Joseph Buscema

Early invasive carcinoma of the vulva

Abstract Early invasive and/or microinvasive carcinomas have presented problems in the areas of histopathologic interpretation and clinical management. The reported and anecdotal cases treated by less than radical procedures with rapid recurrences have increased in the past 5 years. As with cervical cancer, there have been multiple interpretations of “microinvasion.” This series of 58 cases of early invasive disease addresses these controversial issues.

Characterization of human papillomavirus type 45, a new type 18-related virus of the genital tract.

DNA of human papillomavirus (HPV) type 45, a new HPV type 18-related papillomavirus of the genital tract, was cloned from a recurrent cervical lesion displaying mild to moderate dysplasia with koilocytosis. HPV-45 DNA was identified in paraffin sections of biopsies of both the initial and recurrent lesions of the patient, taken 7 months apart. HPV-45 DNA hybridized efficiently to that of many different HPV types under low and moderate stringency conditions (Tm - 37 degrees C to Tm - 25 degrees C) but with only HPV-18 DNA under high stringency conditions (Tm - 17 degrees C). HPV-45 DNA was distinguished from HPV-18 DNA by (i) differences in restriction enzyme digest patterns, (ii) lack of hybridization at Tm - 17 degrees C between HPV-18 and some fragments of HPV-45, (iii) a value of 25% in liquid reassociation kinetics between HPV-18 and HPV-45 and (iv) differences in intensities of hybridization with selected tissue DNAs. The prevalence of HPV-45 infection in the genital tract was low. In tests of over 600 tissue DNAs from female genital tract lesions, HPV-45 sequences were detected in three additional tissues, one each of invasive cervical carcinoma, condyloma, and normal cervical epithelium. HPV-45 is a newly recognized papillomavirus which rarely infects the genital tract and is associated with lesions across a wide histological spectrum.

Ovarian cancer metastatic to the breast.

The breast is an uncommon site for metastasis from epithelial ovarian cancer. Such lesions are purportedly secondary to blood-borne metastases. The accurate classification of ovarian epithelial neoplasms is the cornerstone of decisions regarding therapy and prognosis. Taylor, in 1929, reported a hyperplastic variety of papillary cystadenoma which, on occasion, produced multiple implants on the peritoneum but usually behaved in a benign fashion. The International Federation of Gynecologists and Obstetricians adopted a classification of benign cystadenomas, cystadenocarcinomas of low malignant potential (LMP), and cystadenocarcinomas. The serous tumors of LMP rarely metastasize outside of the abdominopelvic cavity. This case, of a serous tumor of LMP with breast metastasis, permits an analysis of metastatic breast lesions secondary to epithelial ovarian cancer.

Progressive histobiologic alterations in the development of vulvar cancer

Identification of the patient at risk for the development of cancer and the precursory histopathologic changes has led to improvement in 5-year survivals among patients with cancer of the cervix and endometrium. In conrast, there has been controversy as to these factors in discussions of vulvar neoplasia. This report of five cases of patients who developed invasive cancer after treatment for in situ disease attempts to define some of the at-risk factors, including the specific area at which three of the five malignancies subsequently developed.

Investigation of ovarian neoplasia of low malignant potential for human papillomavirus

Recent in situ hybridization studies have suggested the presence of human papillomavirus type 6 (HPV-6) DNA in ovarian cancer cells. An association between HPV and ovarian neoplasia of low malignant potential (LMP) has not been previously identified. Paraffin-embedded tissue blocks from 24 patients with LMP ovarian tumors were screened for human papillomavirus DNA. The patients ranged in age from 18 to 73 years. Corresponding microscopic slides from each tissue block were reviewed to confirm the histopathologic diagnosis. For identification of HPV genome, deparaffinized sections were subjected to the polymerase chain reaction to achieve amplification of DNAs of HPV types 6, 11, 16, and 18. For each HPV type, a 120-base-pair region of the E6 gene was targeted for amplification. Human papillomaviral DNA was not detected in the tissue specimens subjected to polymerase chain reaction. These results suggest that HPV types 6, 11, 16, and 18 are not likely to play a role in LMP ovarian tumors. These results do not totally exclude possible contributions of other HPV types.