# MALT1

Source: https://onco.cc/targets/malt1/  
OnCo record `malt1` (Target). Data CC BY-NC 4.0, attribute "Data from OnCo (onco.cc)"; commercial use needs a licence.

## TL;DR

MALT1 (Mucosa-associated lymphoid tissue lymphoma translocation protein 1) is a gene that drives cell growth when it is altered. The public catalogues list it as an oncogene driver and a fusion partner, and it is called a cancer driver by mutation analysis of patient cohorts. Tied to Skin cancer and Diffuse large B-cell lymphoma.

## Summary

Protease that enhances BCL10-induced activation: acts via formation of CBM complexes that channel adaptive and innate immune signalling downstream of CARD domain-containing proteins (CARD9, CARD11 and CARD14) to activate NF-kappa-B and MAP kinase p38 pathways which stimulate expression of genes encoding pro-inflammatory cytokines and chemokines. Mediates BCL10 cleavage: MALT1-dependent BCL10 cleavage plays an important role in T-cell antigen receptor-induced integrin adhesion. Involved in the induction of T helper 17 cells (Th17) differentiation.

Open Targets scores its association with cancer at 0.62 (direct and indirect evidence; datatypes literature 0.97, genetic association 0.04, somatic mutation 0.97). IntOGen calls it a driver in 1 cohort (1 activating, 0 loss-of-function), covering Diffuse Large B-Cell Lymphoma, NOS.

## Fields

- Kind: Target
- Last checked: 2026-09-23
- Also known as: MALT1 paracaspase; Mucosa-associated lymphoid tissue lymphoma translocation protein 1; PCASP1
- Tags: cancer-genes-wave
- Symbol: MALT1
- Class: oncogene
- Biology: Protease that enhances BCL10-induced activation: acts via formation of CBM complexes that channel adaptive and innate immune signalling downstream of CARD domain-containing proteins (CARD9, CARD11 and CARD14) to activate NF-kappa-B and MAP kinase p38 pathways which stimulate expression of genes encoding pro-inflammatory cytokines and chemokines. Mediates BCL10 cleavage: MALT1-dependent BCL10 cleavage plays an important role in T-cell antigen receptor-induced integrin adhesion. Involved in the induction of T helper 17 cells (Th17) differentiation. Cleaves RC3H1 and ZC3H12A in response to T-cell receptor (TCR) stimulation which releases their cooperatively repressed targets to promote Th17 cell differentiation. Also mediates cleavage of N4BP1 in T-cells following TCR-mediated activation, leading to N4BP1 inactivation. May also have ubiquitin ligase activity: binds to TRAF6, inducing TRAF6 oligomerisation and activation of its ligase activity. Location: Cytoplasm, perinuclear region; Nucleus (UniProt). Locus 18q21.32 (HGNC).
- Where found: Skin cancer: Open Targets association 0.51 with skin cancer (MONDO_0002898); Diffuse large B-cell lymphoma: IntOGen driver in 1 cohort (DLBCLNOS)

## 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: IntOGen calls it an activating (Act) driver in 1 cohort; UniProt disease notes describe a translocation or gene fusion involving the gene. Evidence tier "cohort-driver" is the strongest of those signals.
- Prevalence not recorded: none of the sources gives a positivity rate.
- Lymphoma, t(11;18) API2-MALT1 and the NF-kB lesions of marginal zone lymphoma: Gastric MALT lymphoma begins as a Helicobacter-driven proliferation that still needs the antigen; removing the bacterium removes the stimulus and the lymphoma regresses. The t(11;18) fuses API2 to MALT1 and produces a protein that activates NF-kB on its own, so the lymphoma no longer needs the antigen and no longer cares whether the bacterium is still there. The related translocations, t(1;14) involving BCL10 and t(14;18) involving MALT1, do the same job by a different route, and inactivation of TNFAIP3 removes the brake. Frequency: Among 111 patients with Helicobacter-positive gastric MALT lymphoma treated with antibiotics, the translocation separated the responders from the non-responders: 47 of the 48 patients who regressed completely were negative for the API2-MALT1 transcript (Liu 2002). What it changes about treatment: Yes, and this is one of the few places where a translocation result changes the first decision. A t(11;18)-positive gastric MALT lymphoma should not be treated with eradication alone, whatever the stage; a negative one usually can be.

## Sources

- HGNC HGNC:6819: https://www.genenames.org/data/gene-symbol-report/#!/hgnc_id/HGNC:6819
- UniProt Q9UDY8: https://www.uniprot.org/uniprotkb/Q9UDY8/entry
- NCBI Gene 10892: https://www.ncbi.nlm.nih.gov/gene/10892
- Ensembl ENSG00000172175: https://www.ensembl.org/Homo_sapiens/Gene/Summary?g=ENSG00000172175
- Liu et al., Gastroenterology 2002: t(11;18) marks gastric MALT lymphomas that will not respond to Helicobacter pylori eradication (111 patients): https://doi.org/10.1053/gast.2002.33047

## Connected records

- collections: [IntOGen](https://onco.cc/collections/intogen/), [Open Targets Platform](https://onco.cc/collections/open-targets/)
- cancers: [Diffuse large B-cell lymphoma](https://onco.cc/cancers/dlbcl/), [Extranodal marginal zone lymphoma of mucosa-associated lymphoid tissue (MALT lymphoma)](https://onco.cc/cancers/malt-lymphoma/), [Marginal zone lymphoma](https://onco.cc/cancers/marginal-zone-lymphoma/), [Non-Hodgkin lymphoma (all types)](https://onco.cc/cancers/non-hodgkin-lymphoma/), [Skin cancer (all types)](https://onco.cc/cancers/skin-cancer/)
- pathways: [B-cell receptor / BTK signalling (to NF-κB)](https://onco.cc/pathways/bcr-signalling/), [Inflammation & NF-κB](https://onco.cc/pathways/inflammation-nfkb/), [Microbiome-tumour interactions](https://onco.cc/pathways/microbiome-tumour/)

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JSON: https://onco.cc/api/v1/entities/malt1.json