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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.
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.
In plain words · 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.
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.
Component of the class I major histocompatibility complex (MHC). Involved in the presentation of peptide antigens to the immune system.
No product in this corpus aims at B2M yet. Because the protein is lost rather than overactive, drugs either restore its function or exploit the weakness its loss leaves (synthetic lethality).
Tumour-specific alteration: the catalogues call it an oncogene driver (IntOGen cohort analysis finds it activated more often than chance) and a tumour suppressor (IntOGen finds it knocked out more often than chance), so the direction differs between cohorts but the alteration is somatic either way; what a medicine would aim at or exploit is the altered form or its loss, absent from normal cells; no corpus medicine is aimed at it yet. HPA B2M: RNA low tissue specificity; high antibody staining in 7 normal tissues; highest cancer staining urothelial cancer (2 of 11 high). Distribution: 6 cancer families in the corpus carry a prevalence row, label threshold or catalogue link for it (Lymphoma, Colorectal cancer, Lung cancer (all types), Head and neck squamous cell carcinoma, Cervical cancer, Skin cancer (all types)); Open Targets associates it with 1 specific cancer type at or above 0.5 (diffuse large B-cell lymphoma). (Rule 6 of scripts/fetch-target-specificity.ts.)
Sources: UniProt P61769; CIViC gene B2M; IntOGen B2M; Human Protein Atlas B2M tissue; Open Targets ENSG00000166710 associations
First described 1973. Earliest sequence paper UniProt cites for the protein: Cunningham B.A. et al, Biochemistry, 1973, "The complete amino acid sequence of beta 2-microglobulin". Source.
Sources: HGNC HGNC:914 (approved symbol, name, aliases, locus and cross-references (hgnc_complete_set.txt)); UniProt P61769 (protein name, function text, keywords and locations (REST API)); CIViC gene B2M (7 evidence items, 0 assertions, 4 variants; diseases: Colorectal Cancer, Melanoma, Lung Cancer, Mantle Cell Lymphoma, Diffuse Large B-cell Lymphoma and 1 more (GraphQL API, CC0)); Open Targets ENSG00000166710 (association with cancer (MONDO_0004992) 0.69; per-cancer scores at or above 0.5: colorectal cancer 0.56, melanoma 0.57, diffuse large B-cell lymphoma 0.67, non-Hodgkin lymphoma 0.72 (GraphQL API, CC0)); IntOGen B2M (driver in 10 cohorts (Act 4, LoF 6); Compendium_Cancer_Genes.tsv release 20240920, CC0 1.0)
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).
RNA: low tissue specificity, detected in all normal tissues.
Medium: Adrenal gland, Appendix, Cerebral cortex, Cervix, Colon, Duodenum, Endometrium, Epididymis.
Medium only: carcinoid, cervical cancer, endometrial cancer, glioma.
Human Protein Atlas version 25.1, antibody staining at reliability approved, enhanced or supported; used under CC BY-SA 3.0. Staining counts are patients per level in the atlas cohort, not population prevalence.
| Cancer | Prevalence | Measure | Note | Source |
|---|---|---|---|---|
| Colorectal cancer | 3-7% | Inactivating mutation or deletion (antigen presentation) | cBioPortal: 335 of 7,237, 4.6%, in crc_msk_2026; 39 of 1,134, 3.4%, in crc_msk_2017; 61 of 1,516, 4.0%, in crc_eo_2020; 24 of 534, 4.5%, plus 13 deep deletions of 592, in coadread_tcga_pan_can_atlas_2018; 44 of 619, 7.1%, in coadread_dfci_2016. | cBioPortal (TCGA) |
Approximate, population-level figures; the measure column says what was counted. Ranges show the midpoint as a bar.
It gives a genetic account of both immunotherapy failures: why some mismatch repair deficient tumours resist, and why the microsatellite-stable majority has no T cells in it to begin with.
It is the argument that immune biology matters across the whole disease rather than only in the mismatch repair deficient sixth, and the reason microsatellite-stable tumours with high neoantigen load are still being pursued for immunotherapy.
Query for this target: (TITLE:"B2M" OR ABSTRACT:"B2M" OR TITLE:"beta-2-microglobulin" OR ABSTRACT:"beta-2-microglobulin" OR TITLE:"Beta-2-microglobulin" OR ABSTRACT:"Beta-2-microglobulin") AND (cancer OR tumor OR tumour OR oncology OR carcinoma OR lymphoma OR leukemia OR leukaemia OR myeloma OR sarcoma OR melanoma OR glioma). Results are unfiltered search hits about B2M, not a curated reading list.
Shares Clonal haematopoiesis (CHIP), Nodal T-follicular helper cell lymphoma, angioimmunoblastic type (angioimmunoblastic T-cell lymphoma), Epigenetic reprogramming, CIViC.
Shares Antigen presentation & immune editing, Hodgkin lymphoma, CIViC, IntOGen.
Shares Clonal haematopoiesis (CHIP), Nodal T-follicular helper cell lymphoma, angioimmunoblastic type (angioimmunoblastic T-cell lymphoma), Epigenetic reprogramming, CIViC.
Shares Epigenetic reprogramming, Mantle cell lymphoma, CIViC, IntOGen.
Shares Epigenetic reprogramming, Cervical cancer, CIViC, IntOGen.
Shares Clonal haematopoiesis (CHIP), CIViC, IntOGen, Non-Hodgkin lymphoma (all types).
Shares Clonal haematopoiesis (CHIP), Nodal T-follicular helper cell lymphoma, angioimmunoblastic type (angioimmunoblastic T-cell lymphoma), Epigenetic reprogramming, Non-Hodgkin lymphoma (all types).
Shares Primary CNS lymphoma, Mantle cell lymphoma, Hodgkin lymphoma, Diffuse large B-cell lymphoma.