TPM3
Overview
TPM3 (Tropomyosin 3) encodes a tropomyosin isoform that regulates actin-filament dynamics in non-muscle cells. In cancer genomics, TPM3 is most notable as a fusion partner in oncogenic rearrangements: the TPM3-ALK fusion was originally described in anaplastic large-cell lymphoma and has since been identified in rare solid tumours including renal cell carcinoma.
Alterations observed in the corpus
- TPM3-ALK fusion detected by MSK-IMPACT targeted sequencing and confirmed by ALK break-apart FISH in uRCC case T12, representing the second adult RCC case with this fusion reported; ALK inhibition proposed as a targeted therapeutic option. PMID:27713405
- TPM3-NTRK1 fusion observed in MSI-H mCRC as part of the NTRK1/NTRK3 fusion landscape (8% MSI-H vs 1% MSS). PMID:29316426
Cancer types (linked)
- Unclassified high-grade renal cell carcinoma (URCC): TPM3-ALK fusion observed in one case (1/62, ~2%); defines an emerging RCC entity amenable to ALK-directed therapy. PMID:27713405
Co-occurrence and mutual exclusivity
- TPM3-ALK fusion co-occurs with the ALK alteration in a rare uRCC subset; the single case (T12) was not assigned to any of the four main molecular subsets (NF2-loss, mTORC1-hyperactive, FH-deficient, chromatin/DNA-damage). PMID:27713405
Therapeutic relevance
- The TPM3-ALK fusion raises the possibility of ALK inhibitor use in molecularly selected uRCC, analogous to TPM3-ALK-driven ALCL or inflammatory myofibroblastic tumour. PMID:27713405
Open questions
- Whether the TPM3-ALK fusion in adult RCC responds to ALK inhibitors in vivo has not been tested; clinical data are limited to case reports.
Sources
This page was processed by crosslinker on 2026-05-14. - PMID:29316426
This page was processed by entity-page-writer on 2026-05-15.