表观遗传重编程作为癌症干细胞和治疗耐药性的关联:对生物标志物发现的影响
Chu Xin Ng1, Shin Yuh Lee1, Xin Yi Yap1
1School of Biosciences, Faculty of Health and Medical Sciences, Taylor's University, No.1, Jalan Taylors, 47500, Subang Jaya, Selangor, Malaysia.
Discover oncology
|November 19, 2025
概括
癌细胞通过表观遗传重编程适应压力因素,促进干性和治疗耐药性. 本综述探讨了如何针对这些表观遗传机制可以改善癌症诊断和治疗.
科学领域:
- 在瘤学瘤学.
- 表观遗传学 在表观遗传学中,表观遗传学是指表观遗传学.
- 癌症生物学 癌症生物学
背景情况:
- 癌症治疗失败是由瘤细胞适应药物和免疫监测等压力因素所驱动的.
- 癌症干细胞 (CSC) 在瘤进展过程中出现,有助于抵抗和复发.
- 表观遗传重编程是推动CSC发展和治疗耐药性的关键机制.
研究的目的:
- 审查表观遗传重编程如何影响染色体可塑性,促进癌症干和治疗耐药性.
- 讨论利用表观遗传机制用于精确瘤学的转化研究.
- 突出表观遗传生物标志物的潜力,以改善癌症诊断和治疗疗效.
主要方法:
- 关于表观遗传学,癌症干细胞和治疗耐药性的科学文献的审查.
- 分析基因修饰和染色质结构在调节基因表达中的作用.
- 对瘤分类和预后的表观遗传特征的检查.
主要成果:
- 表观遗传重编程改变染色质以促进干性和沉默分化基因,增强癌细胞的可塑性.
- 特定的表观遗传特征与瘤亚型,预后和治疗反应相关.
- 表观遗传生物标志物对早期发现瘤复发和监测最小残留疾病充满希望.
结论:
- 表观遗传重编程是癌症干细胞和治疗耐药性的关键驱动因素.
- 准表观遗传机制为推进精确瘤学提供了一个有希望的途径.
- 对表观遗传生物标志物的进一步研究可以显著改善癌症诊断,预后和治疗结果.
相关概念视频
Cancer Stem Cells and Tumor Maintenance
5.8K
Early diagnosis and treatment can often cure cancer. However, even with treatment, residual cells called cancer stem cells (CSC) might remain, often causing tumor recurrence. These cancer stem cells possess the potential for self-renewal and multi-lineage differentiation and are often responsible for the therapeutic resistance displayed in most cancers.
Cancer stem cells are thought to originate from tissue-specific normal stem cells or progenitor cells. The normal stem cells usually reside in...
Cancer stem cells are thought to originate from tissue-specific normal stem cells or progenitor cells. The normal stem cells usually reside in...
5.8K
Treatment Resistant Cancers
3.7K
Cancer is the second leading cause of death in the United States. A cancer cell is genetically unstable and hence can mutate faster. They can also modify their microenvironment and escape immune surveillance. The difficulties in treating cancer are further compounded by the emergence of rapid resistance to anticancer drugs. The most common ways to attain resistance in cancer cells include alteration in drug transport and metabolism, modification of drug target, elevated DNA damage response, or...
3.7K
Somatic to iPS Cell Reprogramming
2.6K
Reprogramming alters the gene expression in somatic cells, transforming them into induced pluripotent stem (iPS) cells over several generations. Scientists can reprogram cells by introducing genes for four transcription factors—Oct4, Sox2, Klf4, and c-Myc (OSKM) by viral or non-viral methods. These factors are also known as Yamanaka factors after Shinya Yamanaka, who first generated iPS cells using mouse skin cells. Yamanaka was awarded the Nobel Prize in Physiology or Medicine in 2012...
2.6K
Epigenetic Regulation
3.7K
Epigenetic changes alter the physical structure of the DNA without changing the genetic sequence and often regulate whether genes are turned on or off. This regulation ensures that each cell produces only proteins necessary for its function. For example, proteins that promote bone growth are not produced in muscle cells. Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
X-chromosome...
X-chromosome...
3.7K
Epigenetic Regulation
33.4K
Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
33.4K
Adaptive Mechanisms in Cancer Cells
6.9K
Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
6.9K


