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Related Concept Videos

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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Rous Sarcoma Virus (RSV) and Cancer01:03

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Rous Sarcoma virus or RSV was discovered by F. Peyton Rous in the year 1911 as a filterable transmissible agent that could cause tumors in chickens. He won a Nobel Prize for this discovery in 1966. His experiments clearly demonstrated that some cancers could be caused by infectious agents and led to the discovery of many more cancer-causing viruses in animals as well as humans.
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Cancer-Critical Genes I: Proto-oncogenes01:33

Cancer-Critical Genes I: Proto-oncogenes

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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...
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Small GTPases - Ras and Rho01:24

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Ras and Rho are small monomeric GTPases that act downstream of receptor tyrosine kinase (RTK) and regulate various cellular processes. These GTPases switch between active and inactive states by binding to guanine nucleotides.
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MAPK Signaling Cascades01:07

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Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...
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Abnormal Proliferation02:23

Abnormal Proliferation

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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...
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Updated: Sep 16, 2025

Characterize Disease-related Mutants of RAF Family Kinases by Using a Set of Practical and Feasible Methods
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Genetic and oncogenic features of RASGRF fusions.

Sreya Das1,2,3, Daniel S Lenchner1,2,3, Ellen Jaeger4

  • 1Department of Internal Medicine, Section of Medical Oncology, Yale School of Medicine, New Haven, CT, USA.

NPJ Precision Oncology
|July 4, 2025
PubMed
Summary

RASGRF fusions are newly identified oncogenic drivers in cancers like lung and pancreatic cancer. These fusions activate the RAS pathway and may be targeted by MAPK inhibitors.

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Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Targeted therapies are revolutionizing cancer treatment by focusing on specific oncogenic drivers.
  • RASGRF1 and RASGRF2 are guanine exchange factors (GEFs) that activate RAS signaling, but their role in cancer is not fully understood.

Purpose of the Study:

  • To investigate the prevalence, genetic diversity, and oncogenic mechanisms of RASGRF1 and RASGRF2 fusions in human malignancies.
  • To explore the therapeutic potential of targeting RASGRF fusions.

Main Methods:

  • Analysis of RNA-sequencing data from a large, real-world database of diverse human tumors.
  • Functional assays to assess the transforming activity and oncogenic mechanisms of identified RASGRF fusions.

Main Results:

  • Identified 40 tumors with RASGRF1/2 rearrangements, with half occurring in non-small cell lung carcinoma (NSCLC), pancreatic cancer, and melanoma.
  • RASGRF fusions were enriched in tumors lacking other known driver alterations.
  • Transmembrane partners and loss of N-terminal domains (PH1 and DH) in RASGRF fusions enhanced RAS activation and transforming activity.
  • Loss of the PH1 domain alone was insufficient for cellular transformation.

Conclusions:

  • RASGRF fusions represent a novel class of oncogenic drivers with diverse tissue distribution and structural variations.
  • These fusions activate oncogenic signaling pathways, particularly through enhanced RAS activation.
  • RASGRF fusions are potential therapeutic targets, as cancer models exhibit sensitivity to MAPK pathway inhibition.