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Related Concept Videos

The Ras Gene02:38

The Ras Gene

5.7K
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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Small GTPases - Ras and Rho01:24

Small GTPases - Ras and Rho

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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.
Three regulatory proteins control their activity:
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Cancers Originate from Somatic Mutations in a Single Cell02:21

Cancers Originate from Somatic Mutations in a Single Cell

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Cancer arises from mutations in the critical genes that allow healthy cells to escape cell cycle regulation and acquire the ability to proliferate indefinitely. Though originating from a single mutation event in one of the originator cells, cancer progresses when the mutant cell lines continue to gain more and more mutations, and finally, become malignant. For example, chronic myelogenous leukemia (CML) develops initially as a non-lethal increase in white blood cells, which progressively...
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The Ras Gene02:38

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Mismatch Repair01:20

Mismatch Repair

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Organisms are capable of detecting and fixing nucleotide mismatches that occur during DNA replication. This sophisticated process requires identifying the new strand and replacing the erroneous bases with correct nucleotides. Mismatch repair is coordinated by many proteins in both prokaryotes and eukaryotes.
The Mutator Protein Family Plays a Key Role in DNA Mismatch Repair
The human genome has more than 3 billion base pairs of DNA per cell. Prior to cell division, that vast amount of genetic...
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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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Related Experiment Video

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Single Droplet Digital Polymerase Chain Reaction for Comprehensive and Simultaneous Detection of Mutations in Hotspot Regions
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Single Droplet Digital Polymerase Chain Reaction for Comprehensive and Simultaneous Detection of Mutations in Hotspot Regions

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KRAS mutations: analytical considerations.

Marta Herreros-Villanueva1, Chih-Chieh Chen2, Shyng-Shiou F Yuan3

  • 1Department of Gastroenterology, Hospital Donostia/Instituto Biodonostia, Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Universidad del País Vasco UPV/EHU, San Sebastián, Spain.

Clinica Chimica Acta; International Journal of Clinical Chemistry
|February 19, 2014
PubMed
Summary
This summary is machine-generated.

KRAS mutation testing is crucial for colorectal cancer (CRC) patients treated with anti-EGFR therapy. Identifying these mutations ensures patients receive effective treatments and avoid ineffective therapies like Cetuximab and Panitumumab.

Keywords:
Colorectal cancerKRAS geneMethod and mutation analysisMutation

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Area of Science:

  • Oncology
  • Molecular Diagnostics
  • Cancer Genetics

Background:

  • Colorectal cancer (CRC) is a leading cause of cancer death globally.
  • EGFR inhibitors like Cetuximab and Panitumumab improve survival in metastatic CRC (mCRC).
  • KRAS mutations (codons 12 and 13) are key biomarkers predicting response to anti-EGFR therapy.

Purpose of the Study:

  • To review current KRAS mutation testing techniques for mCRC.
  • To evaluate the effectiveness and limitations of various KRAS testing methods.
  • To highlight the clinical importance of KRAS mutation status in guiding anti-EGFR therapy.

Main Methods:

  • Literature review of recent KRAS mutation testing techniques.
  • Analysis of reliability and feasibility of diagnostic methods.
  • Summary of clinical effectiveness and limitations of KRAS testing.

Main Results:

  • KRAS mutations occur in 35-45% of CRC patients.
  • KRAS mutations predict non-response to Cetuximab and Panitumumab.
  • Various KRAS testing techniques have emerged with distinct advantages and disadvantages.

Conclusions:

  • KRAS mutation testing is essential for all advanced CRC patients.
  • Accurate KRAS testing guides personalized treatment strategies with anti-EGFR inhibitors.
  • Ongoing advancements in testing methods aim to improve diagnostic reliability and clinical utility.