A case of perivascular epithelioid cell tumor (PEComa) at the uterus / 대한산부인과학회지

Perivascular epithelioid cell tumors (PEComas) at the uterus are very rare tumors and about 30 cases have been reported as far as we know. As a case was experienced at our hospital, we would like to report it with a brief review of literature.

One case of primary malignant mixed Mullerian tumor of the pelvic peritoneum / 부인종양

Malignant mixed mullerian tumor (MMMT) is a tumor in which carcinoma (an epithelial malignancy) is mixed with sarcoma (a nonepithelial malignancy). Extrauterine MMMTs are extremely rare, and only 32 cases are reported according to the literature. We experienced a case of primary peritoneal MMMT and repot with a brief review of literature.

When should human papillomavirus (HPV) testing be done after conization? / 대한산부인과학회지

OBJECTIVE: To know when human papillomavirus (HPV) testing should be done after conization. METHODS: Between 1997 to 2004, Large Loop Excisions of the Transformation Zone (LLETZ) were done for conization to women with cervical pathology at A University Hospital. The Pap and HPV typing were done before LLETZ procedures. After conizations, HPV typing were planned to be done every 3 months. Every HPV typing was done by HPV oligonucleotide microarray (Biomedlab Co., Seoul, South Korea). RESULTS: For 8 years, 120 LLETZ were enrolled in this study. There were 8 cases of no neoplasm, 9 cases of CIN 1, 17 cases of CIN 2, 74 cases of CIN 3, 10 cases of microinvasive cervix cancer, and 2 cases of adenocarcinoma in situ. HPV DNA before LLETZ procedures was found about 85.0% and subtype 16 was the most common type among the patients with cervical lesion (40.8%). After LLETZ, 190 HPV typing were done through 1,307 total months (average, 6.9 months/typing). 95 (79.2%) cases had negative results, and 25 (20.8%) cases had positive results. Our data showed that, after conization, about 80% turned out to negative in 6 months. CONCLUSION: Our data suggested HPV DNA testing should be done after 6 months of LLETZ, as about 80% were destined to negative in 6 months.

Relationship between HPV Typing and Expressions of p16 and p53 in Cervical Neoplasia / 대한산부인과학회잡지

OBJECTIVE: To determine the relationships among the grade of cervical pathology, HPV infection status, p16 expression, and p53 expression in cervical neoplasia. METHODS: From July of 2002 to June of 2003, authors did HPV typing with HPV Oligonucleotide Microarray DNA Chip (Biomed, Seoul, Korea), p16 and p53 immunochemical staining in cervical tissues obtained from conization or hysterectomy RESULTS: 41 patients were enrolled in this study. There were 16 normal (WNL) patients, 9 CIN patients, 8 microinvasive cancer (MIC) patients, and 8 invasive cervical cancer (ICC) patients. The HPV infection rate in WNL, CIN, MIC and ICC were 0%, 100%, 50% and 50% retrospectively. The expression rate of p16 was 13% in WNL, 67% in CIN, 50% in MIC and 100% in ICC. That of p53 was 0% in WNL, 67% in CIN, 75% in MIC and 100% in ICC. With regard to p16 staining in HPV negative cases, negative staining was 67%, weakly positive was 13% and strongly positive was 21%. But in HPV-infected cases, negative staining of p16 was 29%, weakly positive was 53% and strongly positive was 18%. With regard to p53 staining in HPV negative cases, without HPV infection, negative staining was 62%, weakly positive was 33% and strongly positive was 4%. But in HPV infected cased, negative staining of p53 was 18%, weakly positive was 53% and strongly positive was 29%. Finally, in p16 negative cases, negative staining of p53 was 62%, weakly positive was 38% and strongly positive was 0%. But in p16 weakly positive cases, with weakly positive p16, negative staining of p53 was 33%, weakly positive was 42%, and strongly positive was 25%. In p16 strongly positive cases, negative staining of p53 was 13%, weakly positive was 50% and strongly positive was 38%. CONCLUSION: There were significant associations among grades of cervical pathology, HPV infection, p16 and p53 expression. Thus there might be some possibilities that expression of p16 and p53 induced by E7 and E6 proteins of HPV can impact on the tumorigenesis.