ISSN:
0730-2312
Schlagwort(e):
retinoic acid (RA)
;
cervical intraepithelial neoplasia (CIN)
;
HPV
;
dysplasia
;
colposcopic examination
;
Life and Medical Sciences
;
Cell & Developmental Biology
Quelle:
Wiley InterScience Backfile Collection 1832-2000
Thema:
Biologie
,
Chemie und Pharmazie
,
Medizin
Notizen:
Retinoids, a family of molecules capable of profound impact on many biological functions, have antiproliferative, differentiative, and immunomodulatory properties. The present study assessed the effect of 13-cis- retinoic acid (13-CRA) treatment in 13 chronic cervicitis and 52 cervical intraepithelial neoplasia patients. We examined low- and high-risk human papilloma virus titer (using the hybrid capture method) and made a colposcopic and cervicographic examination before and after treatment with 13-CRA at 1 mg/kg for 4 to 12 weeks. Patients were between 27 and 64 years, the average age being 36.6 years. Histology revealed chronic cervicitis in 13 cases, mild dysplasia in 18 cases, moderate dysplasia in 18 cases, and severe dysplasia in 16 cases, totaling 65 cases. The expression rate of high-risk human papilloma virus (HPV 16, 18) was 9 of 13 cases (69%) in chronic cervicitis, 7 of 18 cases (38%) in mild dysplasia, 9 of 18 cases (50%) in moderate dysplasia, and 12 of 16 cases (75%) in severe dysplasia, with the overall expression rate being 37 of 65 cases (57%). Following 13-CRA treatment, decreases in high-risk titer were observed in 6 of 9 cases (66%) of chronic cervicitis, 4 of 11 cases (36%) of mild dysplasia, 7 of 9 cases (77%) of moderate dysplasia, and 8 of 12 cases (75%) of severe dysplasia. Overall, HPV titer decreased in 25 of 41 cases (61%). Minimal changes were found in colposcopic and cervicographic observations during the study. In summary, high-risk HPV titer decreased after treatment with 13-CRA in the majority of patients with cervical intraepithelial neoplasia. This study supports the potential of retinoids to interrupt multi-step carcinogenesis, possibly by down-regulation of gene products (E6, E7) produced by HPV infection. J. Cell. Biochem. Suppls. 28/29:133-139. © 1998 Wiley-Liss, Inc.
Zusätzliches Material:
4 Ill.
Materialart:
Digitale Medien
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