<b>Methods:</b> The expression of HUWE1 and p53 in lung cancer cells was modulated and the phenotypes were assessed by performing soft agar colony forming assays, cell cycle analysis, BrdU incorporation assays, and xenograft tumor growth assays.
<b>Methods:</b> We determined that LINC00460 expression in lung cancer tissues and the prognosis in patients with non-small cell lung carcinoma (NSCLC) using Gene Expression Profiling Interactive Analysis (GEPIA) website and The Cancer Genome Atlas (TCGA) database.
<b>Objectives:</b> Ring finger protein 38 (RNF38), as an E3 ubiquitin ligase, plays an essential role in multiple biological processes by controlling cell apoptosis, cell cycle and DNA repair, and resides in chromosome 9 (9p13) which is involvement in cancer pathogenesis including lung cancer.
<b>Objectives:</b> Ring finger protein 38 (RNF38), as an E3 ubiquitin ligase, plays an essential role in multiple biological processes by controlling cell apoptosis, cell cycle and DNA repair, and resides in chromosome 9 (9p13) which is involvement in cancer pathogenesis including lung cancer.
<b>Objectives:</b> Ring finger protein 38 (RNF38), as an E3 ubiquitin ligase, plays an essential role in multiple biological processes by controlling cell apoptosis, cell cycle and DNA repair, and resides in chromosome 9 (9p13) which is involvement in cancer pathogenesis including lung cancer.
<b>Objectives:</b> Ring finger protein 38 (RNF38), as an E3 ubiquitin ligase, plays an essential role in multiple biological processes by controlling cell apoptosis, cell cycle and DNA repair, and resides in chromosome 9 (9p13) which is involvement in cancer pathogenesis including lung cancer.
<b>Objectives:</b> Tumor pathology examination especially epidermal growth factor receptor (<i>EGFR</i>) mutations molecular testing has been integral part of lung cancer clinical practices.
<b>Purpose:</b> Because of emergence of resistance to osimertinib, a third-generation EGFR tyrosine kinase inhibitor (TKI), no targeted treatments are available for patients with lung cancer who lose sensitivity due to new mutations or bypass mechanisms.
<b>Purpose:</b> Drug resistance is a major challenge for epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitors (TKIs) treatment of lung cancer.
<b>Purpose:</b> To identify molecular factors that determine duration of response to EGFR tyrosine kinase inhibitors and to identify novel mechanisms of drug resistance, we molecularly profiled <i>EGFR</i>-mutant tumors prior to treatment and after progression on EGFR TKI using targeted next-generation sequencing.<b>Experimental Design:</b> Targeted next-generation sequencing was performed on 374 consecutive patients with metastatic <i>EGFR</i>-mutant lung cancer.
<b>Results</b>: Decreased susceptibility of LC was found in all genetic models contrast in Bsm1 gene of VDR (a vs. A: OR = 0.62, 95 % CI = 0.44-0.87; aa vs. AA: OR = 0.76, 95 % CI = 0.60-0.96; Aa vs. AA: OR = 0.59, 95 % CI = 0.39-0.88; aa vs. AA+Aa: OR = 0.80, 95 % CI = 0.64-0.99; Aa+aa vs. AA: OR = 0.57, 95 % CI = 0.37-0.86).
<b>Results:</b> Analysis of the Oncomine datasets identified that an elevation of MEOX1 in gene amplification in lung cancer tissues in comparison to normal lung tissues.
<b>Results:</b> Higher levels of ΔNp63α were observed in the lung cancer tissues of smokers than in those of non-smokers, whereas ΔNp63α was positively correlated with CD133 and Oct4 expression in lung cancer tissues.
<b>Results:</b> Higher levels of ΔNp63α were observed in the lung cancer tissues of smokers than in those of non-smokers, whereas ΔNp63α was positively correlated with CD133 and Oct4 expression in lung cancer tissues.
<b>Results:</b> Higher levels of ΔNp63α were observed in the lung cancer tissues of smokers than in those of non-smokers, whereas ΔNp63α was positively correlated with CD133 and Oct4 expression in lung cancer tissues.
<b>Results:</b> Higher levels of ΔNp63α were observed in the lung cancer tissues of smokers than in those of non-smokers, whereas ΔNp63α was positively correlated with CD133 and Oct4 expression in lung cancer tissues.
<b>Results:</b> We found that FRMPD1 expression in lung cancer specimens was lower than that in normal bronchial epithelium and normal submucosal glands.
<b>Results:</b> We showed that CDK16 is frequently overexpressed in lung cancer cells and tissues, and high levels of CDK16 are correlated with lymph node stage and poor prognosis in lung cancer patients.
<i>EGFR</i> rs712829, rs712830, rs2072454, and rs11543848 single nucleotide polymorphisms (SNPs) were genotyped to test for their association with lung cancer risk.
<i>Glutathione S transferase mu 1</i> (<i>GSTM1</i>) gene has been associated with lung cancer (LC) risk, for GSTM1 enzyme playing a vital role in detoxification pathway and protective against toxic insults.
<i>Conclusion:</i> The methylation analysis of the SHOX2 and RASSF1A panel in BALF with RT-PCR achieved a satisfactory sensitivity and specificity in lung cancer diagnosis, especially in an early stage.
<i>Conclusion:</i> The methylation analysis of the SHOX2 and RASSF1A panel in BALF with RT-PCR achieved a satisfactory sensitivity and specificity in lung cancer diagnosis, especially in an early stage.
<i>EGFR</i> mutations in cfDNA, both the activating mutation and <i>EGFR</i> T790M, became undetectable in most patients in the setting of clinical response and reemerged upon disease progression.<b>Conclusions:</b> ASP8273 was well tolerated and promoted antitumor activity in patients with <i>EGFR</i>-mutant lung cancer with disease progression on prior EGFR TKI therapy.<i></i>.