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Lisa Fusetti

Publications -  5
Citations -  679

Lisa Fusetti is an academic researcher. The author has contributed to research in topics: Gene rearrangement & Gene. The author has an hindex of 5, co-authored 5 publications receiving 667 citations.

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Replacement of Fhit in cancer cells suppresses tumorigenicity

TL;DR: No consistent effect of exogenous Fhit on growth in culture was observed, but Fhit and hydrolase "dead" Fhit mutant proteins suppressed tumorigenicity in nude mice, indicating that 5',5"'-P1, P3-triphosphate hydrolysis is not required for tumor suppression.
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Transforming activity of the chimeric sequence formed by the fusion of collagen gene COL1A1 and the platelet derived growth factor b-chain gene in dermatofibrosarcoma protuberans.

TL;DR: All the biochemical and biological assays were consistent with the model of an autocrine mechanism for NIH3T3 transformation by the human rearranged PDGFB gene involving the activation of the endogeneous PDGF receptor.
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Chromosome I rearrangements involving the genes TPR and NTRK1 produce structurally different thyroid‐specific TRK oncogenes

TL;DR: Evidence that TRK‐T2 is generated by different rearrangements in two thyroid tumors, and a detailed analysis of the three different TPR/NTRK1 rearranged genes is reported.
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Role of the TFG N-terminus and coiled-coil domain in the transforming activity of the thyroid TRK-T3 oncogene

TL;DR: It is shown that TRK-T3 activity depends on oligomers formation, and that the TFG coiled-coil domain and its N-terminal region are both required for the activation and the fully transforming activity of the TRK -T3 oncoprotein, although they play a role in different steps of the transforming process.
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The Gly571arg mutation, associated with the autonomic and sensory disorder congenital insensitivity to pain with anhidrosis, causes the inactivation of the NTRK1/nerve growth factor receptor

TL;DR: It is demonstrated clearly that the CIPA mutations cause the inactivation of the NTRK1 receptor, thus exerting a loss of function effect, and an experimental approach to distinguish functional mutations from genetic polymorphisms is provided.