# B2M

Source: https://onco.cc/targets/b2m/  
OnCo record `b2m` (Target). Data CC BY-NC 4.0, attribute "Data from OnCo (onco.cc)"; commercial use needs a licence.

## TL;DR

B2M (Beta-2-microglobulin) is a gene whose normal job is to hold cell growth in check. The public catalogues list it as a drug target, an oncogene driver, a tumour suppressor and a biomarker, and clinical evidence ties its variants to diagnosis, prognosis or drug response. Tied to Non-Hodgkin lymphoma, Colorectal cancer, Lung cancer and 5 more.

## Summary

Component of the class I major histocompatibility complex (MHC). Involved in the presentation of peptide antigens to the immune system. Exogenously applied M.tuberculosis EsxA or EsxA-EsxB (or EsxA expressed in host) binds B2M and decreases its export to the cell surface (total protein levels do not change), probably leading to defects in class I antigen presentation.

CIViC holds 7 clinical evidence items and 0 assertions across 4 variants, naming Pembrolizumab, Nivolumab, Anti-PD-L1 Monoclonal Antibody and Immune Checkpoint Inhibitor and others. Open Targets scores its association with cancer at 0.69 (direct and indirect evidence; datatypes literature 0.98, affected pathway 0.61, genetic association 0.00, somatic mutation 0.88). IntOGen calls it a driver in 10 cohorts (4 activating, 6 loss-of-function), covering Cervical Squamous Cell Carcinoma, Diffuse Large B-Cell Lymphoma, NOS, Head and Neck Squamous Cell Carcinoma, Melanoma, Malignant Lymphoma, Non-Hodgkin Lymphoma and others.

## Fields

- Kind: Target
- Last checked: 2026-09-23
- Also known as: beta-2-microglobulin; Beta-2-microglobulin
- Tags: cancer-genes-wave
- Symbol: B2M
- Class: tumor-suppressor
- Biology: Component of the class I major histocompatibility complex (MHC). Involved in the presentation of peptide antigens to the immune system. Exogenously applied M.tuberculosis EsxA or EsxA-EsxB (or EsxA expressed in host) binds B2M and decreases its export to the cell surface (total protein levels do not change), probably leading to defects in class I antigen presentation. Location: Secreted; Cell surface (UniProt). Locus 15q21.1 (HGNC).
- Where found: Non-Hodgkin lymphoma: Open Targets association 0.72 with non-Hodgkin lymphoma (MONDO_0018908); IntOGen driver in 2 cohorts (MLYM, NHL); Colorectal cancer: Open Targets association 0.56 with colorectal cancer (MONDO_0005575); CIViC evidence names this disease; Lung cancer: CIViC evidence names this disease; Head and neck squamous cell carcinoma: IntOGen driver in 2 cohorts (HNSC); Cervical cancer: IntOGen driver in 1 cohort (CESC); Diffuse large B-cell lymphoma: Open Targets association 0.67 with diffuse large B-cell lymphoma (MONDO_0018905); CIViC evidence names this disease; Colorectal cancer: inactivating mutation or deletion (antigen presentation) 3-7%

