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MYD88 (Myeloid differentiation primary response protein MyD88) is a gene that drives cell growth when it is altered. The public catalogues list it as a drug target, an oncogene driver and a biomarker, and clinical evidence ties its variants to diagnosis, prognosis or drug response. Tied to Non-Hodgkin lymphoma, Leukaemia, Breast cancer and 4 more.
Adapter protein involved in the Toll-like receptor and IL-1 receptor signalling pathway in the innate immune response. Acts via IRAK1, IRAK2, IRF7 and TRAF6, leading to NF-kappa-B activation, cytokine secretion and the inflammatory response. Increases IL-8 transcription.
CIViC holds 5 clinical evidence items and 0 assertions across 2 variants, naming Paclitaxel, Ibrutinib, IRAK-1/4 Inhibitor and IMG-2005-5. Open Targets scores its association with cancer at 0.61 (direct and indirect evidence; datatypes literature 0.98, genetic association 0.00, somatic mutation 0.95). IntOGen calls it a driver in 10 cohorts (10 activating, 0 loss-of-function), covering Chronic Lymphocytic Leukaemia/Small Lymphocytic Lymphoma, Diffuse Large B-Cell Lymphoma, NOS, Malignant Lymphoma, Non-Hodgkin Lymphoma.
In plain words · MYD88 (Myeloid differentiation primary response protein MyD88) is a gene that drives cell growth when it is altered. The public catalogues list it as a drug target, an oncogene driver and a biomarker, and clinical evidence ties its variants to diagnosis, prognosis or drug response. Tied to Non-Hodgkin lymphoma, Leukaemia, Breast cancer and 4 more.
MYD88 (Myeloid differentiation primary response protein MyD88) is a gene that drives cell growth when it is altered. The public catalogues list it as a drug target, an oncogene driver and a biomarker, and clinical evidence ties its variants to diagnosis, prognosis or drug response. Tied to Non-Hodgkin lymphoma, Leukaemia, Breast cancer and 4 more.
Adapter protein involved in the Toll-like receptor and IL-1 receptor signalling pathway in the innate immune response.
No product in this corpus aims at MYD88 yet. Drugs fit a pocket that exists only in one shape of the mutant protein and hold it there, off.
Tumour-specific alteration: the catalogues call it an oncogene driver (IntOGen cohort analysis finds it activated more often than chance); 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 MYD88: RNA low tissue specificity; high antibody staining in 32 normal tissues; highest cancer staining thyroid cancer (3 of 4 high). Distribution: 3 cancer families in the corpus carry a prevalence row, label threshold or catalogue link for it (Lymphoma, Leukaemia, Breast cancer (all types)); Open Targets associates it with 3 specific cancer types at or above 0.5 (B-cell chronic lymphocytic leukemia, diffuse large B-cell lymphoma, lymphoid leukemia). (Rule 6 of scripts/fetch-target-specificity.ts.)
Sources: UniProt Q99836; CIViC gene MYD88; IntOGen MYD88; Human Protein Atlas MYD88 tissue; Open Targets ENSG00000172936 associations
First described 1996. Earliest sequence paper UniProt cites for the protein: Hardiman et al, Oncogene, 1996, "Molecular characterization and modular analysis of human MyD88". Source.
Sources: HGNC HGNC:7562 (approved symbol, name, aliases, locus and cross-references (hgnc_complete_set.txt)); UniProt Q99836 (protein name, function text, keywords and locations (REST API)); CIViC gene MYD88 (5 evidence items, 0 assertions, 2 variants; diseases: Lymphoplasmacytic Lymphoma, Breast Cancer, Diffuse Large B-cell Lymphoma, Chronic Lymphocytic Leukaemia (GraphQL API, CC0)); Open Targets ENSG00000172936 (association with cancer (MONDO_0004992) 0.61; per-cancer scores at or above 0.5: acute lymphoblastic leukaemia 0.70, diffuse large B-cell lymphoma 0.72, B-cell chronic lymphocytic leukaemia 0.70, non-Hodgkin lymphoma 0.83, Waldenstrom macroglobulinemia 0.50, breast cancer 0.54 (GraphQL API, CC0)); IntOGen MYD88 (driver in 10 cohorts (Act 10, LoF 0); Compendium_Cancer_Genes.tsv release 20240920, CC0 1.0)
Adapter protein involved in the Toll-like receptor and IL-1 receptor signalling pathway in the innate immune response. Acts via IRAK1, IRAK2, IRF7 and TRAF6, leading to NF-kappa-B activation, cytokine secretion and the inflammatory response. Increases IL-8 transcription. Involved in IL-18-mediated signalling pathway. Activates IRF1 resulting in its rapid migration into the nucleus to mediate an efficient induction of IFN-beta, NOS2/INOS, and IL12A genes. Upon TLR8 activation by GU-rich single-stranded RNA (GU-rich RNA) derived from viruses such as SARS-CoV-2, SARS-CoV and HIV-1, induces IL1B release through NLRP3 inflammasome activation. Location: Cytoplasm; Nucleus (UniProt). Locus 3p22.2 (HGNC).
