低甲基化剂加上venetoclax与分子定义的二次AML中的强化诱导化疗方案相比
Shai Shimony1,2, Jan Philipp Bewersdorf3, Rory M Shallis4
1Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA. shai_shimony@dfci.harvard.edu.
Leukemia
|February 20, 2024
概括
低甲基化剂加上venetoclax可能是二次急性髓性白血病 (AML) 的首选治疗方法. 与标准化疗相比,这种组合显示出更好的生存率,特别是考虑到特定的遗传突变时.
科学领域:
- 血液学 血液学 血液学
- 在瘤学瘤学.
- 分子生物学分子生物学
背景情况:
- 二次性急性髓性白血病 (AML) 是由于先前的髓性瘤而产生的,并且与较差的患者结局有关.
- 了解分子定义的二次性AML治疗疗效对于改善患者存活率至关重要.
研究的目的:
- 为了比较分子定义的二次AML患者的整体存活期 (OS),用不同的治疗方案治疗.
- 确定影响治疗反应和患者预后的特定分子变化.
主要方法:
- 对395名分子定义的二次AML患者的回顾性分析.
- 用鲁素/细胞氨酸 (7+3),脂质体鲁素/细胞氨酸 (CPX-351) 和低甲基化剂 (HMA) 加上venetoclax (VEN) 治疗的患者的结局的比较.
- 多变量分析和对照比较,调整年龄和分子共同突变.
主要成果:
- 在60岁以上的患者中,治疗组之间的整体存活率是可比的.
- 与7+3 (HR 0.64;P=0.041) 相比,HMA + VEN与更好的生存状况相关,而CPX-351与7+3 (HR 0.79;P=0.31) 并没有显著不同.
- 特定突变,如IDH,BCOR和全原干细胞移植与改善的生存状况相关,而年龄较大,先前的骨髓性疾病,NRAS/KRAS,EZH2和单体型与更糟糕的生存状况相关.
- IDH共同突变受益于7+3,而NRAS/KRAS共同突变则对HMA+VEN和CPX-351产生不利影响.
- 在SF3B1突变患者中,HMA+VEN改善了OS,而在RNA剪接因子突变携带者中,SF3B1突变患者的OS与7+3相比改善,而在RNA剪接因子突变携带者的CPX-351相比改善.
结论:
- 用低甲基化剂加上venetoclax的治疗可能是分子定义的二次AML的首选选择.
- 通过考虑特定的共同突变,可以进一步细化治疗决策,指导个性化治疗策略.
- 需要进一步的前性研究来证实这些发现,并根据分子概况优化治疗选择.
相关概念视频
02:50Combination Therapies and Personalized Medicine
4.9K
Combining two or more treatment methods increases the life span of cancer patients while reducing damage to vital organs or tissue from the overuse of a single treatment. Combination therapy also targets different cancer-inducing pathways, thus reducing the chances of developing resistance to treatment.
The combination of the drug acetazolamide and sulforaphane is a good example of combination therapy to treat cancer. The cells in the interior of a large tumor often die due to the hypoxic and...
The combination of the drug acetazolamide and sulforaphane is a good example of combination therapy to treat cancer. The cells in the interior of a large tumor often die due to the hypoxic and...
4.9K
02:57Targeted Cancer Therapies
7.6K
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...
7.6K
02:49Cancer Therapies
7.7K
Cancer therapies are various modes of treatment, such as surgery, radiation therapy, and chemotherapy that are administered to cancer patients.
However, cancer treatments can pose several challenges, as therapies used to kill cancer cells are generally also toxic to normal cells. Moreover, cancer cells mutate rapidly and can develop resistance to chemical agents or radiation therapy. Besides, all types of cancer cells may not respond to the same therapy. Some cancer cells respond to one...
However, cancer treatments can pose several challenges, as therapies used to kill cancer cells are generally also toxic to normal cells. Moreover, cancer cells mutate rapidly and can develop resistance to chemical agents or radiation therapy. Besides, all types of cancer cells may not respond to the same therapy. Some cancer cells respond to one...
7.7K
01:28Chemotherapy-Induced Nausea and Vomiting: Neurokinin-1 Receptor Antagonists
163
Neurokinin 1 (NK1) receptors are distributed across the GI tract, vagal afferents, and key CNS regions including the central vomiting center and chemoreceptor trigger zone (CTZ) Chemotherapy agents stimulate enterochromaffin cells in the gastrointestinal (GI) tract to release large amounts of substance P (SP). SP is a neuropeptide released by specific sensory nerves in response to many different stressors, including those in the GI mucosa affected by chemotherapy. SP binds and activates...
163