Related Experiment Video

Updated: Aug 14, 2026

Focus Formation: A Cell-based Assay to Determine the Oncogenic Potential of a Gene
08:18

Focus Formation: A Cell-based Assay to Determine the Oncogenic Potential of a Gene

Published on: December 31, 2014

[Expression of transformation characters in colchicine-resistant tumor cells]

E S Kakpakova

    Biulleten' Eksperimental'Noi Biologii I Meditsiny
    |July 1, 1983
    PubMed

    Insights

    Djungarian hamster tumor cell lines resistant to colchicine showed varying malignancy. High colchicine resistance significantly reduced tumorigenicity, but anchorage independence remained unaffected in resistant cell lines.

    Area of Science:

    • Cell Biology
    • Cancer Research
    • Drug Resistance

    Context:

    • Investigating the biological consequences of drug resistance in cancer cells.
    • Utilizing Djungarian hamster tumor cell lines as a model system.

    Purpose:

    • To determine the impact of colchicine resistance on malignancy and anchorage independence.
    • To compare the tumorigenicity and cloning efficiency of colchicine-resistant cells with wild-type cells.

    Summary:

    • Tumorigenicity (TD50) was significantly reduced in highly colchicine-resistant (200-800-fold) Djungarian hamster tumor cell lines compared to wild-type.
    • Low colchicine resistance (15-20-fold) did not alter tumorigenicity.
    • Colchicine resistance did not affect anchorage independence, as evidenced by similar cloning efficiency in semi-solid medium.

    Impact:

    • Highlights a complex relationship between drug resistance and cancer progression.
    • Suggests that while resistance may reduce tumor formation, other factors like anchorage independence are preserved.
    • Provides insights into the phenotypic changes associated with multidrug resistance in cancer models.

    More Related Videos

    Establishing Cell Lines Overexpressing DR3 to Assess the Apoptotic Response to Anti-mitotic Therapeutics12:28

    Establishing Cell Lines Overexpressing DR3 to Assess the Apoptotic Response to Anti-mitotic Therapeutics

    Published on: January 11, 2019

    Testing Targeted Therapies in Cancer using Structural DNA Alteration Analysis and Patient-Derived Xenografts10:27

    Testing Targeted Therapies in Cancer using Structural DNA Alteration Analysis and Patient-Derived Xenografts

    Published on: July 25, 2020

    Related Concept Videos

    Abnormal Proliferation02:23

    Abnormal Proliferation

    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 daughter...
    Cancer-Critical Genes I: Proto-oncogenes01:33

    Cancer-Critical Genes I: Proto-oncogenes

    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...
    Treatment Resistant Cancers02:56

    Treatment Resistant Cancers

    Cancer is the second leading cause of death in the United States. A cancer cell is genetically unstable and hence can mutate faster. They can also modify their microenvironment and escape immune surveillance. The difficulties in treating cancer are further compounded by the emergence of rapid resistance to anticancer drugs. The most common ways to attain resistance in cancer cells include alteration in drug transport and metabolism, modification of drug target, elevated DNA damage response, or...
    Cancer-Critical Genes II: Tumor Suppressor Genes01:05

    Cancer-Critical Genes II: Tumor Suppressor Genes

    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...
    Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase01:11

    Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase

    Genetic polymorphisms in drug targets have emerged as critical determinants of interindividual variability in drug response and toxicity. Pharmacogenomic investigations increasingly focus on identifying these variations to personalize and optimize therapeutic interventions. A drug target may be a receptor, enzyme, or signaling protein involved in pharmacologic responses or disease-related pathways. While early pharmacogenetic studies focused primarily on drug metabolism, current research...