These included many molecular mechanisms of cancer and cancerrelated signaling pathways, such as for instance mammalian target of rapamycin signaling, p53 signaling, Mycmediated apoptosis signaling, vascular endothelial growth factor signaling, phosphoinositide 3 kinase Bosutinib clinical trial /AKT signaling, and phosphatase and tensin homolog signaling, amongst others. We related the mutated, increased or differentially expressed genes with known cancer pathways from the Kyoto Encyclopedia of Genes and Genomes database and to drug targets present in the Drug Bank database. The 15 zoomed, around expressed or mutated genes in cancer pathways targetable by approved medications are listed in Table S2 in Additional file 1. Some increased genes, such as for instance NKX3 1, RBBP8 and CABL1, were implicated in cancer but aren’t well characterized in this role. In addition, they did not have recognized drugs targeting them. The Ret proto-oncogene appeared as a gene of specific interest to us, since it was within a region of genomic amplification and was abundantly expressed. RET is a receptor tyrosine kinase that stimulates signals for cell growth and differentiation via the mitogen activated protein kinase extracellular signal-regulated Carcinoid kinase pathway and its constitutive activation is liable for oncogenic transformation in medullary and papillary thyroid carcinoma. Within the lung tumor, RET was both highly amplified stage 4) and the most highly expressed known oncogene in lung relative to compendium, 123. 2 Hamilton Academical in lung relative to body). Furthermore, many of the MAPK pathway constituents will also be highly expressed in the tumefaction. Interestingly, over-expression of the water channel protein Aquaporin 5 has been implicated in multiple cancers and has been demonstrated to activate Ras and its signaling pathways. Aberrations ultimately causing increased activation of the 2-ME2 2-Methoxyestradiol PI3K/AKT route are common in human cancers and are reviewed in. Inactivating mutations and decreased expression of PTEN, a tumor suppressor that reverses the action of PI3K, would be the most frequently seen aberrations. In the patient tumor, PTEN was under expressed, and we observe that PTEN maps to an area of heterozygous reduction in the tumor genome. Because PTEN mediates cross-talk between PI3K and RET signaling by negatively regulating SHC and ERK and up-regulated RET can also activate the PI3K/AKT process, loss in PTEN could up regulate both the PI3K/ AKT and RET MAPK pathways, leading to decreased apoptosis, increased protein synthesis and cellular growth. However, in the patient, we observed LOH removal in AKT1, under expression of AKT2, mTOR, elF4E, and over expression of the negative regulators eIF4EBP1 and NKX3 1. These changes mitigate the effect of PTEN loss on the PI3K/AKT pathway and suggest that the loss of PTEN serves mainly to further activate the RET pathway to drive tumor growth. The high expression of RET offers a possible explanation of the failure of erlotinib to control proliferation of this tumor.