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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.
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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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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.
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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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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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Ras protein abundance correlates with Ras isoform mutation patterns in cancer.

Fiona E Hood1, Yasmina M Sahraoui1, Rosalind E Jenkins2

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Summary
This summary is machine-generated.

Higher KRAS protein levels, not rare codons, may explain its frequent mutation in cancer. This Ras dosage sweet-spot model impacts cancer and development.

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Area of Science:

  • Molecular Biology
  • Oncology
  • Genetics

Background:

  • Activating Ras gene mutations are common in cancer.
  • KRAS is mutated more frequently than HRAS and NRAS in cancer and RASopathies, but the reasons are unclear.
  • The protein products of Ras genes are nearly identical.

Purpose of the Study:

  • To quantify HRAS, NRAS, KRAS4A, and KRAS4B protein abundance in cell lines and tissues.
  • To investigate the correlation between Ras isoform protein expression and mutation frequencies in cancer.
  • To explore the role of Ras dosage in cancer development and isoform-specific contributions.

Main Methods:

  • Quantitative analysis of HRAS, NRAS, KRAS4A, and KRAS4B protein levels.
  • Comparison of protein abundance across diverse cell lines and healthy tissues.
  • Correlation analysis with known Ras mutation frequencies in various cancers.

Main Results:

  • Consistent KRAS > NRAS > HRAS protein expression patterns were observed.
  • These expression patterns correlate with the rank order of Ras mutation frequencies in cancer.
  • Mutant vs. wild-type KRAS protein abundance showed frequent imbalance, suggesting non-gene duplication mechanisms.

Conclusions:

  • Ras protein dosage, particularly high KRAS levels, may define a 'sweet-spot' influencing cancer and development.
  • High abundance of KRAS, rather than rare codons, likely underlies its predominant mutation in cancer.
  • Isoform-specific Ras dosage contributes to oncogenesis, with HRAS and NRAS typically insufficient for transformation when mutated.