在三阴性乳腺癌中缺少不匹配修复蛋白质
Bayan Maraqa1, Maxim Al-Ashhab1, Hamza Zughaier1
1Department of Pathology and Laboratory Medicine, King Hussein Cancer Center, Amman, Jordan.
The Journal of international medical research
|June 20, 2024
概括
大约9%的三阴性乳腺癌 (TNBC) 患者缺乏不匹配修复蛋白 (dMMR). 这种缺陷可能有助于预测结果,并识别可能受益于免疫治疗的TNBC患者.
科学领域:
- 在瘤学瘤学.
- 癌症研究 癌症研究
- 免疫治疗是一种免疫疗法.
背景情况:
- 三阴性乳腺癌 (TNBC) 是一个重大的全球健康挑战.
- 不匹配修复蛋白 (MMRP) 缺乏发生在0.2%-18.6%的TNBC病例中.
- 免疫疗法对MMRP缺乏的转移性乳腺癌具有前途.
研究的目的:
- 为了确定TNBC患者的MMRP缺陷.
- 评估MMRP缺陷作为TNBC预测生物标志物的潜力.
主要方法:
- 对TNBC患者的回顾性队列研究 (20152021).
- 免疫组织化学用于评估MMRP表达.
- 对152名TNBC患者的分析.
主要成果:
- 在152名患者中,有14名患者 (9.2%) 患有缺陷的MMR (dMMR).
- 最常见的缺陷是PMS2损失,其次是MLH1,MSH6和MSH2.
- dMMR患者的5年生存率 (80.8%) 比熟练的MMR患者 (62.3%) 高,尽管整体存活率没有显著差异.
结论:
- 大约9%的TNBC患者表现出dMMR.
- MMRP 缺陷可能会预测 TNBC 的结果.
- dMMR状态可以识别适合免疫治疗的TNBC患者.
相关概念视频
Mismatch Repair
40.0K
Overview
40.0K
Nucleotide Excision Repair
3.5K
DNA Distortion and Damage
Cells are regularly exposed to mutagens—factors in the environment that can damage DNA and generate mutations. UV radiation is one of the most common mutagens and is estimated to introduce a significant number of changes in DNA. These include bends or kinks in the structure, which can block DNA replication or transcription. If these errors are not fixed, the damage can cause mutations, which in turn can result in cancer or disease depending on which sequences are...
Cells are regularly exposed to mutagens—factors in the environment that can damage DNA and generate mutations. UV radiation is one of the most common mutagens and is estimated to introduce a significant number of changes in DNA. These include bends or kinks in the structure, which can block DNA replication or transcription. If these errors are not fixed, the damage can cause mutations, which in turn can result in cancer or disease depending on which sequences are...
3.5K
Abnormal Proliferation
4.5K
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...
4.5K
Long-patch Base Excision Repair
7.0K
Since the discovery of the two BER pathways, there has been a debate about how a cell chooses one pathway over the other and the factors determining this selection. Numerous in vitro experiments have pointed out multiple determinants for the sub-pathway selection. These are:
7.0K
Base Excision Repair
22.3K
One of the common DNA damages is the chemical alteration of single bases by alkylation, oxidation, or deamination. The altered bases cause mispairing and strand breakage during replication. This type of damage causes minimal change to the DNA double helix structure and can be repaired by the base excision repair (BER) pathways. BER corrects damaged DNA sequences by removing the damaged base and restoring the original base sequence using the complementary strand as a template.
The first step of...
The first step of...
22.3K
DNA Damage can Stall the Cell Cycle
9.1K
In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
9.1K


