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BCL10 (B-cell lymphoma/leukaemia 10) is a gene whose normal job is to hold cell growth in check. The public catalogues list it as an oncogene driver, a tumour suppressor, a biomarker and a fusion partner, and clinical evidence ties its variants to diagnosis, prognosis or drug response. Tied to Non-Hodgkin lymphoma, Lung cancer, Diffuse large B-cell lymphoma and 1 more.
Plays a key role in both adaptive and innate immune signalling by bridging CARD domain-containing proteins to immune activation. Acts by channeling adaptive and innate immune signalling downstream of CARD domain-containing proteins CARD9, CARD11 and CARD14 to activate NF-kappa-B and MAP kinase p38 (MAPK11, MAPK12, MAPK13 and/or MAPK14) pathways which stimulate expression of genes encoding pro-inflammatory cytokines and chemokines. Recruited by activated CARD domain-containing proteins: homooligomerised CARD domain-containing proteins form a nucleating helical template that recruits BCL10 via CARD-CARD interaction, thereby promoting polymerisation of BCL10, subsequent recruitment of MALT1 and formation of a CBM complex.
CIViC holds 1 clinical evidence item and 0 assertions across 1 variant. Open Targets scores its association with cancer at 0.69 (direct and indirect evidence; datatypes literature 0.80, genetic association 0.19, somatic mutation 0.88). IntOGen calls it a driver in 3 cohorts (1 activating, 2 loss-of-function), covering Diffuse Large B-Cell Lymphoma, NOS, Malignant Lymphoma.
In plain words · BCL10 (B-cell lymphoma/leukaemia 10) is a gene whose normal job is to hold cell growth in check. The public catalogues list it as an oncogene driver, a tumour suppressor, a biomarker and a fusion partner, and clinical evidence ties its variants to diagnosis, prognosis or drug response. Tied to Non-Hodgkin lymphoma, Lung cancer, Diffuse large B-cell lymphoma and 1 more.
BCL10 (B-cell lymphoma/leukaemia 10) is a gene whose normal job is to hold cell growth in check. The public catalogues list it as an oncogene driver, a tumour suppressor, a biomarker and a fusion partner, and clinical evidence ties its variants to diagnosis, prognosis or drug response. Tied to Non-Hodgkin lymphoma, Lung cancer, Diffuse large B-cell lymphoma and 1 more.
Plays a key role in both adaptive and innate immune signalling by bridging CARD domain-containing proteins to immune activation.
No product in this corpus aims at BCL10 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) and a fusion partner (UniProt records a translocation), 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 BCL10: RNA low tissue specificity; no normal tissue stained high; highest cancer staining lymphoma (6 of 11 high). Distribution: 2 cancer families in the corpus carry a prevalence row, label threshold or catalogue link for it (Lymphoma, Lung cancer (all types)); Open Targets associates it with 2 specific cancer types at or above 0.5 (MALT lymphoma, testicular germ cell tumor). (Rule 6 of scripts/fetch-target-specificity.ts.)
Sources: UniProt O95999; CIViC gene BCL10; IntOGen BCL10; Human Protein Atlas BCL10 tissue; Open Targets ENSG00000142867 associations
First described 1999. Earliest sequence paper UniProt cites for the protein: Willis T.G. et al, Cell, 1999, "Bcl10 is involved in t(1;14)(p22;q32) of MALT B cell lymphoma and mutated in multiple tumor types". Source.
Sources: HGNC HGNC:989 (approved symbol, name, aliases, locus and cross-references (hgnc_complete_set.txt)); UniProt O95999 (protein name, function text, keywords and locations (REST API)); CIViC gene BCL10 (1 evidence items, 0 assertions, 1 variants; diseases: Diffuse Large B-cell Lymphoma (GraphQL API, CC0)); Open Targets ENSG00000142867 (association with cancer (MONDO_0004992) 0.69; per-cancer scores at or above 0.5: diffuse large B-cell lymphoma 0.54, non-Hodgkin lymphoma 0.71, lung cancer 0.50, marginal zone lymphoma 0.58 (GraphQL API, CC0)); IntOGen BCL10 (driver in 3 cohorts (Act 1, LoF 2); Compendium_Cancer_Genes.tsv release 20240920, CC0 1.0)
Plays a key role in both adaptive and innate immune signalling by bridging CARD domain-containing proteins to immune activation. Acts by channeling adaptive and innate immune signalling downstream of CARD domain-containing proteins CARD9, CARD11 and CARD14 to activate NF-kappa-B and MAP kinase p38 (MAPK11, MAPK12, MAPK13 and/or MAPK14) pathways which stimulate expression of genes encoding pro-inflammatory cytokines and chemokines. Recruited by activated CARD domain-containing proteins: homooligomerised CARD domain-containing proteins form a nucleating helical template that recruits BCL10 via CARD-CARD interaction, thereby promoting polymerisation of BCL10, subsequent recruitment of MALT1 and formation of a CBM complex. This leads to activation of NF-kappa-B and MAP kinase p38 (MAPK11, MAPK12, MAPK13 and/or MAPK14) pathways which stimulate expression of genes encoding pro-inflammatory cytokines and chemokines. Activated by CARD9 downstream of C-type lectin receptors; CARD9-mediated signals are essential for antifungal immunity. Activated by CARD11 downstream of T-cell receptor (TCR) and B-cell receptor (BCR). Location: Cytoplasm, perinuclear region; Membrane raft (UniProt). Locus 1p22.3 (HGNC).
RNA: low tissue specificity, detected in all normal tissues.
No normal tissue stained high; medium in Adrenal gland, Appendix, Bronchus, Cervix, Colon, Duodenum and more.
Medium only: breast cancer, cervical cancer, endometrial cancer, liver 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.
Query for this target: (TITLE:"BCL10" OR ABSTRACT:"BCL10" OR TITLE:"BCL10 immune signaling adaptor" OR ABSTRACT:"BCL10 immune signaling adaptor" OR TITLE:"B-cell lymphoma/leukemia 10" OR ABSTRACT:"B-cell lymphoma/leukemia 10" OR TITLE:"CARMEN" OR ABSTRACT:"CARMEN" OR TITLE:"CIPER" OR ABSTRACT:"CIPER" OR TITLE:"mE10" OR ABSTRACT:"mE10") 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 BCL10, not a curated reading list.
Shares Microbiome-tumour interactions, B-cell receptor / BTK signalling (to NF-κB), Inflammation & NF-κB, Extranodal marginal zone lymphoma of mucosa-associated lymphoid tissue (MALT lymphoma).
Shares Microbiome-tumour interactions, Inflammation & NF-κB, Extranodal marginal zone lymphoma of mucosa-associated lymphoid tissue (MALT lymphoma), Marginal zone lymphoma.
Shares Microbiome-tumour interactions, 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), Inflammation & NF-κB, CIViC, IntOGen.
Shares B-cell receptor / BTK signalling (to NF-κB), Inflammation & NF-κB, CIViC, IntOGen.
Shares B-cell receptor / BTK signalling (to NF-κB), CIViC, IntOGen, Diffuse large B-cell lymphoma.
Shares B-cell receptor / BTK signalling (to NF-κB), Inflammation & NF-κB, CIViC, Lung cancer (all types).
Shares Marginal zone lymphoma, CIViC, Diffuse large B-cell lymphoma, Open Targets Platform.