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The Ras Gene02:38

The Ras Gene

6.4K
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...
6.4K
Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

7.9K
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...
7.9K
Targeted Cancer Therapies02:57

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...
7.8K
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

3.9K
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...
3.9K
Loss of Tumor Suppressor Gene Functions01:12

Loss of Tumor Suppressor Gene Functions

5.1K
Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
When the tumor suppressor genes develop mutations or are lost, cells start growing out of control, leading to cancer. However, a single functional copy of the tumor suppressor gene is enough for the cells to maintain their normal functions and cell...
5.1K
Abnormal Proliferation02:23

Abnormal Proliferation

4.6K
Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
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相关实验视频

Updated: Sep 9, 2025

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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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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一种基因无关突变KRAS抑制剂抑制瘤维护信号并重新编程瘤免疫力

Kathleen M McAndrews1, Francesca Paradiso1, Clint A Stalnecker2,3

  • 1University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.

Science translational medicine
|September 3, 2025
PubMed
概括
此摘要是机器生成的。

一种新的突变KRAS抑制剂 (panKRASi) 在临床前模型中有效抑制胰腺癌的生长. 它还增强了抗瘤免疫力,但通过YAP信号和免疫检查点升级出现了抵抗力.

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相关实验视频

Last Updated: Sep 9, 2025

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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科学领域:

  • 癌症学
  • 分子生物学
  • 免疫学

背景情况:

  • KRAS突变在癌症中很常见,
  • 小分子抑制剂提供了一种直接向突变KRAS的新方法.
  • 胰腺管腺癌 (PDAC) 是一种经常出现KRAS突变的癌症.

研究的目的:

  • 评估BI-2493的临床前疗效,这是一种全RAS抑制剂 (panKRASi),用于胰腺管腺癌 (PDAC).
  • 为了研究基底的分子机制 panKRASi 疗效和耐药性.
  • 探索结合策略以克服耐药性并提高治疗效果.

主要方法:

  • 在各种PDAC模型中进行临床前评估 (细胞系,PDX,同基因或基因工程小鼠模型).
  • 转录基因,蛋白质基因和蛋白质基因分析以评估途径抑制和免疫变化.
  • 对瘤微环境 (TME) 和免疫细胞透的分析.
  • 研究抗性机制,包括YAP信号和免疫检查点.

主要成果:

  • 在各种临床前模型中,BI-2493显示出显著的瘤生长抑制和延长存活时间.
  • 证实了RAS通路的抑制,与此相关的LKB1/ AMPK目标的上调.
  • panKRASi治疗增加了内CD8+T细胞,并重塑了TME,使其对免疫检查点阻塞敏感.
  • 对panKRASi单一治疗的耐药性与增强的YAP信号和免疫检查点表达有关.

结论:

  • 通过抑制RAS通路和调节免疫反应,BI-2493显示出对PDAC的前临床疗效.
  • 了解抗药机制,如YAP激活和免疫逃避,对于持续治疗至关重要.
  • 为了在PDAC中获得持久的反应,可能需要使用包括panKRASi在内的组合策略.