Skip to Main Content
  • Become an Access Reviewer
  • Clinical Phenotypes
  • OMMBID Advisory banner
  • Ommbid banner
  • Ommbid latest banner

Abstract

Abstract 

  1. Based on available worldwide statistics, cervical cancer is the second most common cause of cancer-related mortality in women. Cervical cancers are curable when detected early, and the implementation of effective screening programs has reduced the incidence of and mortality from cervical cancer in industrialized countries substantially.

  2. Neoplastic processes are undoubtedly complex, and cervical tumorigenesis is no exception. Like other adult solid tumors, cervical cancer appears to develop and progress largely as a consequence of activating mutation of oncogenes coupled with inactivation of tumor-suppressor genes. Alterations of such genes have profound effects on the exquisite control of cell growth and differentiation present in normal cells. Based on currently available information, it appears that inherited factors do not play a major role in cervical tumorigenesis.

  3. Cervical cancer is different from most other common malignancies in that it is strongly associated with an infectious agent (human papillomavirus, HPV). This strong association has been used to great advantage in the research laboratory because the HPVs provide powerful tools with which to examine the molecular mechanisms underlying cervical tumor development and progression.

  4. Most studies have focused on the E6 and E7 transforming proteins of the oncogenic HPV types. E6 and E7 interfere with function of the cellular tumor-suppressor proteins p53 and pRB via protein-protein interactions. By interfering with cell cycle control and DNA repair mechanisms, oncogenic HPVs appear to contribute indirectly to cervical tumorigenesis by promoting genetic instability and the accumulation of mutations in HPV-infected cells.

  5. Relatively few specific genes have been identified that are often altered in cervical carcinomas, although frequent amplification of c-myc and HER2-neu has been reported. However, other cytogenetic and molecular genetic studies suggest that genes on chromosomes 1, 3, 5, 11, and others are likely to play important roles in cervical tumorigenesis. Intensive efforts are currently underway to identify specific genes targeted by alterations of these chromosomes.

  6. Animal models of papillomavirus-associated tumorigenesis have been developed, including several species-specific systems. More recently, production of transgenic animals expressing HPV transforming proteins have provided new insights into the mechanisms by which HPVs contribute to cervical cancer.

  7. Cervical cancers are particularly attractive targets for preventive and antitumor vaccines because they virtually always contain tumor-specific antigens (HPV proteins).

Want remote access to your institution's subscription?

Sign in to your MyAccess profile while you are actively authenticated on this site via your institution (you will be able to verify this by looking at the top right corner of the screen - if you see your institution's name, you are authenticated). Once logged in to your MyAccess profile, you will be able to access your institution's subscription for 90 days from any location. You must be logged in while authenticated at least once every 90 days to maintain this remote access.

Ok

About MyAccess

If your institution subscribes to this resource, and you don't have a MyAccess profile, please contact your library's reference desk for information on how to gain access to this resource from off-campus.

Subscription Options

OMMBID Full Site: One-Year Subscription

Connect to the full suite of OMMBID content including new and revised chapters that reflect the latest research, image galleries, clinical phenotypes, and more.

$295 USD
Buy Now

Pay Per View: Timed Access to all of OMMBID

24 Hour Subscription $34.95

Buy Now

48 Hour Subscription $54.95

Buy Now

Pop-up div Successfully Displayed

This div only appears when the trigger link is hovered over. Otherwise it is hidden from view.