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相关概念视频

Targeted Cancer Therapies02:57

Targeted Cancer Therapies

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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...
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Combination Therapies and Personalized Medicine02:50

Combination Therapies and Personalized Medicine

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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...
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The Ras Gene02:38

The Ras Gene

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The Ras-gene-encoded proteins are regulators of signaling pathways controlling cell proliferation, differentiation, or cell survival. The Ras-gene family in humans constitutes three primary members—the HRas, NRas, and KRas. These genes code for four functionally distinct yet closely related proteins—the HRas, NRas, KRas4A, and KRas4B. The involvement of mutant Ras genes in human cancer was first discovered in 1982 and is among the most common causes of human tumorigenesis.
Ras is a...
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Treatment Resistant Cancers02:56

Treatment Resistant Cancers

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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...
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The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
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相关实验视频

Updated: Mar 15, 2026

Utilizing 18F-FDG PET/CT Imaging and Quantitative Histology to Measure Dynamic Changes in the Glucose Metabolism in Mouse Models of Lung Cancer
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对KRAS突变癌症进行系统和精确的干预.

JingHui Liang1, JunXi Wu1, Yuan Zhang1

  • 1State Key Laboratory of Drug Regulatory Sciences, National Institutes for Food and Drug Control, Beijing, 102629, China.

Experimental hematology & oncology
|March 14, 2026
PubMed
概括
此摘要是机器生成的。

针对癌症的关键驱动因素KRAS突变,正在推进新的异位基因特异性药物和组合疗法. 研究重点是克服抗性以持久控制KRAS突变瘤.

关键词:
有KRAS突变的癌症.针对KRAS的向疗法新的KRAS治疗方法治疗耐药性是一种治疗性耐药性.

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科学领域:

  • 在瘤学瘤学.
  • 分子生物学分子生物学
  • 药物发现 药物发现 药物发现

背景情况:

  • KRAS突变是人类癌症中普遍存在的致癌驱动因素,启动和进展固体瘤.
  • 联KRASG12C抑制剂的开发刺激了对基因基因定向疗法和KRAS信号通路调节的兴趣.

研究的目的:

  • 审查了解KRAS结构,构造和异质性的最新进展.
  • 总结针对KRAS突变的直接和间接治疗策略.
  • 分析耐药性机制,并概述长期治疗癌症的对策.

主要方法:

  • 关于KRAS结构,信号通路和治疗干预的文献综述.
  • 对KRAS突变 (G12C,G12D,G12V) 的等位基因特异性和形状选择性抑制剂的分析.
  • 评估间接向策略,包括SHP2/SOS1抑制,MEK阻断,代谢向和免疫疗法组合.

主要成果:

  • 开发针对KRAS G12C,G12D和G12V突变的等位基因特异性药物的进展.
  • 识别对形状选择性宽谱抑制剂的鉴定.
  • 分析耐药机制和潜在的对策,如下一代抑制剂和ctDNA监测.

结论:

  • 克拉斯治疗领域正在向符合形状的,多模式的精密疗法发展.
  • 纵向疾病管理策略对于持久控制KRAS突变瘤至关重要.
  • 进步为治疗由KRAS突变驱动的各种固体瘤提供了新的途径.