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Cervical Cancer: Pathogenesis

by Carlo Raj, MD
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    Pathogenesis of cervical cancer. I'll quickly walk you through the algorithm that's important for you. You’ve seen this before in some way, shape, or form. I like the organization pattern that is being established here for you. Sexual activity. The more that you have a partner that is promiscuous, I mean, in this case, a female, then she increases her risk for HPV exposure. In basic pathology, we talked about neoplasia. In neoplasia, we talked about HPV high-risk strain containing particular oncogenes. And those included E6 and E7. E6 knocked out p53; E7 knocked out Rb. If you knock out the tumor suppressor gene, you are now going to choose a cell in the transformation zone of either becoming an adenocarcinoma or a squamous. Your focus will be on the left branch of this algorithm. Eighty five percent of time, you are going to then start the development of invasive squamous cancer. Squamous differentiation. What does that mean? Now, the squamous cells are undergoing differentiation but not for the good though. They’re going to proliferate, proliferate, proliferate. What’s disorganized or disordered proliferation called to you medically? Good. Dysplasia. So now, you begin the process of dysplasia, and there are three different types. CIN 1, CIN 2, CIN 3. Cervical intraepithelial neoplasia, CIN 1, 2, 3. You go straight to CIN 3. Close your eyes. What’s happening right now? Dysplasia. Dysplasia. Can you picture increased proliferation of squamous cells right now? That means that the membrane is getting more -- it’s bearing more and more weight. Think of it that way. With all this proliferation, the membrane, which is still intact, is now bearing all this weight. Oh my goodness. At some point, from CIN 3, you’re going to become malignant. At this point, what form are you in? You’re in...

    About the Lecture

    The lecture Cervical Cancer: Pathogenesis by Carlo Raj, MD is from the course Disorders of Vulva, Vagina and Cervix.


    Included Quiz Questions

    1. Dysplasia
    2. Metaplasia
    3. Hyperplasia
    4. Hypoplasia
    5. Hypertrophy
    1. Low grade squamous intraepithelial lesion (LSIL)
    2. High grade squamous intraepithelial lesion (HSIL)
    3. Squamous carcinoma in-situ (CIS)
    4. Undifferentiated squamous cell carcinoma of cervix
    5. Highly differentiated squamous cell carcinoma of the cervix
    1. HPV 16, 18 and 45
    2. HPV 3 and 9
    3. HPV 4 and 5
    4. HPV 6 and 8
    5. HPV 5 and 11
    1. HIV infection, high parity, oral contraceptive use, smoking, preexisting gene alterations
    2. Smoking, exposure to rubber chemicals, obesity, pregnancy
    3. Alcohol consumption, concomitant Herpes infection, smoking, intravenous drug use.
    4. Hypertension, Giardia infection, chronic pelvic inflammatory disease
    5. There is no evidence for any risk factor associated with malignant transformation of glandular intraepithelial lesions.

    Author of lecture Cervical Cancer: Pathogenesis

     Carlo Raj, MD

    Carlo Raj, MD


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