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Cervical Cancer: Pathogenesis

by Carlo Raj, MD
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    00:01 Pathogenesis of cervical cancer.

    00:04 I'll quickly walk you through the algorithm that's important for you.

    00:08 You’ve seen this before in some way, shape, or form.

    00:11 I like the organization pattern that is being established here for you.

    00:15 Sexual activity.

    00:17 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.

    00:28 In basic pathology, we talked about neoplasia.

    00:31 In neoplasia, we talked about HPV high-risk strain containing particular oncogenes.

    00:37 And those included E6 and E7.

    00:40 E6 knocked out p53; E7 knocked out Rb.

    00:46 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.

    00:57 Your focus will be on the left branch of this algorithm.

    01:02 Eighty five percent of time, you are going to then start the development of invasive squamous cancer.

    01:10 Squamous differentiation.

    01:12 What does that mean? Now, the squamous cells are undergoing differentiation but not for the good though.

    01:19 They’re going to proliferate, proliferate, proliferate.

    01:21 What’s disorganized or disordered proliferation called to you medically? Good.

    01:29 Dysplasia.

    01:30 So now, you begin the process of dysplasia, and there are three different types.

    01:38 CIN 1, CIN 2, CIN 3.

    01:42 Cervical intraepithelial neoplasia, CIN 1, 2, 3.

    01:48 You go straight to CIN 3.

    01:51 Close your eyes.

    01:52 What’s happening right now? Dysplasia.

    01:53 Dysplasia.

    01:54 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.

    02:04 Think of it that way.

    02:06 With all this proliferation, the membrane, which is still intact, is now bearing all this weight.

    02:12 Oh my goodness.

    02:14 At some point, from CIN 3, you’re going to become malignant.

    02:20 At this point, what form are you in? You’re in dysplasia.

    02:23 That is not a neoplasia.

    02:25 It is a dysplasia, but it’s not a cancer.

    02:28 It’s not malignant.

    02:30 So your next step in terms of malignancy will be in situ.

    02:33 And then you’re going to invade.

    02:35 If you then invade, you become now invasive cervical cancer.

    02:40 Let’s pause here for a second.

    02:42 You should be familiar with CIN 1, 2, and 3.

    02:44 We’ve talked about it in microbiology.

    02:46 I will talk to you about this a little bit more.

    02:47 However, clinically, this might be new information for you, that you need to make sure that you’re familiar with.

    02:56 You no longer will call this CIN when you document it.

    03:00 When you document the changes that you find on Pap smear, okay, you’ve taken a sample of the cell and you’re looking at it now.

    03:08 When you document it, you’ll be writing down what type of SIL has been taking place.

    03:17 SIL stands for squamous intraepithelial lesion, SIL.

    03:22 There is either low grade or high grade.

    03:25 Please focus upon high grade SIL.

    03:29 What high grade SIL means is the fact that you’re getting step by step by step closer to invasive squamous cancer.

    03:40 Here we have the following, high grade and also risk factors that are involved.

    03:45 Smoking, oral contraceptive pills, high parity, altered immune status, and maybe perhaps, host gene alterations All of these factors, high grade, you’re increasing risk of? Invasive squamous cancer.

    04:03 Take a look at the very left. We have low grade.

    04:05 Low grade has a rare chance of going on to invasive squamous cancer.

    04:10 Think of this, please, as being like CIN 1.

    04:16 Once you go past CIN 1 and you go into CIN 2 and 3, this is your high grade.

    04:24 And once again, to high grade, you’ll increase the chance of going on to? Invasive squamous cancer of what organ right now? Cervical.

    04:33 How important is this? Worldwide developing countries, cervical invasive cancer is the number one cancer gynecologically.

    04:45 What about the other side? On the right branch, what part of the cervix are we in if it’s columnar? Endocervical columnar differentiation.

    04:55 If this is endocervical, what kind of cells are these? Good.

    05:00 These are columnar cells.

    05:03 Therefore, why would you ever call this squamous intraepithelial lesion? That makes no sense.

    05:10 You would call this glandular intraepithelial lesion.

    05:13 "But Dr. Raj, I’ve never heard of that before." That’s okay, that’s good, because that means that you’ve been taught that majority of your cervical cancer is of what type? Squamous, squamous, squamous, 85% of the time.

    05:26 A measly 10-15%, sure, you could go into glandular.

    05:30 Just to make sure we’re complete, because on your boards and in your wards, you’d never know.

    05:35 You could be facing both of these differentiation leading into invasive adenocarcinoma.

    05:41 A beautiful algorithm and flow chart to summarize in general the development of your invasive cervical cancer.

    05:49 You’ve understood this.

    05:50 You've pretty much understood everything there is to know about cervical cancer and where it’s coming from.

    05:56 Take your time.

    05:57 Keep repeating what I've taught you here until it becomes firmly implanted in your head.


    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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