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Related Concept Videos

Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

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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...
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Cancer Stem Cells and Tumor Maintenance02:40

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Early diagnosis and treatment can often cure cancer. However, even with treatment, residual cells called cancer stem cells (CSC) might remain, often causing tumor recurrence. These cancer stem cells possess the potential for self-renewal and multi-lineage differentiation and are often responsible for the therapeutic resistance displayed in most cancers.
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Targeted Cancer Therapies02:57

Targeted Cancer Therapies

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The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
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Loss of Tumor Suppressor Gene Functions01:12

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Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
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Related Experiment Video

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Methods for Evaluating the Role of c-Fos and Dusp1 in Oncogene Dependence
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WITHDRAWN: A Druggable Tumor Suppressor and Leukemic Stem Cell Marker.

Yi Pan, Xiaduo Meng, Chen Wang

    Biorxiv : the Preprint Server for Biology
    |January 7, 2026
    PubMed
    Summary

    Chemotherapy-resistant acute myeloid leukemia (AML) relapses due to leukemic stem cells (LSCs) lacking AT2R. Targeting AT2R with buloxibutid (C21) inhibits AML progression and enhances chemotherapy, offering hope for relapsed AML patients.

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    Area of Science:

    • Hematology
    • Oncology
    • Molecular Biology
    • Drug Discovery

    Background:

    • Acute myeloid leukemia (AML) frequently relapses due to chemotherapy-resistant leukemic stem cells (LSCs).
    • Relapsed AML has a poor prognosis and is unresponsive to current therapies.
    • Identifying novel therapeutic targets for AML is crucial.

    Purpose of the Study:

    • To nominate druggable therapeutic targets for AML using a large-language model (LLM) agent.
    • To investigate the role of Angiotensin II Receptor Type 2 (AGTR2/AT2R) in AML pathogenesis and LSC function.
    • To evaluate the therapeutic potential of an AT2R agonist in AML models.

    Main Methods:

    • Developed an LLM agent integrating multi-modal data to identify therapeutic targets.
    • Functional studies on 68 primary human AML samples and 21 patient-derived xenograft (PDX) models.
    • Analysis of AT2R expression, chromatin rearrangements, and epigenetic silencing of AGTR2.
    • Murine AML models with Agtr2 knockdown or enforced expression.
    • Treatment of AML PDX models with buloxibutid (C21), an AT2R agonist.

    Main Results:

    • Higher AGTR2 (AT2R) expression correlated with better chemotherapy response and survival in AML.
    • Leukemic stem cells (LSCs) consistently lacked AT2R expression and were enriched after chemotherapy.
    • Epigenetic silencing, not mutation, was identified as the mechanism for AT2R downregulation in AML.
    • Enforced AT2R expression in murine models delayed AML progression, reduced LSC frequency, and suppressed stemness.
    • Buloxibutid (C21) significantly inhibited AML progression and enhanced chemotherapy efficacy, especially in relapsed AML.

    Conclusions:

    • AT2R absence is a marker for LSCs, and AT2R functions as a tumor suppressor in AML.
    • Epigenetic silencing of AGTR2 contributes to AT2R downregulation and AML relapse.
    • Targeting AT2R with agonists like buloxibutid (C21) represents a promising therapeutic strategy for AML, particularly relapsed cases.