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Related Concept Videos

The Ras Gene02:38

The Ras Gene

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.
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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 daughter...
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Related Experiment Video

Updated: Jun 9, 2026

Characterize Disease-related Mutants of RAF Family Kinases by Using a Set of Practical and Feasible Methods
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Interfering with RAS-effector protein interactions prevent RAS-dependent tumour initiation and causes stop-start

T Tanaka1, T H Rabbitts

  • 1Leeds Institute of Molecular Medicine, Section of Experimental Therapeutics, St James's University Hospital, University of Leeds, Leeds, UK.

Oncogene
|September 7, 2010
PubMed
Summary

Targeting RAS-effector interactions with novel antibody fragments can control cancer growth. This approach offers chemo-preventive effects, suggesting combination therapies are needed for curative outcomes in RAS-dependent cancers.

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Area of Science:

  • Oncology
  • Molecular Biology
  • Drug Discovery

Background:

  • RAS mutations are common in cancer, driving uncontrolled cell growth.
  • Targeting RAS-effector protein-protein interactions presents a novel therapeutic strategy for 'undruggable' targets.

Purpose of the Study:

  • To investigate the efficacy of targeting RAS-effector interactions in preclinical models of RAS-dependent cancers.
  • To evaluate the potential of antibody fragments to block activated RAS and its downstream effectors.

Main Methods:

  • Utilized a transgenic mouse model of lung cancer.
  • Employed an antibody fragment designed to bind activated RAS and inhibit RAS-effector interactions (e.g., with phosphoinositide 3-kinase and RAF).
  • Assessed the impact on tumor initiation, growth control, and cell death in human cancer cells.

Main Results:

  • RAS-effector interactions were demonstrated to be essential for tumor initiation.
  • Interference with oncogenic RAS-effector interactions led to the control of tumor growth in human cancer cells.
  • Tumor regression was not consistently observed, indicating a need for combination strategies.

Conclusions:

  • Ablating RAS-dependent signaling can confer chemo-preventive effects, leading to a chronic cancer state.
  • Mutant RAS-targeted therapies may require combination with other agents or strategies for curative potential.
  • The findings challenge the universal applicability of the oncogene addiction model, suggesting cancer cell death is not always inevitable upon oncogenic protein function loss.