解读敌人的战术 - - 走向最佳抗癌策略的狭窄路径,以华堡效应为目标
Kinga A Kocemba-Pilarczyk1, Barbara Ostrowska2, Sonia E Trojan2
1Chair of Medical Biochemistry, Faculty of Medicine, Jagiellonian University - Medical College, Kopernika 7, Kraków, 31-034, Poland. kinga.kocemba@uj.edu.pl.
Pharmacological reports : PR
|August 1, 2025
概括
在癌症中准华堡效应需要个性化策略来抑制癌细胞代谢,而不会伤害正常细胞. 本综述讨论了针对特定的,个性化的癌症治疗的最佳目标和治疗方法.
科学领域:
- 在瘤学瘤学.
- 生物化学 生物化学
- 代谢途径 代谢途径
背景情况:
- 癌细胞表现出改变的新陈代谢,特别是华堡效应 (有氧糖解),以快速增长.
- 这种代谢重编程提供能量,生物合成中间体和NAD+用于增殖.
- 华堡效应也存在于正常增殖细胞中,使向癌症治疗复杂化.
研究的目的:
- 讨论抑制癌细胞代谢变化的最佳策略,特别是华堡效应.
- 识别特定的蛋白质,酶和途径作为潜在的抗癌标.
- 强调在癌症治疗中需要个性化和神经治疗方法.
主要方法:
- 审查有关癌症代谢重编程的当前知识.
- 确定和讨论关键蛋白质,酶和参与华堡效应的途径.
- 使用可用数据库对癌症患者基因表达异质性的分析.
主要成果:
- 鉴定了华堡效应抑制的关键标:HK2,PKM2,PFKFB3,PFKFB4,NAD+代谢,NADH氧化,MCT4,MCT1,LDHA和LDHB.
- 突出了瘤中代谢基因表达的异质性.
- 强调了向新陈代谢率可能对正常细胞的毒性较小.
结论:
- 针对华堡效应需要个性化策略,以确保特异性并最大限度地减少副作用.
- 综合诊断和治疗的治疗方法对于个性化癌症治疗至关重要.
- 了解新陈代谢重编程异质性是开发有效的,针对患者的治疗方法的关键.
相关概念视频
Targeted Cancer Therapies
7.8K
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...
7.8K
Combination Therapies and Personalized Medicine
5.1K
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...
5.1K
Adaptive Mechanisms in Cancer Cells
5.9K
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,...
5.9K
Cancer Therapies
7.9K
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...
7.9K
Treatment Resistant Cancers
3.4K
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...
3.4K
Inhibition of Cdk Activity
4.9K
The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
4.9K


