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• W2063485349 abstract "The vast majority of tumors, including lung cancer, have several alterations in the PI3K and RAS pathways, as well as in p53. The new challenge in providing better treatment for patients lies in understanding the relationship between different genetic abnormalities that can serve both as prognostic markers and as the basis for novel therapeutic intervention. For example, we have observed that AEG-1 and BRCA1 mRNA expression significantly influences progression-free survival (PFS), either in metastatic non-smallcell lung cancer (NSCLC) patients with or without EGFR mutations. BRCA1 mRNA expression was also an independent prognostic marker in erlotinibtreated EGFR mutated NSCLC patients, with significant differences in the length of PFS according to BRCA1 levels: median PFS was 27 months in patients with low BRCA1 mRNA expression [1]. Moreover, a significantly better PFS was obtained in those patients who had elevated expression of NFKBIA (a gatekeeper of the EGFR pathway and the inhibitor of NFuB activation) [2]. FBW7 is an important tumor suppressor gene that degrades mTORC1 and the loss of FBW7 could be a potential biomarker for treatment with mTOR pathway inhibitors [3]. FBW7 also inhibits the pro-survival protein MCL1 which is a crucial regulator of apoptosis triggered by antitubulin drugs. It has been suggested that profiling FBW7 and MCL1 status of tumors in terms of protein levels, messenger RNA levels and genetic status could be useful for predicting patient response to antitubulin drugs [4,5]. Intriguingly, in a systematic characterisation of somatic mutations in cancer genomes, a high frequency of FBW7 was observed in squamous cell lung cancer. However, in the report no details of the type of EGFR mutations are given [6]. Hotspot mutations have been described in FBW7 that occur in high frequencies, 30%, in cholangiocarcinomas and also in T-ALL [7]. Therefore, it is of great interest to examine FBW7 status, including mRNA expression. EZH2, an oncogene which activates NFuB and RAS, was closely correlated with BRCA1 expression in a series of 60 metastatic NSCLC patients, but with no correlation between levels of EZH2 and K-ras mutations. EZH2 mutations (Try641) have been reported in follicular and diffuse large B-cell lymphomas [8]." @default.
• W2063485349 created "2016-06-24" @default.
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• W2063485349 date "2011-09-01" @default.
• W2063485349 modified "2023-09-25" @default.
• W2063485349 title "New therapeutic avenues in lung cancer based on disturbances in PI3K and RAS pathways" @default.
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• W2063485349 doi "https://doi.org/10.1016/s0959-8049(11)70094-6" @default.
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