| Literature DB >> 33258061 |
Albrecht Stenzinger1, Cornelis M van Tilburg2, Ghazaleh Tabatabai3, Florian Länger4, Norbert Graf5, Frank Griesinger6, Lukas C Heukamp7, Michael Hummel8, Thomas Klingebiel9, Simone Hettmer10, Christian Vokuhl11, Sabine Merkelbach-Bruse12, Friedrich Overkamp13, Peter Reichardt14, Monika Scheer15, Wilko Weichert16, C Benedikt Westphalen17, Carsten Bokemeyer18, Philipp Ivanyi19, Sonja Loges18,20,21,22, Peter Schirmacher23, Bernhard Wörmann24, Stefan Bielack15, Thomas T W Seufferlein25.
Abstract
NTRK gene fusions are sporadic genetic alterations that can occur across tumor entities. Whereas they are quite rare in most solid tumors they are present at much higher frequencies in certain rare tumors such as infantile fibrosarcoma, congenital mesoblastic nephroma, secretory breast, or salivary gland carcinoma. NTRK gene fusions or TRK fusion proteins are considered strong oncogenic drivers. If NTRK gene fusions are detected, TRK inhibitors such as entrectinib and larotrectinib can be used regardless of the tumor entity. So far only larotrectinib is approved in the European Union. Both drugs have been shown to be effective and well tolerated in phase I and phase II studies. The low prevalence of TRK fusion-positive cancers poses challenges for diagnostic and clinical work-flows. On one hand, patients with NTRK gene fusions should be identified; on the other hand, epidemiological, histological, and resource-related aspects have to be taken into account. Based on these premises, we suggest a diagnostic algorithm for TRK fusion cancers and present current data on TRK inhibitors.Entities:
Keywords: Entrectinib; Gene fusion; Larotrectinib; NTRK; Translocation
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Year: 2021 PMID: 33258061 PMCID: PMC7858552 DOI: 10.1007/s00292-020-00864-y
Source DB: PubMed Journal: Pathologe ISSN: 0172-8113 Impact factor: 1.011