Genetic alteration of tumor suppressor gene and microsatellite in nonsmall cell lung cancer

2000 ◽  
Vol 49 (4) ◽  
pp. 453 ◽  
Author(s):  
Tae Rim Shin ◽  
Young Sook Hong ◽  
Jhin Gook Kim ◽  
Jung Hyun Chang
Keyword(s):  
Lung Cancer ◽  
Tumor Suppressor ◽  
Tumor Suppressor Gene ◽  
Cell Lung Cancer ◽  
Nonsmall Cell Lung Cancer ◽  
Suppressor Gene ◽  
Genetic Alteration

scholarly journals UHRF1-mediated tumor suppressor gene inactivation in nonsmall cell lung cancer

Cancer ◽  
2010 ◽  
Vol 117 (5) ◽  
pp. 1027-1037 ◽  
Author(s):  
Alexandros Daskalos ◽  
Urszula Oleksiewicz ◽  
Anastasia Filia ◽  
George Nikolaidis ◽  
George Xinarianos ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Tumor Suppressor ◽  
Tumor Suppressor Gene ◽  
Cell Lung Cancer ◽  
Nonsmall Cell Lung Cancer ◽  
Suppressor Gene ◽  
Gene Inactivation ◽  
Tumor Suppressor Gene Inactivation

scholarly journals TSLC1 is a tumor-suppressor gene in human non-small-cell lung cancer

10.1038/86934 ◽  
2001 ◽  
Vol 27 (4) ◽  
pp. 427-430 ◽  
Author(s):  
Masami Kuramochi ◽  
Hiroshi Fukuhara ◽  
Takahiro Nobukuni ◽  
Takamasa Kanbe ◽  
Tomoko Maruyama ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Tumor Suppressor ◽  
Small Cell Lung Cancer ◽  
Tumor Suppressor Gene ◽  
Cell Lung Cancer ◽  
Suppressor Gene ◽  
Small Cell ◽  
Small Cell Lung

Prognostic Significance of the Tumor Suppressor Gene Maspin in Non–Small Cell Lung Cancer

2005 ◽  
Vol 79 (1) ◽  
pp. 248-253 ◽  
Author(s):  
Kyoji Hirai ◽  
Kiyoshi Koizumi ◽  
Shuji Haraguchi ◽  
Tomomi Hirata ◽  
Iwao Mikami ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Tumor Suppressor ◽  
Small Cell Lung Cancer ◽  
Tumor Suppressor Gene ◽  
Cell Lung Cancer ◽  
Prognostic Significance ◽  
Suppressor Gene ◽  
Small Cell ◽  
Small Cell Lung

scholarly journals The Nonreceptor-Type Tyrosine Phosphatase PTPN13 Is a Tumor Suppressor Gene in Non–Small Cell Lung Cancer

2012 ◽  
Vol 180 (3) ◽  
pp. 1202-1214 ◽  
Author(s):  
Marianna Scrima ◽  
Carmela De Marco ◽  
Fernanda De Vita ◽  
Fernanda Fabiani ◽  
Renato Franco ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Tumor Suppressor ◽  
Small Cell Lung Cancer ◽  
Tumor Suppressor Gene ◽  
Cell Lung Cancer ◽  
Tyrosine Phosphatase ◽  
Suppressor Gene ◽  
Small Cell ◽  
Small Cell Lung

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.

scholarly journals Epigenetic Silencing of the Candidate Tumor Suppressor Gene Per1 in Non–Small Cell Lung Cancer

