Protocadherin 10 is frequently downregulated by promoter methylation and functions as a tumor suppressor gene in non-small cell lung cancer

2013 ◽  
Vol 12 (1) ◽  
pp. 11-19 ◽  
Author(s):  
Xiaokui Tang ◽  
Xuedong Yin ◽  
Tingxiu Xiang ◽  
Hongzhong Li ◽  
Fan Li ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Tumor Suppressor ◽  
Small Cell Lung Cancer ◽  
Tumor Suppressor Gene ◽  
Cell Lung Cancer ◽  
Promoter Methylation ◽  
Suppressor Gene ◽  
Small Cell ◽  
Small Cell Lung

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 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.

ARNT2 is downregulated and serves as a potential tumor suppressor gene in non-small cell lung cancer

Tumor Biology ◽  
2015 ◽  
Vol 36 (3) ◽  
pp. 2111-2119 ◽  
Author(s):  
Bo Yang ◽  
Ende Yang ◽  
Hehe Liao ◽  
Zhouquan Wang ◽  
Zhiping Den ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Tumor Suppressor ◽  
Small Cell Lung Cancer ◽  
Tumor Suppressor Gene ◽  
Cell Lung Cancer ◽  
Suppressor Gene ◽  
Small Cell ◽  
Small Cell Lung ◽  
Potential Tumor Suppressor
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