原著＿王

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1 HPV The Prognosis of the HPV Infected Cer vical Lesions after Followed-up for a Long Term O Jou (Department of Gynecology and Obstetrics, Saitama Medical School, Moroyama, Iruma-gun, Saitama , Japan) Objective: HPV infections are very common in women, only very few develop clinically relevant dysplastic lesions or even cancer. Some infected cases experienced spontaneous regression, and some showed persistent infection. On the other hand, cervical dysplasia that displays a certain persistent process from the normal to tumorigenic state in the tissues, is a precancerous lesion on the histopathological viewpoint. Unfortunately, long-term follow-up cases on HPV-infected uterocervixes are limited. In this study, patients with cervical dysplasia were monitored with the attempt of detecting the continuous changes in cervical lesions. Furthermore, treatments for the HPV-infected cases in progression group were attempted and progresses in these cases were observed. Materials and methods: We examined 573 women aged who visited our Department of OB/Gyn between April 1992 and October 2002 for Papanicolaou Smear Testing and HPV examination. All the patients were divided into 3 groups. Progression group includes patients with developed process of cervical lesions, which were from smear Class II to mild dysplasia, or from mild to severe dysplasia, or from dysplasia to carcinoma in situ. Regression group consisted of patients with regression, or reducing from dysplasia to smear Class II or from severe to mild dysplasia. In the dysplasia cases, patients whose lesions persisted in one stage were classifi ed in persistence group. Results: Of 206 women who were followed-up for 2 years, 118(57.3%) were HPV-positive. Among these, the numbers of the three groups were 56(47.5%) in regression group, 35(29.6%) in persistence group, and 27(22.8%) in progression group. Among 29 women infected with HPV-16, their distribution in the three groups were 5(17.2%), 12(41.4%) and 12(41.4%) respectively. Eighty-eight (42.7%) cases of 206 women were HPV-negative and their distribution in the three groups were 57(64.7%), 26(29.5%), and 5(5.7%), respectively. Of the post-operation cases, 16 were followed-up and their HPV persistencies were reevaluated. Within these 16 cases, 14 were turned out to be HPV-negative and got a smear Class II. Conclusion: The results confi rm an important pathogenic role of high-risk-types HPV infections in cervical dysplasia as well as in cervical cancers. After an effective treatment, HPV-positive cases have a strong tendency of negative conversion, and most of them have an HPV-negative report and normal histologycal fi ndings fi nally. Keywords: HPV types, high-risk-type HPV, progression group, cervical dysplasia, carcinoma in situ J Saitama Med School 2003;30: (Received February 14, 2003) sex activity 1983 Zur Hausen Dursthuman HPV: human papilloma virus, PCR: polymerase chain reaction papilloma virus (HPV) 16 HPV HPV 55 nm papovavirus 80002DNA HPV 90 E1 E2 E4 E5 E6 E7 L1 L2 8 open reading frame

2 E1 E7 6 E6 E7 E6 E7in vitro 2-4) p53 RB binding 5-7) 6, 7) HPV E6 E7 HPV HPV HPV 8-11) HPV Kataja 12 HPV high risk intermediate risk 6 11 low risk 13 HPV16 HPV 2 HPV HPV HPV HPV HPV HPV HPV II II 3 2 HPV DNA Medscand Medical AB(Sweden) 10 mm Tris-HCl ph 8.0, 150 mm NaCl, 10 mm EDTA 1ml4 DNA- SDS (0.1 ) proteinase K 20 µg/ml min 1 / 1 DNA DNA TE 1 mm Tris-HCl PH 8.0, 1 mmedta ph 8.0PCR template DNA 4 HPV E6 E7 primer denature 95 1 min annealing 57 1 min extension 72 1 min 35 cycles PCR (primer HPV E6U 5 -TGTCAAAAACCGTTGTGTCC primer HPV E7U 5 -GAGCTGTCGCTTAATTGCTC) 14,15) 3 HPV PCR 5 µl TAE buffer ethidium bromide 320 nm UV RELP restriction fragment length polymorphism Perkin Elmer Applied Biosystems 310 Genetic Analyzer PCR direct sequence HPV genotype III 206 II 5 II II

3 HPV high risk type HPV HPV HPV 2 HPVHPV HPV HPV HPV wilcoxon signed ranks test (20.7 ) HPV (13.1 ) (22.1 ) (25.5 )16 (11.0 ) Table 4a Table HPV G0 P0 G8 P7, G2.30 P HPV HPV HPV II HPV Table 2 HPV HPV II HPV HPV (Table 3) HPV P HPV HPV HPV Table Table 2. HPV Table 3. HPV Table 4. HPV Table 4a. HPV

4 4HPV HPV HPV 88HPV 118 HPV HPV HPV Table 5 HPVHPV HPV52 58 HPV 3Table HPV HPV HPV II Table 7 HPV HPV Table 8 HPV HPV 2 Table 9 23 HPV16 5 HPV 119 HPV 2 HPV II Table 5. HPV HPV Table 6. Table 7. HPV16 12 Table 8. HPV52 6

