No abstract

We have investigated the prevalence of HPV DNA in cervical samples collected from 1335 women with abnormal Pap test and analysed the degree of association of HPV genotype with cervical cytological abnormality and also with patient age. The study was principally aimed at providing some cross-sectional figures on the epidemiology of HPV in our area, where the ethnic background is expected to rapidly evolve due to extensive immigration from overseas. 471 (35.3%) of the 1335 patients screened were positive for HPV DNA. A clear association was observed between cytological findings and the proportion of patients with positive HPV PCR, namely 24.0% HPV positivity in the ASCUS group (atypical squamous cells of undetermined significance), 48.7% in LSIL group (low grade squamous intraepithelial lesions), and 71.9% in HSIL group (high grade squamous intraepithelial lesions) (p-value < 0.001). High-risk (HR) HPV prevalence appeared to be different from other areas of the world; we have detected a high prevalence rate of HPV-16, 31, and 58 and a low prevalence rate of HPV-18 and 11. The prevalence of both HR and low risk (LR) genotype groups was clearly related to age (p-value < 0.001), since the prevalence of LR group had a nadir between 41 and 50 y of age and 2 peaks at 15-20 y and at over 60 y, while the curve of prevalence of HR genotypes displayed an almost inverse trend.

Recent studies have implicated Chlamydia pneumoniae (now Chlamydophila pneumoniae) in the pathogenesis of atherosclerosis and demonstrated its presence within human peripheral blood mononuclear cells (PBMCs). In this study the presence of C. pneumoniae DNA was assessed, using nested PCR, in PBMCs from 169 active blood donors as a function of age, of speci®c antibodies and C-reactive protein. The results obtained demonstrated a high degree of global positivity (46.15%), which was higher in females (52%) than in males (43.7%). Seroepidemiological studies showed a high percentage of positivity both in subjects positive by PCR (65.91%) and negative by PCR (71.74%). The clinical implication of such ®nding are under study.

Treatment of mouse Lewis lung carcinoma with razoxane or dacarbazine was protracted for 10 transplant generations. While the capacity of the treated tumors to grow locally in immuno‐competent or in immuno‐depressed hosts was retained and not significantly modified, the metastatic phenotype was eliminated when the treated tumor cells were transplanted into immuno‐competent hosts. The reduction in metastatic potential was slightly less pronounced, in terms of both number and volume of metastases, when the treated tumor cells were transplanted into immuno‐depressed hosts. These properties were retained after 3 transplant generations without treatment. Northern blotting and zymography of primary‐tumor crude extracts revealed that treatment with either razoxane or dacarbazine for one generation approximately doubled the expression of MMP‐2 and MMP‐9, while lacking any effect on that of 1.0 and of 3.5 kb TIMP‐2. When the treatment was maintained for 10 generations, the expression of MMP‐2 and MMP‐9 for both drugs showed up‐regulation of approximately 10‐ and 2‐fold respectively. TIMP‐2 mRNA of 1.0 kb doubled its expression, while that of 3.5 kb registered just above the control. Dacarbazine doubled the expression of uPA after 10 generations, while razoxane boosted it approximately 3‐fold after either 1 or 10 generations. The permanent loss of metastatic phenotype induced in Lewis lung carcinoma by dacarbazine and razoxane is thus attributable to biological mechanisms independent of down‐regulation of expression and/or activation of the 2 gelatinases. Int. J. Cancer 72:1056–1061, 1997. © 1997 Wiley‐Liss, Inc.

Treatment of mouse Lewis lung carcinoma with razoxane or dacarbazine was protracted for 10 transplant generations. While the capacity of the treated tumors to grow locally in immuno-competent or in immuno-depressed hosts was retained and not significantly modified, the metastatic phenotype was eliminated when the treated tumor cells were transplanted into immuno-competent hosts. The reduction in metastatic potential was slightly less pronounced, in terms of both number and volume of metastases, when the treated tumor cells were transplanted into immuno-depressed hosts. These properties were retained after 3 transplant generations without treatment. Northern blotting and zymography of primary-tumor crude extracts revealed that treatment with either razoxane or dacarbazine for one generation approximately doubled the expression of MMP-2 and MMP-9, while lacking any effect on that of 1.0 and of 3.5 kb TIMP-2. When the treatment was maintained for 10 generations, the expression of MMP-2 and MMP-9 for both drugs showed up-regulation of approximately 10-and 2-fold respectively. TIMP-2 mRNA of 1.0 kb doubled its expression, while that of 3.5 kb registered just above the control. Dacarbazine doubled the expression of uPA after 10 generations, while razoxane boosted it approximately 3-fold after either 1 or 10 generations. The permanent loss of metastatic phenotype induced in Lewis lung carcinoma by dacarbazine and razoxane is thus attributable to biological mechanisms independent of downregulation of expression and/or activation of the 2 gelatinases.