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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...
Mouse Models of Cancer Study02:43

Mouse Models of Cancer Study

Mice have long served as models for studying human biology and pathology because of their phylogenetic and physiological similarity with humans. They are also easy to maintain and breed in the laboratory, and hence, many inbred strains are now available for research. Studies on mice have contributed immeasurably to our understanding of cancer biology.
The development of transgenic, knockout, and knock-in mice has led to an exponential increase in their use as model organisms in research,...
Mouse Models of Cancer Study02:43

Mouse Models of Cancer Study

Mice have long served as models for studying human biology and pathology because of their phylogenetic and physiological similarity with humans. They are also easy to maintain and breed in the laboratory, and hence, many inbred strains are now available for research. Studies on mice have contributed immeasurably to our understanding of cancer biology.
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Adaptive Mechanisms in Cancer Cells02:53

Adaptive Mechanisms in Cancer Cells

Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
Adaptive Mechanisms in Cancer Cells02:53

Adaptive Mechanisms in Cancer Cells

Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
Cancer Survival Analysis01:21

Cancer Survival Analysis

Cancer survival analysis focuses on quantifying and interpreting the time from a key starting point, such as diagnosis or the initiation of treatment, to a specific endpoint, such as remission or death. This analysis provides critical insights into treatment effectiveness and factors that influence patient outcomes, helping to shape clinical decisions and guide prognostic evaluations. A cornerstone of oncology research, survival analysis tackles the challenges of skewed, non-normally...

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Related Experiment Video

Updated: Jul 18, 2026

Generation of Genomic Deletions in Mammalian Cell Lines via CRISPR/Cas9
09:40

Generation of Genomic Deletions in Mammalian Cell Lines via CRISPR/Cas9

Published on: January 3, 2015

Modeling non-random deletions in cancer.

Maria Kost-Alimova1, Stefan Imreh

  • 1Karolinska Institutet, Microbiology Tumor and Cell Biology Center (MTC), Box 280, 171 77 Stockholm, Sweden.

Seminars in Cancer Biology
|December 19, 2006
PubMed
Summary

Chromosome deletions in cancer often lead to growth advantages. Researchers used an elimination test (Et) to identify critical tumor suppressor genes on chromosome 3, pinpointing three key deletion regions.

Area of Science:

  • Oncology
  • Genetics
  • Cancer Biology

Background:

  • Chromosome deletions are common in cancer and non-randomly located.
  • Segmental losses are believed to confer a selective growth advantage to cancer cells.
  • These deletions may harbor genes that regulate normal growth and suppress malignancy.

Purpose of the Study:

  • To develop an experimental model, the elimination test (Et), for generating and analyzing chromosome deletions.
  • To functionally analyze deletions on human chromosome 3, focusing on the 3p region known for tumor suppressor activity.
  • To narrow down the 3p tumor suppressor region and identify candidate genes crucial for inhibiting cancer growth.

Main Methods:

  • Development of a monochromosomal hybrid-based experimental model called the "elimination test" (Et).

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  • Application of the Et to human chromosome 3 to analyze 3p deletions.
  • Identification and characterization of frequently deleted regions (CER1, CER2, FER) and a retained region (CRR).

    • Main Results:

    • Three critical deletion regions (CER1, CER2, FER) on chromosome 3p were identified in tumors.
    • A 3q26-qter region (CRR) was consistently retained across tumors.
    • CER1 contains potential tumor suppressor genes, with RIS1, LF (LTF), and LIMD1 showing strong evidence of tumor suppressor activity.
    • Breakpoint regions exhibit instability features like evolutionary breaks, horizontal evolution, and pseudogene insertions, driven by segmental duplications.

    Conclusions:

    • The elimination test (Et) is effective for identifying tumor suppressor regions and candidate genes.
    • Specific regions on chromosome 3p (CER1, CER2, FER) are critical in cancer development.
    • Tumor suppressor region borders are unstable and prone to alterations, contributing to cancer-associated genomic instability.