被动吸烟诱导的突变性作为肺癌发生的促进者
Akifumi Mochizuki1, Kouya Shiraishi2, Takayuki Honda3
1Division of Genome Biology, National Cancer Center Research Institute, Tokyo, Japan; Department of Respiratory Medicine, Tokyo Medical and Dental University, Tokyo, Japan.
概括
接触二手烟会增加瘤突变负担,并通过诱导APOBEC类型突变促进肺癌. 特定的遗传变异可以识别患肺癌高风险的个体.
科学领域:
- 在瘤学瘤学.
- 遗传学 遗传学是一种遗传学.
- 环境健康 环境健康
背景情况:
- 被动吸烟 (二手烟) 是一种已知的致癌物质,与肺癌有关.
- 与积极吸烟相比,被动吸烟的突变效应尚不清楚.
研究的目的:
- 为了研究被动吸烟在肺腺癌中的突变性特性.
- 为了确定与被动吸烟引起的肺癌相关的遗传变化和生物标志物.
主要方法:
- 来自女性从未吸烟者,有详细的被动吸烟暴露史的肺腺癌样本的全外基因组和全基因组测序.
- 对瘤突变负担和突变特征与被动吸烟暴露相关的分析.
- 研究亚洲人群中APOBEC3A/3B多态性及其对突变负载的影响.
主要成果:
- 被动吸烟暴露与瘤突变负担的统计显著增加有关.
- 被动吸烟引起的突变表现出APOBEC类型的特征,包括SMAD4和ADGRG6热点突变.
- 在亚洲人群中常见的APOBEC3A / 3B多态变异在青少年被动吸烟暴露的个体中放大了突变负载.
结论:
- 被动吸烟诱导的突变发生有助于肺癌发生.
- APOBEC3A / 3B多态可能作为生物标志物来识别由于被动烟雾暴露导致肺癌风险较高的个体.
关键词:
这是APOBECAPOBECAPOBECAPOBECAPOBECAPOBECAPOBECAPOBECAPOBECAPOBECAPOBECAPOBECAPOBEC肺部腺癌瘤是肺部腺癌.突变的签名 突变的签名被动吸烟是一种被动吸烟.多态性多态性多态性更多相关视频
相关概念视频
Mutagenicity and Carcinogenicity
1.3K
Mutagenicity and carcinogenicity refer to the ability of drugs to cause genetic defects and induce cancer, respectively. The International Agency for Research on Cancer (IARC) classifies agents into four groups based on their carcinogenic potential. Group 1 agents are known human carcinogens; group 2A agents are probably carcinogenic to humans; group 3 agents lack data to support their role in carcinogenesis; and group 4 includes agents for which data support that they are not likely to be...
1.3K
Cancer Prevention
6.2K
Several factors can increase the risk of cancer in an individual. About 50% of cancer cases can be prevented by adopting a healthy lifestyle, regular exercise, eating healthy, and following a modest cancer prevention diet. Epidemiological studies have consistently shown that populations with vegetable and fruit-rich diets have reduced the incidence of cancer. On the other hand, populations who have a diet rich in animal fat, red meat, junk food, or high calories are predisposed to cancer.
Some...
Some...
6.2K
Mutations
82.2K
Overview
82.2K
Chronic Obstructive Pulmonary Disease-II: Pathophysiology
2.8K
Chronic Obstructive Pulmonary Disease (COPD) pathophysiology is intricate and multifaceted, involving a complex interplay of physiological processes. Understanding these mechanisms is crucial for effectively managing and treating COPD. Here is an in-depth look at the critical elements in the pathophysiology of COPD:
Chronic Inflammation
Chronic Inflammation
2.8K
Cancer-Critical Genes I: Proto-oncogenes
8.9K
Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
8.9K
Cancers Originate from Somatic Mutations in a Single Cell
11.9K
Cancer arises from mutations in the critical genes that allow healthy cells to escape cell cycle regulation and acquire the ability to proliferate indefinitely. Though originating from a single mutation event in one of the originator cells, cancer progresses when the mutant cell lines continue to gain more and more mutations, and finally, become malignant. For example, chronic myelogenous leukemia (CML) develops initially as a non-lethal increase in white blood cells, which progressively...
11.9K


