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  • HPV Dr. Dr. Prasetyadi Mawardi, Sp. KK (K)

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    This document discusses the role of high-risk HPV in cervical carcinogenesis. It shows how the viral oncoproteins E6 and E7 disrupt key tumor suppressor pathways like p53 and Rb, leading to aberrant cell proliferation, immortalization, and genomic instability. This enables the virus to overcome cellular checkpoints like senescence and apoptosis, allowing malignant progression through additional mutations in host cell DNA.

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    HPV Dr. Dr. Prasetyadi Mawardi, Sp. KK(K) (1)

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    This document discusses the role of high-risk HPV in cervical carcinogenesis. It shows how the viral oncoproteins E6 and E7 disrupt key tumor suppressor pathways like p53 and Rb, leading to aberrant cell proliferation, immortalization, and genomic instability. This enables the virus to overcome cellular checkpoints like senescence and apoptosis, allowing malignant progression through additional mutations in host cell DNA.

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    3 views6 pages

    HPV Dr. Dr. Prasetyadi Mawardi, Sp. KK (K)

    Uploaded by

    sesia
    This document discusses the role of high-risk HPV in cervical carcinogenesis. It shows how the viral oncoproteins E6 and E7 disrupt key tumor suppressor pathways like p53 and Rb, leading to aberrant cell proliferation, immortalization, and genomic instability. This enables the virus to overcome cellular checkpoints like senescence and apoptosis, allowing malignant progression through additional mutations in host cell DNA.

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    © All Rights Reserved
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    of 6

    HIGH RISK HPV IN THE DEVELOPMENT OF HPV ASSOCIATED CARCINOGENESIS

    Extended Telomere Replicative


    E6-AP proliferation Erosion senescence
    E6

    Cellular
    DNA damage hTERT immortalization

    E7 Aberrant Tropic sentinel


    proliferation response

    P53

    DNA damage Abnomal Telomere


    proliferation erosion Hypoxia/ Loss of Chemoresistance
    angiogenesis support/
    survival factors

    Increased Overcome Decreased Invasion/


    sensitivity to Reduced Decreased
    senescence death metastasis
    mutagens/ apoptosis death in
    Increased response to
    carcinogens following
    tumour size chemotherape
    deregulation of
    the cell cycle utics

    Loss of p53
    HPV LIFE CYCLE
    EPITHELIAL CELL RESPONSES TO HPV INFECTION
    VIRUS HPV

    HPV 11 HPV 16 HPV 18


    HPV 6
    ONKOGENESIS PADA HPV

    ONKOGENESIS PADA HPV

    Malignant Benign
    Lession Lession
    Malignant
    Lession Virus Particles Parakeratosis
    Rb
    inactivation
    Other
    Other
    mutations
    mutations p53 L1, L2
    degradation Koilocytosis

    E6
    overexpressio Replication
    Proliferation
    E7
    overexpressio
    Co-factors E1, E2
    Imunosupresion E6, E7
    Smoking
    E2 disruption
    Other infectious
    agents Basal Cell
    Oncogene
    activation integration

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