Interleukin 17A Polymorphism Elevates Gene Expression and Is Associated with Increased Risk of Nonsmall Cell Lung Cancer

2015 ◽  
Vol 34 (1) ◽  
pp. 63-68 ◽  
Author(s):  
Sensen Cheng ◽  
Zhulin Shao ◽  
Xiuchun Liu ◽  
Liangjun Guo ◽  
Xia Zhang ◽  
...  
Keyword(s):  
Gene Expression ◽  
Lung Cancer ◽  
Cell Lung Cancer ◽  
Nonsmall Cell Lung Cancer ◽  
Interleukin 17A ◽  
Increased Risk

Prediction of nonsmall cell lung cancer sensitivity to cisplastin and paclitaxel based on marker gene expression

2011 ◽  
Vol 45 (4) ◽  
pp. 600-607 ◽  
Author(s):  
U. A. Boyarskikh ◽  
Yu. V. Kondrakhin ◽  
I. S. Yevshin ◽  
R. N. Sharipov ◽  
A. V. Komelkov ◽  
...  
Keyword(s):  
Gene Expression ◽  
Lung Cancer ◽  
Cell Lung Cancer ◽  
Marker Gene ◽  
Nonsmall Cell Lung Cancer ◽  
Marker Gene Expression

scholarly journals Gene expression profiling reveals novel biomarkers in nonsmall cell lung cancer

2010 ◽  
Vol 129 (2) ◽  
pp. 355-364 ◽  
Author(s):  
Abel Sanchez-Palencia ◽  
Mercedes Gomez-Morales ◽  
Jose Antonio Gomez-Capilla ◽  
Vicente Pedraza ◽  
Laura Boyero ◽  
...  
Keyword(s):  
Gene Expression ◽  
Lung Cancer ◽  
Gene Expression Profiling ◽  
Cell Lung Cancer ◽  
Expression Profiling ◽  
Nonsmall Cell Lung Cancer ◽  
Novel Biomarkers

scholarly journals Serial Cancer Development Three Times in a Patient with Fanconi Anemia

2021 ◽  
pp. 1168-1174
Author(s):  
Katsuya Yanagisawa ◽  
Toshimichi Horiuchi ◽  
Akemi Matsuo ◽  
Hiroshi Kuraishi ◽  
Hidetoshi Satomi ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Solid Tumors ◽  
Fanconi Anemia ◽  
Cell Lung Cancer ◽  
Bone Marrow Failure ◽  
Nonsmall Cell Lung Cancer ◽  
Cancer Development ◽  
Hematopoietic Stem ◽  
Anal Squamous Cell Carcinoma ◽  
Increased Risk

Fanconi anemia (FA) is characterized clinically by bone marrow failure, congenital malformations, sensitivity to DNA cross-linking agents, and increased risk of malignancy. Hematological cancer is the best-described malignancy in patients with FA, but the susceptibility to the development of solid tumors is also well documented, especially after hematopoietic stem cell transplantation (HSCT). With regard to the development of solid tumors in patients with FA, head and neck, esophageal, and anal squamous cell carcinoma are well known, but reports of lung cancer are extremely rare. Here, we describe an FA patient with a history of HSCT that developed 3 serial cancers – oral, esophageal, and nonsmall cell lung cancer – over a period of 6 years. The third lesion was nonsmall cell lung cancer and its location corresponded closely to the field of irradiation treatment for prior esophageal cancer. The occurrence of lung cancer in patients with FA is uncommon, but FA patients should be screened regularly and serially. Our case also indicated the importance of the irradiated field as a location for subsequent cancer development.

scholarly journals Wnt Pathway Activation Predicts Increased Risk of Tumor Recurrence in Patients With Stage I Nonsmall Cell Lung Cancer

2013 ◽  
Vol 257 (3) ◽  
pp. 548-554 ◽  
Author(s):  
Mark Shapiro ◽  
Gal Akiri ◽  
Cynthia Chin ◽  
Juan P. Wisnivesky ◽  
Mary B. Beasley ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Lung Cancer ◽  
Tumor Recurrence ◽  
Wnt Pathway ◽  
Nonsmall Cell Lung Cancer ◽  
Stage I ◽  
Pathway Activation ◽  
Increased Risk

scholarly journals STAT3 rs3816769 polymorphism correlates with gene expression level and may predispose to nonsmall cell lung cancer: a preliminary study

2013 ◽  
Vol 123 (12) ◽  
pp. 672-679 ◽  
Author(s):  
Daria Domańska ◽  
Adam Antczak ◽  
Dorota Pastuszak‑Lewandoska ◽  
Paweł Górski ◽  
Jacek Kordiak ◽  
...  
Keyword(s):  
Gene Expression ◽  
Lung Cancer ◽  
Cell Lung Cancer ◽  
Nonsmall Cell Lung Cancer ◽  
Gene Expression Level ◽  
Expression Level ◽  
Preliminary Study

scholarly journals Epigenome-wide association study of whole blood gene expression in Framingham Heart Study participants provides molecular insight into the potential role of CHRNA5 in cigarette smoking-related lung diseases

2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Chen Yao ◽  
Roby Joehanes ◽  
Rory Wilson ◽  
Toshiko Tanaka ◽  
Luigi Ferrucci ◽  
...  
Keyword(s):  
Gene Expression ◽  
Lung Cancer ◽  
Dna Methylation ◽  
Cigarette Smoking ◽  
Association Study ◽  
Whole Blood ◽  
Lung Diseases ◽  
Epigenetic Modification ◽  
Blood Gene Expression ◽  
Increased Risk

Abstract Background DNA methylation is a key epigenetic modification that can directly affect gene regulation. DNA methylation is highly influenced by environmental factors such as cigarette smoking, which is causally related to chronic obstructive pulmonary disease (COPD) and lung cancer. To date, there have been few large-scale, combined analyses of DNA methylation and gene expression and their interrelations with lung diseases. Results We performed an epigenome-wide association study of whole blood gene expression in ~ 6000 individuals from four cohorts. We discovered and replicated numerous CpGs associated with the expression of cis genes within 500 kb of each CpG, with 148 to 1,741 cis CpG-transcript pairs identified across cohorts. We found that the closer a CpG resided to a transcription start site, the larger its effect size, and that 36% of cis CpG-transcript pairs share the same causal genetic variant. Mendelian randomization analyses revealed that hypomethylation and lower expression of CHRNA5, which encodes a smoking-related nicotinic receptor, are causally linked to increased risk of COPD and lung cancer. This putatively causal relationship was further validated in lung tissue data. Conclusions Our results provide a large and comprehensive association study of whole blood DNA methylation with gene expression. Expression platform differences rather than population differences are critical to the replication of cis CpG-transcript pairs. The low reproducibility of trans CpG-transcript pairs suggests that DNA methylation regulates nearby rather than remote gene expression. The putatively causal roles of methylation and expression of CHRNA5 in relation to COPD and lung cancer provide evidence for a mechanistic link between patterns of smoking-related epigenetic variation and lung diseases, and highlight potential therapeutic targets for lung diseases and smoking cessation.

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