Detection of Mycoplasma ribosomal DNA sequences in ovarian tumors by nested PCR.

OBJECTIVE: The aim of this study was to investigate the reported association between mycoplasma infection and ovarian cancer by screening ovarian tumor tissues for the presence of mycoplasma DNA. METHODS: Forty-six benign and malignant ovarian tumors were obtained from patients undergoing pelvic surgery at a regional cancer center. DNA was isolated from snap-frozen tumor tissues, and commercial nested polymerase chain reaction (PCR) kits were used to detect the presence of 12 species of mycoplasma in tumor DNA samples. PCR products were isolated from ethidium bromide-stained agarose gels, and sequenced with an automated DNA sequencer. Species were identified through nucleotide sequence similarity searches using the National Center for Biotechnology Information BLAST program. RESULTS: Mycoplasma DNA was detected in 6 (13.0%) of the 46 tumor DNA samples. Nucleotide sequence similarity searches of nested PCR products revealed that one Mycoplasma salivarium and five M. arginini DNA sequences were amplified from the ovarian tissues. CONCLUSIONS: Since M. salivarium and M. arginini are frequently encountered laboratory contaminants that do not have a recognized role as human pathogens, our findings do not support an association between human mycoplasma pathogens and ovarian cancer.

Chronic infection, inflammation, and epithelial ovarian cancer.

At the present time, the etiology of epithelial ovarian cancer is poorly understood. It has recently been recognized that certain chronic infectious agents may contribute to carcinogenesis by inducing a state of persistent inflammation. Since the female upper genital tract is a frequent site of chronic infections, we propose various strategies that may be useful for determining the potential role of chronic infection and persistent inflammation in the pathogenesis of epithelial ovarian cancer.

Human immunodeficiency virus p24 antigen testing in cornea donors.

PURPOSE: Testing for the p24 antigen of the human immunodeficiency virus (HIV) may detect early HIV infection in the seronegative window; however, falsely reactive results may occur in cadaver specimens. Although neither the Food and Drug Administration (FDA) nor the Eye Bank Association of America requires p24 testing of cornea donors, many tissue banks using other organs from cornea donors do perform this assay, and the FDA requires that eye banks reject corneal tissue if a reactive p24 assay is reported. We investigated the impact of p24 testing on eye banking and corneal transplantation. METHODS: Two clinical cases and records from the Lions Eye Bank of Delaware Valley (LEBDV) were reviewed retrospectively. RESULTS: Two corneas from the LEBDV were transplanted before the reporting of p24 reactivity by other tissue banks. In one case, because of the young age of the recipient, the surgeon elected to replace the cornea with new tissue hours after the original transplant, and later polymerase chain reaction (PCR) testing was negative. In the other case, there was not enough specimen to perform Western blot or PCR confirmatory testing. The patient was followed with periodic serologic testing for HIV and has remained seronegative. To avoid such problems in the future, the LEBDV initiated testing of all donors with p24 and other nonrequired screening tests. Over a 2-month period, 22 corneas (from 11 donors) were discarded because of these tests: 4 donors had reactive p24 tests, 6 were reactive for antibody to hepatitis B core antigen, and 1 had a reactive syphilis test. CONCLUSIONS: Results from p24 assays by other tissue banks may cause difficult clinical situations when the results are received after transplantation of the tissue, but the use of the p24 assay in the screening of cornea donors may result in excessive waste of donor tissue. Further guidance is needed regarding the management of positive results from this and other nonrequired screening tests.

Breast cancer risk factors and HER2 over-expression in tumors.

Few epidemiologic studies have investigated the potential role of HER2 in the etiology of breast cancer. We conducted a case-case study of 156 women with incident, invasive ductal carcinoma. Multivariate unconditional logistic regression was used to estimate the odds ratios for a HER2 positive tumor in relation to known and putative risk factors of breast cancer. HER2 status was detected by immunohistochemistry on archival tissue. HER2 positive breast cancers tended to be larger and were less likely to express estrogen receptors, and the incidence rate was higher in patients less than 40 years old. We observed an association between a self-reported history of benign breast disease and the occurrence of HER2 positive breast cancer (OR, 2.1;95% CI, 1.1-4.1). We did not detect associations between HER2 over-expression and family history of breast cancer, parity, late age at first birth, ever having breast fed an infant, or oral contraceptive use. Our findings merit consideration in light of recent evidence of HER2 amplification or over-expression in benign breast disease. Should the link to breast cancer be established, HER2 positive benign breast disease could potentially serve as an early marker for preventive intervention.