BCL2L11
Overview
BCL2L11 (BCL2-like 11, also known as BIM) encodes a pro-apoptotic BH3-only protein that promotes cell death by binding and neutralizing anti-apoptotic BCL2-family members. In endometrial carcinoma, BCL2L11 was detected in recurrent translocations forming predicted in-frame fusions associated with increased BCL-family expression.
Alterations observed in the corpus
- Recurrent translocation involving BCL2L11 detected by low-pass WGS in 5/106 endometrial carcinoma tumors (ucec_tcga_pub); predicted in-frame fusions with increased BCL family expression. PMID:23636398
- Pro-apoptotic BIM protein inhibited by EBV BART-cluster microRNAs in NPC, contributing to apoptosis resistance PMID:24952746
Cancer types (linked)
- UCEC (uterine corpus endometrial carcinoma): recurrent BCL-family translocations in ~5% of tumors; BCL2L11 identified alongside BCL2, BCL7A, and BCL9 as translocation partners. PMID:23636398
Co-occurrence and mutual exclusivity
- Co-occurs with BCL2, BCL7A, and BCL9 in the BCL-family translocation subgroup detected in 5/106 endometrial tumors. PMID:23636398
Therapeutic relevance
- BIM (BCL2L11) loss is a known resistance mechanism to targeted therapies; BCL2L11 translocations in endometrial cancer may have implications for BH3-mimetic drug susceptibility. PMID:23636398
Open questions
- The specific fusion partners and functional consequences of BCL2L11 translocations in endometrial carcinoma are not individually resolved in this study; whether the predicted in-frame fusions are tumorigenic drivers requires experimental validation. PMID:23636398
Sources
This page was processed by crosslinker on 2026-05-09. - PMID:24952746
This page was processed by wiki-cli on 2026-05-11.