Cervical cancer pathophysiology: Difference between revisions
Jump to navigation
Jump to search
Nima Nasiri (talk | contribs) |
Nima Nasiri (talk | contribs) |
||
| Line 4: | Line 4: | ||
{{CMG}}}{{AE}}{{Nnasiri}}{{MD}} {{AIDA}} | {{CMG}}}{{AE}}{{Nnasiri}}{{MD}} {{AIDA}} | ||
==Overview== | ==Overview== | ||
It is established that human papillomavirus (HPV) is | It is established that human papillomavirus (HPV) is the main cause of development of cervical neoplasia, only high risk strain of HPV can cause cervical cancer among women whom are affected. This is because of HPV produced proteins E7 which alters epithelium of cervix mainly at junctional zone. | ||
==Pathophysiology== | ==Pathophysiology== | ||
| Line 14: | Line 14: | ||
* Sex steroid hormons | * Sex steroid hormons | ||
* Smoking | * Smoking | ||
Role of HPV in pathogenesis of cervical cancer includes:<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> | Role of HPV in pathogenesis of cervical cancer includes:<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> | ||
* The high risk HPV E6 gene product binds to p53 and prevents its normal activities which is G1 arrest, apoptosis, and DNA repair. | |||
* HPV enters the host cell which are squamous cells of epithelium in cervix, mainly in junctional zone and viral transcription and replication begins. | |||
* [[HPV|Human papillomaviruses]], a sexually transmitted virus, subtypes 16 and 18 (High risk) play an important role in the pathogenesis of cervical cancer. | |||
* [[HPV|Human papillomaviruses]], a sexually transmitted virus, subtypes 16 and 18 (High risk) play an important role in the pathogenesis of cervical cancer. | |||
== Genetic: == | == Genetic: == | ||
Revision as of 16:02, 12 February 2019
|
Cervical cancer Microchapters |
|
Diagnosis |
|---|
|
Treatment |
|
Case Studies |
|
Cervical cancer pathophysiology On the Web |
|
American Roentgen Ray Society Images of Cervical cancer pathophysiology |
|
Risk calculators and risk factors for Cervical cancer pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]}Associate Editor(s)-in-Chief: Nima Nasiri, M.D.[2]Monalisa Dmello, M.B,B.S., M.D. [3] Aida Javanbakht, M.D.
Overview
It is established that human papillomavirus (HPV) is the main cause of development of cervical neoplasia, only high risk strain of HPV can cause cervical cancer among women whom are affected. This is because of HPV produced proteins E7 which alters epithelium of cervix mainly at junctional zone.
Pathophysiology
Pathogenesis:
Role of high risk strains of HPV, mainly HPV types 16 and 18 had been identified as a potent cause of cancer of cervix, but there are other cofactors that cause progression of cervical neoplasia, some of these include:[1]
- HLA type
- Immunosuppression
- Sex steroid hormons
- Smoking
Role of HPV in pathogenesis of cervical cancer includes:[2]
- The high risk HPV E6 gene product binds to p53 and prevents its normal activities which is G1 arrest, apoptosis, and DNA repair.
- HPV enters the host cell which are squamous cells of epithelium in cervix, mainly in junctional zone and viral transcription and replication begins.
- Human papillomaviruses, a sexually transmitted virus, subtypes 16 and 18 (High risk) play an important role in the pathogenesis of cervical cancer.
Genetic:
- L-1β, encoded by the IL-1B gene, is an inflammatory cytokine and part of the innate immune system.[3]
- TNF-α, encoded by the TNFA gene, is another potent pro-inflammatory cytokine that has been implicated in the control of HPV infection.
- Polymorphisms within HLA plays a role in pathogenesis of cervical neoplasia.
- Interleukin-12 A and B gene (IL12A and IL12B)
- IFN-γ, encoded by the IFNG gene has defensive role against viruses and induces immune mediated inflammatory responses
- Interleukin-10 and the risk and the progression of cervical cancer have been associated with increased IL-10 serum levels
- Cytotoxic T-lymphocyte antigen-4
- HPV E6/E7 oncogenes, proteins that interfere with cell cycle growth and tumor supressor genes.
- Primary microRNA-218 (pri-miR-218) and laminin-5 β3 (LAMB3)
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.
-
Uterus: Cervical Carcinoma: Gross, an excellent example of tumor (labeled as invasive)
Image courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology -
Histopathologic image (H&E stain) of cervical intraepithelial neoplasia.
_CIN3.jpg)
Video
{{#ev:youtube|J3kULzKGzws}}
References
- ↑ Arends MJ, Buckley CH, Wells M (February 1998). "Aetiology, pathogenesis, and pathology of cervical neoplasia". J. Clin. Pathol. 51 (2): 96–103. PMID 9602680.
- ↑ Burd EM (January 2003). "Human papillomavirus and cervical cancer". Clin. Microbiol. Rev. 16 (1): 1–17. PMC 145302. PMID 12525422.
- ↑ . doi:10.1016/S1674-8301(11)60020-1. Check
|doi=value (help). Missing or empty|title=(help)