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Related Concept Videos

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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Tumor Progression02:07

Tumor Progression

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Tumor progression is a phenomenon where the pre-formed tumor acquires successive mutations to become clinically more aggressive and malignant. In the 1950s, Foulds first described the stepwise progression of cancer cells through successive stages.
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Pleiotropy01:33

Pleiotropy

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Pleiotropy is the phenomenon in which a single gene impacts multiple, seemingly unrelated phenotypic traits. For example, defects in the SOX10 gene cause Waardenburg Syndrome Type 4, or WS4, which can cause defects in pigmentation, hearing impairments, and an absence of intestinal contractions necessary for elimination. This diversity of phenotypes results from the expression pattern of SOX10 in early embryonic and fetal development. SOX10 is found in neural crest cells that form melanocytes,...
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Canonical Wnt Signaling Pathway02:54

Canonical Wnt Signaling Pathway

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The gene encoding the main signaling molecules of the Wnt signaling pathways (the Wnt proteins) was discovered almost four decades ago by Nüsslein-Volhard and Wieschaus. They identified and originally named the gene "wingless" (wg) after a phenotype discovered during their landmark genetic screen in Drosophila for body pattern defects. At around the same time, another researcher named Harold Varmus found that a murine tumor virus activates the mammalian wg homolog, Int-1, which...
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Loss of Tumor Suppressor Gene Functions01:12

Loss of Tumor Suppressor Gene Functions

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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.
When the tumor suppressor genes develop mutations or are lost, cells start growing out of control, leading to cancer. However, a single functional copy of the tumor suppressor gene is enough for the cells to maintain their normal functions and cell...
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The Ras Gene02:38

The Ras Gene

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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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  11. The Selenoprotein P-lrp5/6-wnt3a Complex Promotes Tumorigenesis In Sporadic Colorectal Cancer.

The selenoprotein P-LRP5/6-WNT3A complex promotes tumorigenesis in sporadic colorectal cancer.

K Sandeep Prabhu

    The Journal of Clinical Investigation
    |July 3, 2023

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    A Multiplexed Luciferase-based Screening Platform for Interrogating Cancer-associated Signal Transduction in Cultured Cells
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    In vitro Organoid Culture of Primary Mouse Colon Tumors
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    In vitro Organoid Culture of Primary Mouse Colon Tumors

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    View abstract on PubMed

    Summary
    This summary is machine-generated.

    Selenoprotein P (SELENOP) surprisingly promotes colorectal cancer progression by modulating WNT signaling. This finding challenges selenium

    Area of Science:

    • Oncology
    • Molecular Biology
    • Gastroenterology

    Background:

    • Selenium's role in cancer prevention is debated.
    • Selenoprotein P (SELENOP), a selenium-containing protein, is expressed in the gut.
    • Its specific role in colorectal cancer (CRC) is unclear.

    Purpose of the Study:

    • To investigate the role of SELENOP in sporadic colorectal carcinogenesis.
    • To elucidate the molecular mechanisms by which SELENOP influences CRC progression.

    Main Methods:

    • Analysis of SELENOP expression in colorectal tissues.
    • In vivo and in vitro studies to assess SELENOP's functional impact.
    • Investigation of SELENOP's interaction with WNT signaling pathways.

    Main Results:

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    Development and Maintenance of a Preclinical Patient Derived Tumor Xenograft Model for the Investigation of Novel Anti-Cancer Therapies
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    In vitro Organoid Culture of Primary Mouse Colon Tumors
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    In vitro Organoid Culture of Primary Mouse Colon Tumors

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    • Increased SELENOP expression was found to promote the transition of adenomas to carcinomas.
    • SELENOP was identified as a modulator of canonical WNT signaling.
    • SELENOP interacts with WNT3A and LRP5/6, potentially amplifying WNT activity along the gut crypt axis.

    Conclusions:

    • SELENOP plays a pro-tumorigenic role in colorectal cancer, contrary to some selenium-related protective effects.
    • The interaction of SELENOP with the WNT pathway represents a novel mechanism in colorectal tumorigenesis.
    • Targeting SELENOP and its WNT signaling interactions may offer new therapeutic strategies for CRC.