TWIST2
Overview
TWIST2 encodes a basic helix-loop-helix (bHLH) transcription factor that drives epithelial-to-mesenchymal transition (EMT). TWIST2 promotes invasion and metastasis by repressing E-cadherin and activating mesenchymal gene expression programs. In the context of cancer immunotherapy, TWIST2 upregulation is part of a transcriptional program associated with innate resistance to anti-PD-1 therapy.
Alterations observed in the corpus
- Mesenchymal-transition transcript up-regulated in pretreatment melanoma tumors that failed to respond to anti-PD-1 therapy; co-enriched within the IPRES (innate anti-PD-1 resistance) transcriptional signature in a 28-sample RNA-seq cohort PMID:26997480.
Cancer types (linked)
- SKCM / Melanoma: Overexpressed in innately anti-PD-1-resistant pretreatment tumors as part of the IPRES signature PMID:26997480.
Co-occurrence and mutual exclusivity
Therapeutic relevance
- TWIST2 and the IPRES signature are proposed as candidate transcriptomic biomarkers of innate anti-PD-1 resistance; the IPRES program is enriched across multiple cancer types, suggesting that EMT modulators or anti-angiogenics in combination with checkpoint blockade could overcome this resistance mechanism PMID:26997480.
Open questions
- The IPRES signature (including TWIST2) is correlative, not causal; whether pharmacologically suppressing TWIST2/IPRES restores anti-PD-1 sensitivity has not been demonstrated PMID:26997480.
Sources
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