Abstracts: Fall 2007The following abstracts are taken from journals of interest to our readers and are reviewed by Thomas M. Julian (TMJ). Comprehensive Analysis of 130 Multicentric Intraepithelial Female Lower Genital Tract Lesions by HPV Typing and p16 Expression Profile M Hampl, N Wentzensen, S Vinokurova, M von Knebel-Doeberitz, C Poremba, HG Bender, V Kueppers J Cancer Res Clin Oncol 2007 Apr;133(4):235Y45. [e-pub November 2006]Purpose. HPV associated cervical transformation is characterized by well-defined steps, including persistent HPV infection and deregulated oncogene expression. Recent studies suggest a number of lower genital tract lesions are clonally related to cervical lesions. In the current study, HPV infections and oncogene expression were assessed in a large series of patients with multicentric lower genital tract disease to analyze the transformation steps in extracervical disease.Methods. One hundred thirty biopsies of 52 women treated for multicentric synchronous or metachronous lower genital tract intraepithelial neoplasias were collected. Up to seven multicentric specimens taken from one patient were studied with a maximum follow up of 20 years. HPV typing and p16(ink4a) immunostaining was performed.Results. HPV DNA was present in 121 of 130 specimens (93%). HPV16 was frequently found in VIN, VaIN and AIN (73, 60 and 77%, respectively), whereas only 37% of CIN were HPV16 positive. Infections with identical HPV types in multicentric lesions were diagnosed in 46% of the HPV positive patients. p16INK4a expression was negative in the nine HPV negative lesions whereas about 90% of the high grade lesions showed diffuse p16 staining.Conclusion. Our findings indicate that multicentric lower genital tract disease evolves through different pathways. Some cases were related to a high susceptibility towards HPV infections, while others exhibited features of clonal propagation of transformed cervical cell clones. The clinical management of the latter group is particularly challenging, because malignant cell clones can persist over a long time course. Comment: This study is interesting in that it shows that multicentric lesions may be from multiple infections in some patients or at least more than 1 HPV type. The multicenter genital intraepithelial neoplasia syndrome was described by many authors quite some time ago, but never followed over such a long period and with evidence suggesting multiple types of HPV. (TMJ)
SummaryThe tumour suppressor gene CDKN2A, located on chromosome 9p21, encodes the cell cycle regulatory protein p16. Inactivation of the CDKN2A gene could lead to uncontrolled cell growth. In order to determine the role of CDKN2A in the development of sporadic ovarian cancer, loss of heterozygosity at 9p21-22, homozygous deletion, mutation and methylation status of the CDKN2A gene as well as CDKN2A expression were examined in a panel of serous papillary ovarian cancer. The frequency of loss of heterozygosity (LOH) for one or more informative markers at 9p21-22 was 65% (15/23). The most common deleted region was located between interferon (IFN)-α and D9S171. Homozygous deletions and mutations of the CDKN2A gene were not found. There was no evidence of methylation in exon 1, but methylation in exon 2 of CDKN2A gene was found in 26% (6/23). Absence of CDKN2A gene expression was shown in 27% (6/22) at mRNA level and 21% (4/19) at protein level. These data suggest that the CDKN2A gene is involved in the tumorigenesis of ovarian cancer, but the mechanisms of CDKN2A gene inactivation in serous papillary ovarian cancer remains unclear.
We retrospectively analyzed methods of follow-up and subsequent clinical outcome in 399 breast cancer patients treated with curative intent. Radioisotope liver scans, liver sonograms and laboratory investigations were of little value in detecting metastases. Mammography detected 2 of 6 contralateral breast cancers in an asymptomatic stage. Of 92 metastatic diseases, 24 were disclosed by a total of 871 radioisotope bone scans, and 17 were disclosed by a total of 2409 chest x-rays. The detection of distant metastases in an asymptomatic stage by diagnostic procedures vs detection by symptoms was not correlated with a survival benefit. The survival times for the two groups were 6.4 years vs 6.7 years (p = 0.7) after initiation of primary therapy, and 20.8 vs 20.4 months (p = 0.9) after the diagnosis of metastatic disease. Our study does not lend support to the hypothesis that the detection of metastatic disease in an asymptomatic stage or regular follow-up visits are associated with a survival benefit. We conclude that clinical history, physical examination, and mammography are the most important procedures in the follow-up of breast cancer patients.
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