癌症干细胞模拟用于免疫逃避和治疗耐药性
Phei Er Saw1, Qiang Liu2, Ping-Pui Wong1
1Guangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Guangdong-Hong Kong Joint Laboratory for RNA Medicine, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou 510120, China; Nanhai Clinical Translational Center, Sun Yat-sen Memorial Hospital, Foshan, China.
Cell stem cell
|June 26, 2024
概括
癌症干细胞 (CSCs) 表现出模仿性,冒充其他细胞类型以促进瘤生长并逃避免疫检测. 针对这种模仿提供了一种新的策略,以克服治疗耐药性并提高免疫治疗的有效性.
科学领域:
- 在瘤学瘤学.
- 癌症生物学 癌症生物学
- 免疫学 免疫学 免疫学
背景情况:
- 癌症干细胞 (CSCs) 是一个异质的群体,对瘤生长和抵抗至关重要.
- CSCs具有自我更新的能力,并在瘤微环境中调解复杂的细胞间通信.
研究的目的:
- 提出和探索 CSC 模仿作为表型可塑性的驱动器的概念.
- 阐明CSC模仿如何促进免疫逃避和治疗耐药性.
- 突出针对CSC模拟的治疗策略,以改善免疫疗法.
主要方法:
- 基于现有文献的概念框架开发.
- 对CSC与免疫,血管和淋巴细胞相互作用的分析.
- 对参与CSC介导重编程的信号通路 (副和副) 的审查.
主要成果:
- 瘤细胞可以模仿免疫,血管和淋巴细胞,促进瘤的进展.
- 中枢细胞中心模拟促进了对和对的信号传递,促进了 stromal 和免疫细胞中的前瘤表型.
- 这种模仿是免疫逃避的关键机制,导致免疫治疗耐药性.
结论:
- 脑中枢细胞模仿是癌症进展和治疗失败的关键因素.
- 准CSC模仿是一种克服治疗耐药性的有希望的途径.
- 开发针对CSC模拟的向疗法可以显著提高免疫疗法的疗效.
相关概念视频
Cancer Stem Cells and Tumor Maintenance
4.9K
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...
4.9K
Treatment Resistant Cancers
3.3K
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...
3.3K
Adaptive Mechanisms in Cancer Cells
5.7K
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,...
5.7K
Tumor Immunotherapy
510
Immunotherapy is a treatment that boosts or manipulates the immune system to fight diseases, including cancer. For instance, by stimulating an immune response through vaccinations against viruses that cause cancers, like hepatitis B virus and human papillomavirus, these diseases can be prevented. Nonetheless, some cancer cells can avoid the immune system due to their rapid mutation and division. The immune response to many cancers involves three phases: elimination, equilibrium, and escape.
510
Metastasis
5.5K
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...
5.5K
The Tumor Microenvironment
6.6K
Every normal cell or tissue is embedded in a complex local environment called stroma, consisting of different cell types, a basal membrane, and blood vessels. As normal cells mutate and develop into cancer cells, their local environment also changes to allow cancer progression. The tumor microenvironment (TME) consists of a complex cellular matrix of stromal cells and the developing tumor. The cross-talk between cancer cells and surrounding stromal cells is critical to disrupt normal tissue...
6.6K


