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FHIT is a tumor suppressor gene that is frequently inactivated in human cancer. Although the Fhit protein is known to hydrolyze diadenosine triphosphate (Ap3A), this hydrolase activity is not required for Fhit-mediated oncosuppression. Indeed, the molecular mechanisms and the regulatory elements of Fhit oncosuppression are largely unknown. Here, we review physiological and pathological aspects of Fhit in the context of the ApnA family of signaling molecules, as well as the involvement of Fhit in apoptosis and the cell cycle in cancer models. We also discuss recent findings of novel Fhit interactions that may lead to new hypotheses about biochemical mechanisms underlying the oncosuppressor activity of this gene. J. Cell. Physiol. 208: 274–281, 2006. © 2006 Wiley-Liss, Inc.

Surgical removal is the mainstay for early lung cancer treatment and persistent air leaks represent one of the most common clinical complications after lung surgery. Adipose tissue transplantation has been proposed as a new strategy for regenerative therapy after breast cancer surgery; however its efficacy and safety of lung tissue healing after lung resections are unknown. The purpose of this study was to test the biological activity of adipose tissue to facilitate lung tissue healing and evaluate its effect on cancer cells growth, thus providing insight for a possible clinical application. Different in vitro cellular models were used to prove the potential biologic effect of autologous fat tissue (AFT) in repairing injured lung tissue, and in vivo xenograft models were used to evaluate tumor promoting potential of AFT on putative residual cancer cells. Treatment of both embryonic (WI-38) and adult lung fibroblasts and of normal bronchial epithelial cells (HBEC-KT) with AFT samples, harvested from subcutaneous tissue layer of 20 patients undergoing pulmonary metastasectomy, improved wound healing and cell proliferation indicating a trophic effect on both mesenchymal and epithelial cell types. Conversely AFT-conditioned medium was unable to stimulate in vitro proliferation of a lung adenocarcinoma reporter cellular system (A549). Moreover, co-injection of AFT and A549 cells in nude mice did not promote engraftment and progression of A549 cells. These preclinical findings provide preliminary evidence on the potential efficacy of AFT to accelerate lung tissue repair without undesired tumor promoting effects on putative residual cancer cells. J. Cell. Physiol. 228: 1166–1173, 2013. © 2012 Wiley Periodicals, Inc.