长期存在的癌细胞:致命的幸存者
Shensi Shen1, Stéphan Vagner2, Caroline Robert3
1INSERM U981, Gustave Roussy Cancer Campus, Villejuif, France.
Cell
|November 13, 2020
概括
持续的癌细胞在治疗中存活,导致失败. 了解它们复杂的生存机制为癌症治疗提供了新的治疗点,
科学领域:
- 癌症学
- 癌症生物学
- 细胞机制
背景情况:
- 持续的癌细胞逃避治疗,导致治疗失败.
- 这些细胞表现出缓慢的增殖,代谢灵活性和表型可塑性.
- 它们的生存涉及表观遗传,转录和转化调节,以及细胞相互作用.
研究的目的:
- 探索癌细胞持续存活的机制.
- 确定消除这些细胞的潜在治疗点.
主要方法:
- 对持续性癌细胞生物学最新文献的审查.
- 对表观遗传,转录和转化调节过程的分析.
- 研究癌症持久性中的细胞相互作用.
主要成果:
- 癌症细胞具有独特的适应性生存策略.
- 不同的分子和细胞机制有助于它们的持续存在.
- 临床前研究表明这些生存途径具有前景.
结论:
- 针对持久性癌细胞对于改善癌症治疗结果至关重要.
- 需要对其复杂生物学的进一步研究进行临床转化.
- 开发针对这些细胞的疗法具有显著的治疗潜力.
相关概念视频
Cancer Stem Cells and Tumor Maintenance
5.5K
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...
5.5K
Adaptive Mechanisms in Cancer Cells
6.4K
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,...
6.4K
Treatment Resistant Cancers
3.5K
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...
3.5K
Cancer
52.6K
Cancers arise due to mutations in genes involved in the regulation of cell division, which leads to unrestricted cell proliferation. Modern science and medicine have made great strides in the understanding and treatment of cancer, including eradicating cancer in some patients. However, there is still no cure for cancer. This is largely due to the fact that cancer is a large group of many diseases.
52.6K
Metastasis
6.1K
Metastasis is the spread of cancer cells from the original site to distant locations in the body. Cancer cells can spread via blood vessels (hematogenous) as well as lymph vessels in the body.
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...
6.1K
Cancers Originate from Somatic Mutations in a Single Cell
13.9K
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...
13.9K