5 HPV Table 9. HPV58 5 HPV 90 2) high risk intermediate risk low risk high risk low risk HPV LCR (long control region) E1 E2 E4 E5 E6 E7 L1 L2 5) E6 E7 E6 E7 p53rb 2-7) Bosch 16) 22 1 HPV HPV high risk 2, 17) HPV HPV HPV HPV HPV HPV 2 P high risk HPV HPV II high risk HPV Bosch 16) HPV HPV HPV HPV HPV HPV18 HPV18 HPV16 13) HPV HPV HPV HPV Wilcoxon signed ranks test p HPV16 risk Nobbenhuis 18) high risk HPV HPV CIN3 high risk HPV6 40 CIN3 95 (98/103) high risk HPV HPV118 HPV 88 HPV HPV HPV Wilcoxon signed ranks test P Nobbenhuis 18) HPV high risk HPV HPV HPV HPV HPV HPV HPV52 HPV58 HPV HPV16(p 0.01) HPV Kataja 12) HPVhigh risk intermediate riskhpv HPV HPV HPV HPV

6 HPV 6.1HPV HPV HPV HPV HPV HPV HPV HPV 5.7 HPV18 Nobbenhuis 18) high risk HPV 6 HPV high risk HPV 6 3 HPV16 high risk HPV high risk HPV HPV16 risk HPV HPV16 high risk HPV HPV HPV HPV HPV 1) Durst M, Gissman L, Ikenberg H, Zur Hausen H. A papillomavirus DNA from a cervical carcinoma and its prevalance in cancer biopsy samples from different geographic regions. Proc Natl Acad Sci USA 1983;80: ). HPV. 1997;41: ) Berger AJ, Baege A, Guillemette T, Deeds J, Meyer R, Disbrow G, et al. Insulin-like growth factor-binding protein 3 expression increases during immortalization of cervical keratinocytes by human papillomavirus type 16 E6 and E7 proteins. American Journal of Pathology 2002;161(2): ) Steenbergen RD, OudeEngberink VE, Kramer D, Schrijnemakers HF, Verheijen RH, Meijer CJ, et al. Down-regulation of GATA-3 expression during human papillomavirus-mediated immortalization and cervical carcinogenesis. American Journal of Pathology 2002;160(6): ),,. HPV. 1998;50: ) Chen QM, Merrett JB, Dilley T, Purdom S. Down regulation of p53 with HPV E6 delays and modifi es cell death in oxidant response of human diploid fi broblasts: an apoptosis-like cell death associated with mitosis. Oncogene 2002;21(34): ) Ferency A, Franco E. Persistent human papillomavir us infection and cer vical neoplasia. Lancet Oncology 2002;3(1): ) Saito J, Sumiyoshi M, Nakatani H, Ikeda M, H o s h i a i H, N o d a K. D y s p l a s i a a n d H P V infection initally detected by DNA analysis in cytomorphologically normal cer vical semears. International Journal of Gynecology & Obstetrics 1995;51: ) Syrjanen K, Hakama M, Saarikoski S, Vayrynen M, Yliskoski M, Syrjanen S, et al. Prevalence, incidence, and estimated life-time risk of cervical human papillomavirus infections in a nonseledected fi nnish female papulation. Sexually Transmitted Diseases 1990;17: ) Moscicki AB, Palefsky J, Smith G, Siboshski S, Schoolnik G. Variability of human papillomavirus DNA testing in a longitudinal cohort of young women. Obstet Gynecol 1993;82: ) Katase K, Teshima H, Hirai Y, Hasumi K. Natural history of cervical human papillomavirus lesions. Intervirology 1995;38(3-4): ) Kataja V, Syrjanen K, Syrjanen S, Mantyjarvi R, Yliskoski M, Saarikoski S, et al. Prospective follow-up of genital HPV infectino: survial analysis of the HPV typing data. Eur J Epidemiol 1990;6: ),. HPV. 1998; 50: ),,, : PCR. 1996;41: ) Fujinaga Y, Shimada M, Okazawa K, Fukushima M, Kato I, Fujinaga K. Simultaneous detection and typing of genital human papillomavirus DNA using

7 HPV the polymerase chain reaction. J General Virology 1991;72: ) Bosch FX, Manos MM, Munoz N, Sherman M, Jansen AM, Peto J, et al. Prevalence of human papillomavirus in cer vical cancer: a worldwide perspective. International biological study on cervical cancer (IBSCC) Study Group. Journal of the National Cancer Institute 1995;87: ) Liaw KL, Hildesheim A, Burk RD, Gravitt P, Wacholder S, Manos MM, et al. A prospective study of human papillomavirus (HPV) type 16 DNA detection by polymerase chain reaction and its association with acquisition and persistence of other HPV types. Source Journal of Infectious Diseases 2001;183(1): ) Nobbenhuis MA, Walboomers JM, Helmerhorst TJ, Rozendaal L, Remmink AJ, Risse EK, et al. Relation of human papillomavirus status to cervical lesions and consequences for cervical-cancer screening: a prospective study. Lancet 1999;354(9172): The Medical Society of Saitama Medical School

Studies of Foot Form for Footwear Design (Part 9) : Characteristics of the Foot Form of Young and Elder Women Based on their Sizes of Ball Joint Girth

Studies of Foot Form for Footwear Design (Part 9) : Characteristics of the Foot Form of Young and Elder Women Based on their Sizes of Ball Joint Girth and Foot Breadth Akiko Yamamoto Fukuoka Women's University,