这就是HER-2 SMASH
Celal Alandağ1, Ayşegül Öztürk2, Fatih Yulak3
1Department of Medical Oncology, Sivas Medicana Hospital, Sivas, Türkiye. dralandag@hotmail.com.
Cancer chemotherapy and pharmacology
|December 23, 2024
概括
拉巴提尼布治疗可提高癌细胞中人体表皮生长因子-2 (HER-2) 受体的调节,从而提高了 HER-2 向疗法的有效性,如 trastuzumab 和 T-DM1. 这种新的"粉碎方法"扩大了对HER-2低或负瘤的治疗适用性.
科学领域:
- 在瘤学瘤学.
- 分子生物学分子生物学
- 药理学 药理学是指药理学的学科.
背景情况:
- 针对HER-2的向疗法只有在HER-2过度表达的部分癌症中才有效.
- 许多癌症类型,包括乳腺癌和结肠癌,自然表现出低或不存在的HER-2表达,限制了治疗选择.
研究的目的:
- 研究HER-2阴性/低癌细胞系 (MCF-7和HT-29) 中人体表皮生长因子-2 (HER-2) 受体的上调.
- 评估拉帕提尼布诱导的HER-2上调对HER-2向治疗 (特拉斯图祖马布,T-DM1) 的疗效的影响.
主要方法:
- 对MCF-7和HT-29细胞系进行了10天的非细胞毒性拉帕提尼布剂量,以诱导HER-2的过度表达.
- 在拉帕提尼布治疗前后使用ELISA和免疫光分析量化HER-2水平.
- 评估了trastuzumab和T-DM1对细胞活性的影响,并对HER-2通路蛋白进行分析以阐明机制.
主要成果:
- 拉帕提尼布在10天的时间内成功诱导了MCF-7和HT-29细胞中显著的HER-2受体过度表达.
- 在拉帕提尼布诱导的HER-2上调后,观察到trastuzumab和T-DM1抗癌活性和细胞毒性显著增加.
结论:
- 开发的"粉碎方法"有效地将HER-2阴性或低瘤转化为HER-2过度表达的瘤.
- 这种方法有可能扩大符合HER-2向治疗的患者人数,改善各种癌症类型的治疗结果.
相关概念视频
Cancer-Critical Genes II: Tumor Suppressor Genes
7.3K
Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
7.3K
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
Mitogens and the Cell Cycle
6.4K
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...
6.4K