2007 ◽  
Vol 13 (5) ◽  
pp. 1399-1404 ◽  
Author(s):  
Sigal Gery ◽  
Naoki Komatsu ◽  
Norihiko Kawamata ◽  
Carl W. Miller ◽  
Julian Desmond ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Tumor Suppressor ◽  
Small Cell Lung Cancer ◽  
Tumor Suppressor Gene ◽  
Cell Lung Cancer ◽  
Suppressor Gene ◽  
Small Cell ◽  
Epigenetic Silencing ◽  
Small Cell Lung ◽  
Candidate Tumor Suppressor Gene

scholarly journals The Predictive Values of Advanced Non-Small Cell Lung Cancer Patients Harboring Uncommon EGFR Mutations—The Mutation Patterns, Use of Different Generations of EGFR-TKIs, and Concurrent Genetic Alterations

2021 ◽  
Vol 11 ◽  
Author(s):  
Jiarong Tan ◽  
Chengping Hu ◽  
Pengbo Deng ◽  
Rongjun Wan ◽  
Liming Cao ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Tumor Suppressor ◽  
Small Cell Lung Cancer ◽  
Tumor Suppressor Gene ◽  
Cell Lung Cancer ◽  
Suppressor Gene ◽  
Genetic Alterations ◽  
Small Cell ◽  
Small Cell Lung ◽  
Gene Alterations

IntroductionEpidermal growth factor receptor (EGFR) 19del and L858R mutation are known as “common mutations” in non-small cell lung cancer (NSCLC) and predict sensitivities to EGFR tyrosine kinase inhibitors (TKIs), whereas 20ins and T790M mutations confer drug-resistance to EGFR-TKIs. The role of the remaining uncommon EGFR mutations remains elusive.MethodsWe retrospectively screened a group of NSCLC patients with uncommon EGFR mutations other than 20ins and T790M. The mutation patterns, use of different generations of EGFR-TKIs, and concurrent genetic alterations were analyzed. Meanwhile, a cohort of patients with single 19del or L858R were included for comparison.ResultsA total of 180/1,300 (13.8%) patients were identified. There were 102 patients with advanced or recurrent NSCLC that received first-line therapy of gefitinib/erlotinib/icotinib and afatinib and were eligible for analysis. The therapeutic outcomes among patients with common mutations (EGFRcm, n = 97), uncommon mutation plus common mutations (EGFRum+EGFRcm, n = 52), complex uncommon mutations (complex EGFRum, n = 22), and single uncommon mutations (single EGFRum, n = 28) were significantly different (ORRs: 76.3%, 61.5%, 54.5%, and 50.0%, respectively, p = 0.023; and mPFS: 13.3, 14.7, 8.1, and 6.0 months, respectively, p = 0.004). Afatinib showed superior efficacy over gefitinib/erlotinib/icotinib in EGFRcm (ORR: 81.0% vs. 75.0%, p = 0.773; mPFS: 19.1 vs. 12.0m, p = 0.036), EGFRum+EGFRcm (ORR: 100% vs. 54.5%, p = 0.017; mPFS: NE vs. 13.6m, p = 0.032), and single EGFRum (ORR: 78.6% vs. 21.4%, p = 0.007; mPFS: 10.1 vs. 3.0m, p = 0.025) groups. Comprehensive genomic profiling by Next Generation Sequencing encompassing multiple cancer-related genes was performed on 51/102 patients; the mPFS of patients without co-mutation (n = 16) and with co-mutations of tumor-suppressor genes (n = 31) and driver oncogenes (n = 4) were 31.1, 9.2, and 12.4 months, respectively (p = 0.046). TP53 mutation was the most common co-alteration and showed significantly shorter mPFS than TP53 wild-type patients (7.0 vs. 31.1m, p < 0.001). Multivariate analysis revealed that concurrent 19del/L858R and tumor-suppressor gene alterations independently predicted better and worse prognosis in patients with uncommon mutations, respectively.ConclusionsUncommon EGFR mutations constitute a highly heterogeneous subgroup of NSCLC that confer different sensitivities to EGFR-TKIs with regard to the mutation patterns. Afatinib may be a better choice for most uncommon EGFR mutations. Concurrent 19del/L858R and tumor-suppressor gene alterations, especially TP53, can be established as prognostic biomarkers.

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