RNA: low tissue specificity, detected in many normal tissues.
Medium: Adipose tissue, Cervix, Epididymis, Esophagus, Heart muscle, Oral mucosa, Ovary, Skeletal muscle.
Medium only: breast cancer, carcinoid, head and neck cancer, skin cancer.
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.
The piece that turns a research classification into something a trial can use on one person's biopsy, with a probability attached rather than a flat label. It is the reason genetics-directed lymphoma trials became possible at all.
The genetic nosology that precision-medicine trials in diffuse large B-cell lymphoma now use to pick patients. It gives a mechanism, not just a label: two of the four subtypes point at a drug class that already exists.
One of the two foundational genetic classifications of diffuse large B-cell lymphoma. Neither has yet changed what a patient receives outside a trial, but together they are the reason precision-medicine trials in this disease now select by genetics rather than by cell of origin.
Query for this target: (TITLE:"MYD88" OR ABSTRACT:"MYD88" OR TITLE:"MYD88 innate immune signal transduction adaptor" OR ABSTRACT:"MYD88 innate immune signal transduction adaptor" OR TITLE:"Myeloid differentiation primary response protein MyD88" OR ABSTRACT:"Myeloid differentiation primary response protein MyD88") 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 MYD88, not a curated reading list.
Shares Cell of origin in practice: Hans against expression profiling, and what it changes, CD79B ITAM mutation, Assign first-line treatment in diffuse large B-cell lymphoma by genetic subtype, not by a three-antibody stain, MYD88 L265P and CXCR4 mutations.
Shares Molecular subtypes of diffuse large B cell lymphoma are associated with distinct pathogenic mechanisms and outcomes, LymphGen and the genetic clusters of large B-cell lymphoma, A probabilistic classification tool for genetic subtypes of diffuse large B cell lymphoma with therapeutic implications, Genetics and pathogenesis of diffuse large B-cell lymphoma.
Shares Cell of origin in practice: Hans against expression profiling, and what it changes, Molecular subtypes of diffuse large B cell lymphoma are associated with distinct pathogenic mechanisms and outcomes, LymphGen and the genetic clusters of large B-cell lymphoma, A probabilistic classification tool for genetic subtypes of diffuse large B cell lymphoma with therapeutic implications.
Shares Inflammation & NF-κB, Extranodal marginal zone lymphoma of mucosa-associated lymphoid tissue (MALT lymphoma), Marginal zone lymphoma, Leukaemia (all types).
Shares B-cell receptor / BTK signalling (to NF-κB), Inflammation & NF-κB, Extranodal marginal zone lymphoma of mucosa-associated lymphoid tissue (MALT lymphoma), Marginal zone lymphoma.
Shares Inflammation & NF-κB, Extranodal marginal zone lymphoma of mucosa-associated lymphoid tissue (MALT lymphoma), Marginal zone lymphoma, Leukaemia (all types).
Shares B-cell receptor / BTK signalling (to NF-κB), Inflammation & NF-κB, Extranodal marginal zone lymphoma of mucosa-associated lymphoid tissue (MALT lymphoma), Marginal zone lymphoma.
Shares B-cell receptor / BTK signalling (to NF-κB), Leukaemia (all types), Acute lymphoblastic leukaemia, CIViC.