Alterations of tumor suppressor genes (Rb, p16, p27 and p53) and an increased FDG uptake in lung cancer

2003 ◽  
Vol 17 (3) ◽  
pp. 189-196 ◽  
Author(s):  
Masayuki Sasaki ◽  
Kenji Sugio ◽  
Yasuo Juwabara ◽  
Hirofumi Koga ◽  
Makoto Nakagawa ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Tumor Suppressor ◽  
Tumor Suppressor Genes ◽  
Suppressor Genes ◽  
Fdg Uptake

scholarly journals CRISPR-mediated modeling and functional validation of candidate tumor suppressor genes in small cell lung cancer

2019 ◽  
Vol 117 (1) ◽  
pp. 513-521 ◽  
Author(s):  
Sheng Rong Ng ◽  
William M. Rideout ◽  
Elliot H. Akama-Garren ◽  
Arjun Bhutkar ◽  
Kim L. Mercer ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Tumor Suppressor ◽  
Small Cell Lung Cancer ◽  
Tumor Progression ◽  
Cell Lung Cancer ◽  
Tumor Suppressor Genes ◽  
Small Cell ◽  
Small Cell Lung ◽  
Suppressor Genes ◽  
Sequencing Studies

Small cell lung cancer (SCLC) is a highly aggressive subtype of lung cancer that remains among the most lethal of solid tumor malignancies. Recent genomic sequencing studies have identified many recurrently mutated genes in human SCLC tumors. However, the functional roles of most of these genes remain to be validated. Here, we have adapted the CRISPR-Cas9 system to a well-established murine model of SCLC to rapidly model loss-of-function mutations in candidate genes identified from SCLC sequencing studies. We show that loss of the genep107significantly accelerates tumor progression. Notably, compared with loss of the closely related genep130, loss ofp107results in fewer but larger tumors as well as earlier metastatic spread. In addition, we observe differences in proliferation and apoptosis as well as altered distribution of initiated tumors in the lung, resulting from loss ofp107orp130. Collectively, these data demonstrate the feasibility of using the CRISPR-Cas9 system to model loss of candidate tumor suppressor genes in SCLC, and we anticipate that this approach will facilitate efforts to investigate mechanisms driving tumor progression in this deadly disease.

scholarly journals P2-041: Epigenetic changes of the tumor suppressor genes SHP1, SHP2 SOCS1, SOCS3 and the transcription factor STAT1 in human lung cancer

2007 ◽  
Vol 2 (8) ◽  
pp. S506-S507
Author(s):  
Joachim Gullbo ◽  
Michael Bergqvist ◽  
Linda Sooman ◽  
Peter Ericsson ◽  
Johan Lennartsson ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Transcription Factor ◽  
Tumor Suppressor ◽  
Tumor Suppressor Genes ◽  
Human Lung ◽  
Human Lung Cancer ◽  
Epigenetic Changes ◽  
Suppressor Genes

scholarly journals Peperomin E reactivates silenced tumor suppressor genes in lung cancer cells by inhibition of DNA methyltransferase

2016 ◽  
Vol 107 (10) ◽  
pp. 1506-1519 ◽  
Author(s):  
Xin‐zhi Wang ◽  
Ying Cheng ◽  
Kui‐long Wang ◽  
Rui Liu ◽  
Xiao‐lin Yang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Tumor Suppressor ◽  
Cancer Cells ◽  
Tumor Suppressor Genes ◽  
Dna Methyltransferase ◽  
Lung Cancer Cells ◽  
Suppressor Genes

scholarly journals Genetic and Epigenetic Tumor Suppressor Gene Silencing Are Distinct Molecular Phenotypes Driven by Growth Promoting Mutations in Nonsmall Cell Lung Cancer

2008 ◽  
Vol 2008 ◽  
pp. 1-8 ◽  
Author(s):  
Carmen J. Marsit ◽  
E. Andres Houseman ◽  
Heather H. Nelson ◽  
Karl T. Kelsey
Keyword(s):  
Lung Cancer ◽  
Tumor Suppressor ◽  
Cell Lung Cancer ◽  
Tumor Suppressor Genes ◽  
Nonsmall Cell Lung Cancer ◽  
Promoter Hypermethylation ◽  
Genetic Alteration ◽  
Suppressor Genes ◽  
Growth Promoting ◽  
Molecular Phenotypes

Both genetic and epigenetic alterations characterize human nonsmall cell lung cancer (NSCLC), but the biological processes that create or select these alterations remain incompletely investigated. Our hypothesis posits that a roughly reciprocal relationship between the propensity for promoter hypermethylation and a propensity for genetic deletion leads to distinct molecular phenotypes of lung cancer. To test this hypothesis, we examined promoter hypermethylation of 17 tumor suppressor genes, as a marker of epigenetic alteration propensity, and deletion events at the 3p21 region, as a marker of genetic alteration. To model the complex biology between these somatic alterations, we utilized an item response theory model. We demonstrated that tumors exhibiting LOH at greater than 30% of informative alleles in the 3p21 region have a significantly reduced propensity for hypermethylation. At the same time, tumors with activatingKRASmutations showed a significantly increased propensity for hypermethylation of the loci examined, a result similar to what has been observed in colon cancer. These data suggest that NSCLCs have distinct epigenetic or genetic alteration phenotypes acting upon tumor suppressor genes and that mutation of oncogenic growth promoting genes, such asKRAS, is associated with the epigenetic phenotype.

Methylation Profile of Several Tumor Suppressor Genes in Non-Small-Cell Lung Cancer

2003 ◽  
Vol 37 (6) ◽  
pp. 836-840 ◽  
Author(s):  
V. V. Zemlyakova ◽  
A. I. Zhevlova ◽  
I. B. Zborovskaya ◽  
V. V. Strelnikov ◽  
K. K. Laktionov ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Tumor Suppressor ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Tumor Suppressor Genes ◽  
Small Cell ◽  
Methylation Profile ◽  
Small Cell Lung ◽  
Suppressor Genes

scholarly journals Simultaneous down-regulation of tumor suppressor genes RBSP3/CTDSPL, NPRL2/G21 and RASSF1A in primary non-small cell lung cancer

BMC Cancer ◽  
2010 ◽  
Vol 10 (1) ◽  
Author(s):  
Vera N Senchenko ◽  
Ekaterina A Anedchenko ◽  
Tatiana T Kondratieva ◽  
George S Krasnov ◽  
Alexei A Dmitriev ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Tumor Suppressor ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Tumor Suppressor Genes ◽  
Small Cell ◽  
Small Cell Lung ◽  
Down Regulation ◽  
Suppressor Genes
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