Notch gene mutation is associated with lung cancer
Italian researchers have announced that they have discovered a genetic variant associated with lung cancer.
Researchers at institutions such as the University of Milan in Italy have discovered that a gene variant called NOTCH is associated with lung cancer because the Numb protein responsible for controlling this gene has lost control of it. Studies have shown that 33% of patients with lung cancer have a mutation in the NOTCH gene.
The researchers will next carry out clinical trials to study the therapeutic effect of intervention on the NOTCH gene.
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PNAS December 10, 2009, doi: 10.1073 / pnas.0907781106
Alterations of the Notch pathway in lung cancer
Britta Westhoffa, b, 1, Ivan N. Colalucaa, b, 1, Giovanni DArioa, Maddalena Donzellia, b, Daniela Tosonia, b, Sara Volorioa, b, Giuseppe Pelosib, c, Lorenzo Spaggiarib, c, Giovanni Mazzarola, b, Giuseppe Vialeb, c, Salvatore Pecea, b, c, 2 and Pier Paolo Di Fiorea, b, c, 2
aIFOM, Fondazione Istituto FIRC di Oncologia Molecolare, Milan, Italy;
bEuropean Institute of Oncology, Milan, Italy; and
CDipartimento di Medicina, Chirurgia ed Odontoiatria, UniversitÃ degli Studi di Milano, Milan, Italy
Notch signaling regulates cell specification and homeostasis of stem cell compartments, and it is counteracted by the cell fate determinant Numb. Both Numb and Notch have been implicated in human tumors. Here, we show that Notch signaling is altered in approximately one third of nonâ€“ small-cell lung carcinomas (NSCLCs), which are the leading cause of cancer-related deaths: in â‰ˆ30% of NSCLCs, loss of Numb expression leads to increased Notch activity, while in a smaller fraction of cases (around 10%), gain-of-function mutations of the NOTCH-1 gene are present. Activation of Notch correlates with poor clinical outcomes in NSCLC patients without TP53 mutations. Finally, primary epithelial cell cultures, derived from NSCLC harboring constitutive activation of the Notch pathway, are selectively killed by inhibitors of Notch (Î³-secretase inhibitors), showing that the proliferative advantage of these tumors is dependent upon Notch signaling. Our results show that the deregulation of the No tch pathway is a relatively frequent event in NSCLCs and suggest that it might represent a possible target for molecular therapies in these tumors.
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