关于癌症风险的TERT基因MNS16A多态性:系统性审查和元分析
Hao Yuan1, Zhenwei Han1, Zhihai Teng1
1Department of Urology, the Second Hospital of Hebei Medical University, Shijiazhuang, China.
Nucleosides, nucleotides & nucleic acids
|June 22, 2023
概括
端粒酶逆转录酶 (TERT) MNS16A多态性没有显示出整体癌症风险相关性. 然而,分层分析显示,大脑癌症风险增加,特别是在亚洲人群中.
科学领域:
- 遗传学和基因组学 遗传学和基因组学
- 癌症研究 癌症研究
- 分子生物学分子生物学
背景情况:
- 端粒酶逆转录酶 (TERT) 基因中的MNS16A多态性已被研究其与癌症风险的潜在关联.
- 之前的研究对TERT MNS16A多态和各种癌症类型之间的联系产生了相互矛盾的结果.
- 需要进行全面的评估,以澄清这种多态性在癌症易感性中的作用.
研究的目的:
- 进行元分析,准确评估TERT MNS16A多态和癌症风险之间的关联.
- 调查现有研究中的潜在异质性和出版偏见.
- 通过分层分析,探索特定种族群体,控制来源和癌症类型之间的关联.
主要方法:
- 对17项研究 (12篇文章) 进行了元分析,包括7132例癌症病例和13764例对照.
- 使用固定效应或随机效应模型计算了几率比率 (OR) 和95%置信区间 (CI).
- 基于种族,控制来源和癌症类型进行了分层分析,以确定特定的关联.
主要成果:
- 在五种遗传模型中,总体的元分析没有显示TERT MNS16A多态和癌症风险之间的显著关联.
- 按种族分层分析表明,亚洲人群中存在显著的关联.
- 根据癌症类型进行进一步分层,发现与这种多态性有关的大脑癌症的风险显著增加.
结论:
- 虽然整体相关性并不显著,但TERT MNS16A多态可能会导致特定亚组的癌症风险增加.
- 这些发现表明它可能在脑癌的发展中发挥作用,特别是在亚洲人群中.
- 需要进一步的研究来阐明这种关联背后的确切机制.
更多相关视频
11:15Next Generation Sequencing for the Detection of Actionable Mutations in Solid and Liquid Tumors
Published on: September 20, 2016
24.4K
07:47Author Spotlight: Unveiling Transmembrane Protein Family-Related Markers in Gastric Cancer and Implications for Targeted Therapies
Published on: September 15, 2023
1.5K
相关概念视频
Cancer-Critical Genes II: Tumor Suppressor Genes
7.5K
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...
7.5K
Mismatch Repair
4.9K
Organisms are capable of detecting and fixing nucleotide mismatches that occur during DNA replication. This sophisticated process requires identifying the new strand and replacing the erroneous bases with correct nucleotides. Mismatch repair is coordinated by many proteins in both prokaryotes and eukaryotes.
The Mutator Protein Family Plays a Key Role in DNA Mismatch Repair
The human genome has more than 3 billion base pairs of DNA per cell. Prior to cell division, that vast amount of genetic...
The Mutator Protein Family Plays a Key Role in DNA Mismatch Repair
The human genome has more than 3 billion base pairs of DNA per cell. Prior to cell division, that vast amount of genetic...
4.9K
Cancers Originate from Somatic Mutations in a Single Cell
12.1K
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...
12.1K
Cancer-Critical Genes I: Proto-oncogenes
9.0K
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...
9.0K
Abnormal Proliferation
4.6K
Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
4.6K
Loss of Tumor Suppressor Gene Functions
4.9K
Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
When the tumor suppressor genes develop mutations or are lost, cells start growing out of control, leading to cancer. However, a single functional copy of the tumor suppressor gene is enough for the cells to maintain their normal functions and cell...
When the tumor suppressor genes develop mutations or are lost, cells start growing out of control, leading to cancer. However, a single functional copy of the tumor suppressor gene is enough for the cells to maintain their normal functions and cell...
4.9K
