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Related Concept Videos

Cancers Originate from Somatic Mutations in a Single Cell02:21

Cancers Originate from Somatic Mutations in a Single Cell

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...
Cancers Originate from Somatic Mutations in a Single Cell02:21

Cancers Originate from Somatic Mutations in a Single Cell

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...
Mismatch Repair01:20

Mismatch Repair

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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Related Experiment Video

Updated: Jul 12, 2026

Simple and Rapid Method to Obtain High-quality Tumor DNA from Clinical-pathological Specimens Using Touch Imprint Cytology
11:20

Simple and Rapid Method to Obtain High-quality Tumor DNA from Clinical-pathological Specimens Using Touch Imprint Cytology

Published on: March 21, 2018

Somatic Mutation Profiles in Colorectal Cancers Differ by Population.

Batsirai M Mabvakure, Patharapa Promprasert, Lucia Martinez Cruz

    Medrxiv : the Preprint Server for Health Sciences
    |July 10, 2026
    PubMed
    Summary
    This summary is machine-generated.

    Colorectal cancer (CRC) tumor profiles vary by geographic origin and age. African Americans and White individuals share similar early-onset CRC tumor characteristics, influenced by age and environmental factors.

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    Published on: July 28, 2010

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    Published on: March 21, 2018

    Deficient Pms2, ERCC1, Ku86, CcOI in Field Defects During Progression to Colon Cancer
    28:15

    Deficient Pms2, ERCC1, Ku86, CcOI in Field Defects During Progression to Colon Cancer

    Published on: July 28, 2010

    Area of Science:

    • Genomics and Cancer Research
    • Population Genetics
    • Tumor Biology

    Background:

    • Colorectal cancer (CRC) incidence and mortality show population-specific variations.
    • Genetic differences are suspected to influence CRC biology, but studies in diverse populations are scarce.
    • Understanding CRC variants across different ethnic groups is crucial for personalized medicine.

    Purpose of the Study:

    • To investigate somatic tumor mutation profiles in colorectal cancer (CRC) across genetically diverse populations.
    • To explore correlations between population group (African Americans, Ghanaians, Ethiopians, Non-Hispanic Whites) and CRC-specific tumor variants.
    • To identify population-specific variants enriched in underrepresented groups.

    Main Methods:

    • Somatic DNA sequencing of 150 CRC tumors (43 African Americans, 53 Non-Hispanic Whites, 21 Ghanaians, 33 Ethiopians) using Illumina NovaSeq platform targeting 290 genes.
    • Comparative analysis of mutations between African cohorts (African Americans, Ghanaians, Ethiopians) and Non-Hispanic Whites.
    • Identification of enriched variants in historically underrepresented populations.

    Main Results:

    • CRC tumors in US cohorts were diagnosed at significantly younger ages compared to African cohorts.
    • Significant differences observed in primary tumor location, mismatch repair (MMR) phenotypes, KRAS mutations, and tumor mutational burden distribution by population.
    • While BRAF V600E mutations were rare, non-V600E BRAF mutation rates were higher in African American and Non-Hispanic White samples. APC, CTNNB1, RNF43, PIK3CA, and TP53 mutation rates also showed population-specific differences.

    Conclusions:

    • Geographic origin and age of onset are key determinants of the CRC mutational landscape.
    • The similar tumor profiles between African Americans and Non-Hispanic Whites likely stem from their shared early-onset CRC cases.
    • Age and geography-associated factors, potentially including environmental exposures, significantly influence CRC tumor phenotypes.