scholarly journals Downregulation of the KIP family members p27KIP1and p57KIP2by SKP2 and the role of methylation in p57KIP2inactivation in nonsmall cell lung cancer

2006 ◽  
Vol 119 (11) ◽  
pp. 2546-2556 ◽  
Author(s):  
Ioannis S. Pateras ◽  
Kalliopi Apostolopoulou ◽  
Marilena Koutsami ◽  
Kostas Evangelou ◽  
Petros Tsantoulis ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Lung Cancer ◽  
Family Members ◽  
Nonsmall Cell Lung Cancer

Role of Inhibitor of Apoptosis Protein Livin in Radiation Resistance in Nonsmall Cell Lung Cancer

2011 ◽  
Vol 26 (5) ◽  
pp. 585-592 ◽  
Author(s):  
Jian-Guo Sun ◽  
Rong-Xia Liao ◽  
Shao-Xiang Zhang ◽  
Yu-Zhong Duan ◽  
Wen-Lei Zhuo ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Lung Cancer ◽  
Radiation Resistance ◽  
Nonsmall Cell Lung Cancer ◽  
Inhibitor Of Apoptosis ◽  
Inhibitor Of Apoptosis Protein ◽  
Apoptosis Protein

scholarly journals Differential prognostic values of mRNA expression of CEACAM gene family members in nonsmall cell lung cancer

2016 ◽  
Vol Volume 6 ◽  
pp. 23-30 ◽  
Author(s):  
Haruhiko Nakamura ◽  
Hiroki Sakai ◽  
Tomoyuki Miyazawa ◽  
Toshiaki Somehara ◽  
Noboru Nakayama ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Gene Family ◽  
Mrna Expression ◽  
Cell Lung Cancer ◽  
Family Members ◽  
Nonsmall Cell Lung Cancer ◽  
Em Gene

scholarly journals Role of gender in the survival of surgical patients with nonsmall cell lung cancer

2013 ◽  
Vol 8 (3) ◽  
pp. 142 ◽  
Author(s):  
JoséM Chatkin ◽  
JoséA Pinto ◽  
MariaT.R. Tsukazan ◽  
MárioB Wagner ◽  
AdrianaF Saldanha ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Lung Cancer ◽  
Nonsmall Cell Lung Cancer ◽  
Surgical Patients

scholarly journals Classic oncogene family Myc defines unappreciated distinct lineage states of small cell lung cancer

2019 ◽  
Author(s):  
Ayushi S. Patel ◽  
Seungyeul Yoo ◽  
Ranran Kong ◽  
Takashi Sato ◽  
Abhilasha Sinha ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Molecular Subtypes ◽  
Family Members ◽  
Small Cell ◽  
Small Cell Lung ◽  
Genomic Amplification ◽  
Mesenchymal Transition

AbstractComprehensive genomic analyses of small cell lung cancer (SCLC), the most aggressive form of lung cancer, have revealed near universal loss of tumor suppressors (RB1 and TP53) and frequent genomic amplification of all three MYC family members. The amplification of each Myc family member is mutually exclusive; hence it had been long suggested that they are functionally equivalent. However, their expression has more recently been associated with specific neuroendocrine markers and distinct histopathology. In this study, we explored a novel role of c-Myc and L-Myc as lineage determining factors contributing to SCLC molecular subtypes and histology. Integrated analyses of a gene regulatory network generated from mRNA expression of primary SCLC tumor and chromatin state profiling of SCLC cell lines showed that Myc family members impart distinct transcriptional programs associated with lineage state; wherein the L-Myc signature was enriched for neuronal pathways while the c-Myc signature was enriched for Notch signaling and epithelial-to-mesenchymal transition. We investigated the functional redundancy and distinction of c-Myc and L-Myc, and noted the insufficiency of L-Myc to induce lineage switch in contrast to the potential of c-Myc to induce trans-differentiation. c-Myc rewires the Myc-accessible landscape and activates neuron al repressor, Rest to mediate transition from ASCL1-SCLC to NeuroD1-SCLC characterized by distinct LCNEC-like histopathology. Collectively, our findings reveal a previously undescribed role of historically defined general oncogenes, c-Myc and L-Myc, for regulating lineage plasticity across molecular subtypes as well as histological subclasses.

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