## Notes

- Written by scripts/fetch-cancer-genes.ts from CIViC, Open Targets, IntOGen, HGNC and UniProt; the function text is UniProt's, condensed and in UK spelling. Roles: CIViC lists 5 therapies; IntOGen calls it an activating (Act) driver in 4 cohorts; IntOGen calls it a loss-of-function (LoF) driver in 6 cohorts; CIViC holds 7 clinical evidence items on its variants. Evidence tier "clinical-evidence" is the strongest of those signals.
- Prevalence not recorded: none of the sources gives a positivity rate.
- Colorectal cancer: inactivating mutation in 3 to 7% overall but 31.0% of MSI-high against 1.5% of microsatellite-stable samples in crc_msk_2026, with biallelic B2M and HLA loss by copy-number change and copy-neutral loss of heterozygosity documented across 1,211 tumours (Grasso 2018). It is an immunoediting scar and the best available explanation for the mismatch repair deficient patients who do not respond to a checkpoint inhibitor.
- Lymphoma, RHOA G17V and the epigenetic mutations of T-follicular-helper lymphoma: A single substitution, G17V, in the small GTPase RHOA produces a protein that does not bind GTP and that blocks the wild-type protein as well. It is specific to the tumour cell, whereas the TET2 mutations that accompany it are found in non-tumour haematopoietic cells too, which places the TET2 lesion earlier, in the stem cell, and makes this lymphoma a disease that grows out of clonal haematopoiesis. Frequency: RHOA G17V in 68% of angioimmunoblastic T-cell lymphoma samples, with every G17V case also carrying a TET2 mutation (Sakata-Yanagimoto 2014); independently, in 22 of 35 angioimmunoblastic cases, 67%, and 8 of 44 peripheral T-cell lymphoma not otherwise specified, 18%, alongside recurrent TET2, DNMT3A and IDH2 mutations and less frequent FYN, ATM, B2M and CD58 lesions (Palomero 2014). What it changes about treatment: Not through an approved test. The hypomethylating agents are used in this disease on the strength of the TET2 and DNMT3A biology rather than on a mutation result, and azacitidine-containing regimens have shown activity in T-follicular-helper histology specifically.

## Sources

- HGNC HGNC:914: https://www.genenames.org/data/gene-symbol-report/#!/hgnc_id/HGNC:914
- UniProt P61769: https://www.uniprot.org/uniprotkb/P61769/entry
- NCBI Gene 567: https://www.ncbi.nlm.nih.gov/gene/567
- Ensembl ENSG00000166710: https://www.ensembl.org/Homo_sapiens/Gene/Summary?g=ENSG00000166710
- Sakata-Yanagimoto et al., Nat Genet 2014: somatic RHOA G17V in angioimmunoblastic T-cell lymphoma: https://doi.org/10.1038/ng.2872
- Palomero et al., Nat Genet 2014: recurrent mutations in epigenetic regulators, RHOA and FYN in peripheral T-cell lymphoma: https://doi.org/10.1038/ng.2873

## Connected records

- collections: [CIViC](https://onco.cc/collections/civic/), [IntOGen](https://onco.cc/collections/intogen/), [Open Targets Platform](https://onco.cc/collections/open-targets/)
- cancers: [Cervical cancer](https://onco.cc/cancers/cervical/), [Colorectal cancer](https://onco.cc/cancers/colorectal/), [Diffuse large B-cell lymphoma](https://onco.cc/cancers/dlbcl/), [Head and neck squamous cell carcinoma](https://onco.cc/cancers/head-and-neck/), [Hodgkin lymphoma](https://onco.cc/cancers/hodgkin-lymphoma/), [Lung cancer (all types)](https://onco.cc/cancers/lung-cancer/), [Mantle cell lymphoma](https://onco.cc/cancers/mantle-cell-lymphoma/), [Melanoma](https://onco.cc/cancers/melanoma/), [Nodal T-follicular helper cell lymphoma, angioimmunoblastic type (angioimmunoblastic T-cell lymphoma)](https://onco.cc/cancers/angioimmunoblastic-t-cell-lymphoma/), [Non-Hodgkin lymphoma (all types)](https://onco.cc/cancers/non-hodgkin-lymphoma/), [Primary CNS lymphoma](https://onco.cc/cancers/primary-cns-lymphoma/)
- pathways: [Antigen presentation & immune editing](https://onco.cc/pathways/antigen-presentation-immunoediting/), [Clonal haematopoiesis (CHIP)](https://onco.cc/pathways/clonal-haematopoiesis/), [Epigenetic reprogramming](https://onco.cc/pathways/epigenetic-reprogramming/)
- key papers: [Genetic mechanisms of immune evasion in colorectal cancer](https://onco.cc/key-papers/paper-grasso-immune-evasion-colorectal-cancer-discov-2018/), [Genomic correlates of immune-cell infiltrates in colorectal carcinoma](https://onco.cc/key-papers/paper-giannakis-genomic-correlates-immune-colorectal-cell-rep-2016/)

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