NTRK1 holds the blueprint for a protein called TRKA, which dangles from the surface of cells and receives growth signals from other cells. The joining of NTRK1 to other genes causes TRKA to issue cell-growth orders on its own, without being prompted by outside signals.
In the laboratory, investigators mixed NTRK1-inhibiting agents into lung adenocarcinoma cells harboring NTRK1 fusions. The result was a dampening of TRKA’s activity and the death of the cancer cells.
Leila Varella-Garcia, PhD, at CU Cancer Center then designed a new test using fluorescence in situ hybridization (FISH) to detect NTRK1 fusions and tested an additional 56 tumor samples. Three of 91 tumor samples, which had no other sign of cancer-causing genetic abnormalities, had fusions involving NTRK1.
“These findings suggest that in a few percent of lung adenocarcinoma patients – people in whose cancer cells we had previously been able to find no genetic abnormality – tumor growth is driven by a fusion involving NTRK1,” says Pasi A. Jänne, MD, PhD, of Dana-Farber, the senior co-author of the paper. “Given that lung cancer is a common cancer, even a few percent is significant and translates into a large number of patients.”
The co-lead authors of the study are Aria Vaishnavi, BS, of the University of Colorado School of Medicine and Marzia Capelletti, PhD, of Dana-Farber. Co-authors include Anh Le, BA, Severine Kako, Sakshi Mahale, MS, Kurtis Davies, PhD, Dara Aisner, MD, PhD, Amanda Pilling, PhD Eamon Berge, MD, and Marileila Varella-Garcia, PhD, of the University of Colorado School of Medicine; Mohit Butaney, Dalia Ercan, and Peter Hammerman, MD, PhD, of Dana-Farber; Levi Garraway, MD, PhD, of Dana-Farber and the Broad Institute of MIT and Harvard; Gregory Kryukov, PhD, of the B
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