Cervical dysplasia natural history: Difference between revisions
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[[HPV|Human papillomaviruses]] subtypes 16 and 18 (High risk) play an essential role in the pathogenesis of cervical dysplasia. Once [[HPV]] enters an epithelial cell, the virus begins to make the proteins it encodes. Two of the proteins made by high-risk HPVs (E6 and E7) interfere with cell functions that normally prevent excessive growth, helping the cell to grow in an uncontrolled manner and to avoid cell death. Many times these infected cells are recognized by the immune system and eliminated. Sometimes, however, these infected cells are not destroyed, and a persistent infection results. As the persistently infected cells continue to grow, they may develop mutations in cellular genes that promote even more abnormal cell growth, leading to the formation of an area of precancerous cells.<ref>{{Cite web | title =HPV | url = http://www.cancer.gov/about-cancer/causes-prevention/risk/infectious-agents/hpv-fact-sheet}}</ref> | |||
* Cervical dysplasia has its origins at the squamous-columnar junction; it can involve the outer squamous cells, the inner glandular cells, or both. The precursor lesion is [[dysplasia]]: [[cervical intraepithelial neoplasia]] (CIN) or adenocarcinoma in situ.<ref>{{Cite web | title= cervical cancer| url = http://www.cancer.gov/types/cervical/hp/cervical-treatment-pdq#link/_532_toc</ref> | |||
==Natural history== | |||
*Cervical cancer arises from squamous-columnar junction. | |||
*The earliest microscopic change corresponding to [[cervical intraepithelial neoplasia]](CIN) is [[dysplasia]] of the epithelial or surface lining of the cervix,are associated with HPV infection, such as koilocytes, are also commonly seen in Cervical intraepithelial neoplasia (CIN). | |||
*However most CIN spontaneously regress. Left untreated, about 70% of CIN-1 will regress within one year, and 90% will regress within two years. About 50% of CIN 2 will regress within 2 years without treatment. | |||
*Progression to cervical cancer in situ (CIS) occurs in approximately 11% of [[cervical intraepithelial neoplasia]](CIN1) and 22% of [[cervical intraepithelial neoplasia]](CIN2). Progression to invasive cancer occurs in approximately 1% of [[cervical intraepithelial neoplasia]] (CIN1), 5% in [[cervical intraepithelial neoplasia]] (CIN2) and at least 12% in [[cervical intraepithelial neoplasia]] (CIN3). | |||
* This process can be quite slow. Longitudinal studies have shown that in patients with untreated in situ cervical cancer, 30% to 70% will develop invasive carcinoma over a period of 10 to 12 years. However, in about 10% of patients, lesions can progress from in situ to invasive in a period of less than 1 year. As it becomes invasive, the tumor breaks through the basement membrane and invades the cervical stroma.<ref>https://en.wikipedia.org/wiki/Cervical_intraepithelial_neoplasia</ref> | |||
*Extension of the tumor in the cervix may ultimately manifest as ulceration, exophytic tumor, or extensive infiltration of underlying tissue, including the bladder or rectum. | |||
*In advanced disease, [[metastasis|metastases]] may be present in the [[abdomen]], [[lung]]s. | |||
*The patient may present with dyspnea, cough with blood-stained sputum, persistent pain or discomfort in the chest, edema hands/feet. | |||
*Once the cancer spreads to the other organs, it is most likely fatal. | |||
==Prognosis== | ==Prognosis== | ||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Human papillomaviruses subtypes 16 and 18 (High risk) play an essential role in the pathogenesis of cervical dysplasia. Once HPV enters an epithelial cell, the virus begins to make the proteins it encodes. Two of the proteins made by high-risk HPVs (E6 and E7) interfere with cell functions that normally prevent excessive growth, helping the cell to grow in an uncontrolled manner and to avoid cell death. Many times these infected cells are recognized by the immune system and eliminated. Sometimes, however, these infected cells are not destroyed, and a persistent infection results. As the persistently infected cells continue to grow, they may develop mutations in cellular genes that promote even more abnormal cell growth, leading to the formation of an area of precancerous cells.[1]
- Cervical dysplasia has its origins at the squamous-columnar junction; it can involve the outer squamous cells, the inner glandular cells, or both. The precursor lesion is dysplasia: cervical intraepithelial neoplasia (CIN) or adenocarcinoma in situ.[2]
Natural history
- Cervical cancer arises from squamous-columnar junction.
- The earliest microscopic change corresponding to cervical intraepithelial neoplasia(CIN) is dysplasia of the epithelial or surface lining of the cervix,are associated with HPV infection, such as koilocytes, are also commonly seen in Cervical intraepithelial neoplasia (CIN).
- However most CIN spontaneously regress. Left untreated, about 70% of CIN-1 will regress within one year, and 90% will regress within two years. About 50% of CIN 2 will regress within 2 years without treatment.
- Progression to cervical cancer in situ (CIS) occurs in approximately 11% of cervical intraepithelial neoplasia(CIN1) and 22% of cervical intraepithelial neoplasia(CIN2). Progression to invasive cancer occurs in approximately 1% of cervical intraepithelial neoplasia (CIN1), 5% in cervical intraepithelial neoplasia (CIN2) and at least 12% in cervical intraepithelial neoplasia (CIN3).
- This process can be quite slow. Longitudinal studies have shown that in patients with untreated in situ cervical cancer, 30% to 70% will develop invasive carcinoma over a period of 10 to 12 years. However, in about 10% of patients, lesions can progress from in situ to invasive in a period of less than 1 year. As it becomes invasive, the tumor breaks through the basement membrane and invades the cervical stroma.[3]
- Extension of the tumor in the cervix may ultimately manifest as ulceration, exophytic tumor, or extensive infiltration of underlying tissue, including the bladder or rectum.
- In advanced disease, metastases may be present in the abdomen, lungs.
- The patient may present with dyspnea, cough with blood-stained sputum, persistent pain or discomfort in the chest, edema hands/feet.
- Once the cancer spreads to the other organs, it is most likely fatal.
Prognosis
Early diagnosis and prompt treatment cure nearly all cases of cervical dysplasia. Sometimes, the condition returns.
Without treatment, severe cervical dysplasia may develop invasive cancer. It can take 10 or more years for cervical dysplasia to develop into cancer. The risk of cancer is lower for mild dysplasia.
References
- ↑ "HPV".
- ↑ {{Cite web | title= cervical cancer| url = http://www.cancer.gov/types/cervical/hp/cervical-treatment-pdq#link/_532_toc
- ↑ https://en.wikipedia.org/wiki/Cervical_intraepithelial_neoplasia