BCL2L1

Overview

BCL2L1 (BCL2-Like 1), also known as BCL-XL, is an anti-apoptotic member of the BCL-2 protein family that regulates mitochondrial outer membrane permeabilization and cell survival. Amplification of BCL2L1 promotes evasion of apoptosis and is associated with therapeutic resistance. In lung squamous cell carcinoma, BCL2L1 amplification has been identified as a somatic copy number alteration.

Alterations observed in the corpus

• Amplification/copy number alteration identified in TCGA lung squamous cell carcinoma cohort (178 tumors) as part of the landscape of somatic copy number alterations PMID:22960745
• Focal amplification in 11% of muscle-invasive bladder carcinomas (BLCA); one HPV16-positive tumour had the virus integrated into BCL2L1, which was amplified (~6x) and overexpressed (~10x median) PMID:24476821
• Bcl-xL-mediated survival downstream of STAT3 phosphorylation; loss of FXR/NR1H4 activity unleashes STAT3 signaling and BCL2L1-mediated apoptosis resistance in cholangiocarcinoma PMID:25608663
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Cancer types (linked)

• LUSC: BCL2L1 amplification observed among recurrent somatic copy number alterations in the TCGA LUSC cohort (178 tumors) PMID:22960745

Co-occurrence and mutual exclusivity

• No specific co-occurrence or mutual exclusivity patterns reported in the corpus.

Therapeutic relevance

• BCL2L1/BCL-XL is a known anti-apoptotic target; navitoclax (ABT-263) targets BCL-XL, though no specific therapeutic data in LUSC is reported in the corpus.

Open questions

• The functional significance of BCL2L1 amplification as a driver versus passenger event in LUSC requires further investigation.

Sources

• PMID:22960745 — TCGA comprehensive genomic characterization of lung squamous cell carcinoma (178 tumors)

This page was processed by crosslinker on 2026-05-14. - PMID:24476821

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This page was processed by crosslinker on 2026-05-14. - PMID:28988769

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