Cervical cancer pathophysiology: Difference between revisions

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=== '''Pathogenesis:''' ===
=== '''Pathogenesis:''' ===
Two major viral oncogenes, E6 and E7, directly coupled to viral enhancers and promoters, allowing their continued expression after integration. High risk HPV E7 proteins bind and inactivate the Rb protein, whereas E6 proteins bind p53 and direct its rapid degradation. A range of putative cofactors has been implicated in progression: HLA type, immunosuppression, sex steroid hormones, and smoking; most of these cofactors appear to influence progression to CIN 3. The natural history includes progression to CIN 3 in 10% of CIN 1 and 20% of CIN 2 cases, whereas at least 12% of CIN 3 cases progress to invasive carcinoma. Cervical glandular intraepithelial neoplasia (CGIN) often coexists with squamous CIN, and the premalignant potential of high grade CGIN is not in doubt, but the natural history of low grade CGIN remains uncertain. A high proportion of CGIN lesions and adenocarcinomas are HPV positive, and HPV18 has been implicated more in glandular than in squamous lesions. A strong clinical case for the application of HPV typing of cells recovered from cervical scrapes can be made; however, a rigorous cost-benefit analysis of introducing HPV typing into the cervical screening programme is required. Prophylactic and therapeutic HPV vaccines are under development. This article reviews the aetiology, pathogenesis, and pathology of cervical neoplasia, emphasising the role of HPVs.
A range of putative cofactors has been implicated in progression: HLA type, immunosuppression, sex steroid hormones, and smoking; most of these cofactors  


Infection with Human papilloma virus is the main cause of cervical cancer, only certain strain of high risk HPV can cause cervical cancer. <ref name="pmid12525422">{{cite journal |vauthors=Burd EM |title=Human papillomavirus and cervical cancer |journal=Clin. Microbiol. Rev. |volume=16 |issue=1 |pages=1–17 |date=January 2003 |pmid=12525422 |pmc=145302 |doi= |url=}}</ref>
Infection with Human papilloma virus is the main cause of cervical cancer, only certain strain of high risk HPV can cause cervical cancer. <ref name="pmid12525422">{{cite journal |vauthors=Burd EM |title=Human papillomavirus and cervical cancer |journal=Clin. Microbiol. Rev. |volume=16 |issue=1 |pages=1–17 |date=January 2003 |pmid=12525422 |pmc=145302 |doi= |url=}}</ref>
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*Two major viral oncogenes, E6 and E7, directly coupled to viral enhancers and promoters, allowing their continued expression after integration. High risk HPV E7 proteins bind and inactivate the Rb protein, whereas E6 proteins bind p53 and direct its rapid degradation.
*Two major viral oncogenes, E6 and E7, directly coupled to viral enhancers and promoters, allowing their continued expression after integration. High risk HPV E7 proteins bind and inactivate the Rb protein, whereas E6 proteins bind p53 and direct its rapid degradation.
* Important factors in causing cervical cancer:
* Important factors in causing cervical cancer:
[[Immune system]] condition of the patient.
** HLA type
 
** Immunosuppression
Smocking.
** Sex steroid hormones
 
** Smoking
Subtypes of the HPV.
 
High numbers of sexual partners.


== Genetic: ==
== Genetic: ==

Revision as of 20:52, 8 February 2019

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]}Associate Editor(s)-in-Chief: Monalisa Dmello, M.B,B.S., M.D. [2] Aida Javanbakht, M.D.

Overview

It is estalished that human papillomavirus (HPV) is central to the development of cervical neoplasia, only high risk strain of HPV can cause cervical cancer among women whom are affected. This is mainly because of HPV produced proteins E7 which alters epithelium of cervix mainly at junctional zone.

Pathophysiology

Pathogenesis:

A range of putative cofactors has been implicated in progression: HLA type, immunosuppression, sex steroid hormones, and smoking; most of these cofactors

Infection with Human papilloma virus is the main cause of cervical cancer, only certain strain of high risk HPV can cause cervical cancer. [1]

  • Human papillomaviruses, a sexually transmitted virus, subtypes 16 and 18 (High risk) play an important role in the pathogenesis of cervical cancer. Once HPV enters an epithelial cell, begins to make the proteins.
  • Two major viral oncogenes, E6 and E7, directly coupled to viral enhancers and promoters, allowing their continued expression after integration. High risk HPV E7 proteins bind and inactivate the Rb protein, whereas E6 proteins bind p53 and direct its rapid degradation.
  • Important factors in causing cervical cancer:
    • HLA type
    • Immunosuppression
    • Sex steroid hormones
    • Smoking

Genetic:

Associated Conditions:

Gross Pathology:

Microscopic pathology

  • Prominent nucleoli.
  • Blurred or scalloped epithelial-stromal interface.
  • Loss of nuclear polarity.
  • Pseudoglandular pattern because of acantholysis and central necrosis.

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References

  1. Burd EM (January 2003). "Human papillomavirus and cervical cancer". Clin. Microbiol. Rev. 16 (1): 1–17. PMC 145302. PMID 12525422.


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