肺癌和免疫治疗中瘤微环境中的血管生成和EMT调节器
Taotao Yan1,2,3, Jiahai Shi2,3
1Medical School of Nantong University, Nantong University, Nantong, China.
Frontiers in immunology
|December 31, 2024
概括
肺癌免疫疗法研究至关重要. 了解瘤微环境调节器如何驱动血管新生和上皮-介质细胞过渡 (EMT) 可以改善肺癌治疗和克服耐药性.
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:
- 肺癌是癌症死亡的主要原因,复发,转移和药物耐药性恶化的结果.
- 免疫疗法为肺癌治疗提供了一个有前途的新范式.
- 瘤微环境 (TME) 显著影响瘤的进展和治疗反应.
研究的目的:
- 审查TME中瘤血管生成和上皮-介质细胞过渡 (EMT) 的关键调节者.
- 检查这些调节剂对肺癌进展和免疫治疗的影响.
- 探索未来肺癌治疗策略的潜在新调节剂.
主要方法:
- 关于血管新生,EMT和肺癌免疫治疗的最新研究的文献综述.
- 在TME中分析血管生成和EMT之间的相互作用.
- 研究影响肺癌治疗的新型调节因素.
主要成果:
- 瘤血管生成和EMT是TME内部相互依存的过程.
- 这些过程促进瘤转移,入侵和治疗药物耐药性.
- 血管新生导致的缺氧区域可以促进药物耐药性.
结论:
- 在TME中准血管生成和EMT的调节剂对于推进肺癌免疫疗法至关重要.
- 了解这些过程之间的相互作用为克服治疗阻力提供了洞察力.
- 对新型调节剂的进一步研究可能会导致改善肺癌治疗策略.
相关概念视频
The Tumor Microenvironment
6.3K
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...
6.3K
Regulation of Angiogenesis and Blood Supply
2.5K
Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits. Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl...
2.5K
Tumor Immunotherapy
394
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.
394
Mitogens and the Cell Cycle
6.3K
Mitogens and their receptors play a crucial role in controlling the progression of the cell cycle. However, the loss of mitogenic control over cell division leads to tumor formation. Therefore, mitogens and mitogen receptors play an important role in cancer research. For instance, the epidermal growth factor (EGF) - a type of mitogen and its transmembrane receptor (EGFR), decides the fate of the cell's proliferation. When EGF binds to EGFR, a member of the ErbB family of tyrosine kinase...
6.3K
Targeted Cancer Therapies
7.4K
The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against...
There are several types of targeted therapies against...
7.4K
Metastasis
5.4K
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...
5.4K


