 controls miRNA processing and its interactome is linked to cancer RNA metabolism.
Nat Commun. 2017; 8(1):797 [PubMed] Free Access to Full Article Related Publications
Mammalian apurinic/apyrimidinic endonuclease 1 is a DNA repair enzyme involved in genome stability and expression of genes involved in oxidative stress responses, tumor progression and chemoresistance. However, the molecular mechanisms underlying the role of apurinic/apyrimidinic endonuclease 1 in these processes are still unclear. Recent findings point to a novel role of apurinic/apyrimidinic endonuclease 1 in RNA metabolism. Through the characterization of the interactomes of apurinic/apyrimidinic endonuclease 1 with RNA and other proteins, we demonstrate here a role for apurinic/apyrimidinic endonuclease 1 in pri-miRNA processing and stability via association with the DROSHA-processing complex during genotoxic stress. We also show that endonuclease activity of apurinic/apyrimidinic endonuclease 1 is required for the processing of miR-221/222 in regulating expression of the tumor suppressor PTEN. Analysis of a cohort of different cancers supports the relevance of our findings for tumor biology. We also show that apurinic/apyrimidinic endonuclease 1 participates in RNA-interactomes and protein-interactomes involved in cancer development, thus indicating an unsuspected post-transcriptional effect on cancer genes.APE1 plays an important role in the cellular response to oxidative stress, and mutations are linked to tumor progression and chemoresistance. Here, the authors characterize the interactions of APE1 with RNA and demonstrate a role in microRNA processing.

Catalan-Dibene J, Vazquez MI, Luu VP, et al.
Identification of IL-40, a Novel B Cell-Associated Cytokine.
J Immunol. 2017; 199(9):3326-3335 [PubMed] Free Access to Full Article Related Publications
We describe a novel B cell-associated cytokine, encoded by an uncharacterized gene (

Liao YH, Ren JT, Zhang W, et al.
Polymorphisms in homologous recombination repair genes and the risk and survival of breast cancer.
J Gene Med. 2017; 19(9-10) [PubMed] Related Publications
BACKGROUND: Immunoglobulin (Ig)A antibody of Epstein-Barr virus (EBV) was found to associate with breast cancer (BC), whereas IgA positivity was related to a series of genetic markers in the genes of homologous recombination repair system (HRRs). We assessed the associations of the polymorphisms in HRR genes with the risk and survival of BC.
METHODS: A case-control study was conducted with 1551 bc cases and 1605 age-matched healthy controls between October 2008 and March 2012 in the Guangzhou Breast Cancer Study (GZBCS), China, and the case population were followed up until 31 January 2016. Five single nucleotide polymorphisms of candidate genes in HRR system were genotyped. Odds ratios (ORs) and hazards ratios (HRs) were calculated using multivariate logistic regression and Cox proportional hazards regression to estimate the risk and prognostic effect, respectively.
RESULTS: RFC1 rs6829064 (AA) was associated with an increased BC risk [OR = 1.35; 95% confidence interval (CI) = 1.06-1.73] compared to the wild genotype (GG). NRM rs1075496 (GT/TT versus GG) was associated with a worse progression-free survival (PFS) and the HR was 1.34 (95% CI = 1.01-1.78), particularly among advanced patients. LIG3 rs1052536 (CT/TT versus CC) was associated with a better PFS and the HR was 0.70 (95% CI = 0.53-0.93). However, RAD54L rs1710286 and RPA1 rs11078676 were not observed to be associated with either the risk or survival of BC.
CONCLUSIONS: The findings of the present study suggest that the polymorphisms in HRR genes were associated with BC risk (RFC1 rs6829064) and prognosis (NRM rs1075496 and LIG3 rs1052536), whereas RAD54L rs1710286 and RPA1 rs11078676 had null associations with BC.

Disclaimer: This site is for educational purposes only; it can not be used in diagnosis or treatment.

Cite this page: Cotterill SJ. CD79A, Cancer Genetics Web: Accessed:

Creative Commons License
This page in Cancer Genetics Web by Simon Cotterill is licensed under a Creative Commons Attribution-ShareAlike 4.0 International License.
Note: content of abstracts copyright of respective publishers - seek permission where appropriate.

 [Home]    Page last revised: 30 August, 2019     Cancer Genetics Web, Established 1999