Document 0060
 DOCN  M9580060
 TI    Etiology of cervical cancer: current concepts.
 DT    9506
 AU    Bornstein J; Rahat MA; Abramovici H; Department of Obstetrics and
       Gynecology, Carmel Medical Center,; Haifa, Israel.
 SO    Obstet Gynecol Surv. 1995 Feb;50(2):146-54. Unique Identifier : AIDSLINE
       MED/95249184
 AB    The data on the etiological factors presented here may enable us to
       suggest a synergism between the various factors associated with the
       pathogenesis of cervical cancer. Infection of the cervix by HPV 16/18
       may result in persistence of viral DNA. The persistent HPV-DNA undergoes
       disruption at the E2 region, when integrated into the host genome. The
       transcriptional products E6 and E7 oncoproteins bind to and cause the
       degradation of p53 and Rb tumor-suppressor gene products. It is possible
       that, at that point, other cofactors may be involved in the progression
       toward a precancerous or cancerous condition. Those cofactors may
       include cigarette smoking, by introducing co-carcinogens to the tissue
       or by suppressing the local or systemic immune resistance similar to the
       effect of depressed immune resistance seen in AIDS or immunosuppression
       of transplant patients; hormones, by enhancing growth of HPV and
       transformation of HPV infected cells; low serum vitamin levels leading
       to decreased tissue resistance; or other infections causing local
       inflammation and the production of free radicals. CIN develops, leading
       eventually to cervical cancer.
 DE    Cervix Neoplasms/*ETIOLOGY  Contraception  Female  Human
       Immunosuppression  Risk Factors  Sexually Transmitted
       Diseases/*COMPLICATIONS  Smoking/ADVERSE EFFECTS  JOURNAL ARTICLE
       REVIEW  REVIEW LITERATURE

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