[Membrane platelet receptors and cardiovascular risk: from structure to potential clinical implications]. / Recettori piastrinici di membrana e rischio cardiovascolare: dalla struttura alle possibili implicazioni cliniche.

Platelets exhibit membrane receptor proteins the structure of which has adapted, in the course of evolution, to halt hemorrhage. These receptors are also implicated in thrombosis, and their structural variability is likely able to account for part of the variability in intraindividual susceptibility to thrombotic events. This review offers a summary of current knowledge on the molecular structure and function of platelet membrane receptors, here studied also in relation to the variability of platelet function in the general population, with the aim of discussing possible implications for the atherothrombotic risk.

p53 codon 72 polymorphism does not affect the risk of cervical cancer in patients from northern Italy.

A case-control study was performed to investigate the risk of cervical cancer associated with p53 polymorphism at codon 72, encoding either arginine or proline. It has been recently suggested that the arginine isoform increases the susceptibility to invasive cervical cancer; however, data remain controversial. The polymorphism was examined by both allele-specific PCR and RFLP analysis in 101 patients with primary cervical cancer and in 140 healthy women of the same age and from the same geographical area. The distribution of p53 genotypes in cervical cancer patients and in controls was not significantly different (P = 0.445), and homozygosity for arginine at residue 72 was not associated with an increased risk for cervical cancer (odds ratio, 0.81; 95% confidence interval, 0.47-1.42; P = 0.52). Similarly, different genotype distribution and increased risk were not observed when patients versus controls were analyzed according to human papillomavirus status and cancer histotype. Therefore, no evidence of association between homozygosity for p53 arginine and cervical cancer was found in our population sample.

Analysis and clinical implications of p53 gene mutations and human papillomavirus type 16 and 18 infection in primary adenocarcinoma of the uterine cervix.

Mutant p53 is frequently detected in endometrial and ovarian carcinoma, but it is rare in cervical cancers. Previous reports focused on cervical squamous cell carcinoma, whereas cervical adenocarcinoma was given little attention. We searched for p53 gene mutations in 74 primary cervical adenocarcinomas with known human papillomavirus (HPV) status. Our aim was to evaluate the prevalence of p53 mutations and to investigate their possible role as an independent prognostic factor. We found mutations in 13.5% with a high rate of G:C --> A:T transitions as observed in endometrial adenocarcinoma. As p53 mutations are more frequently detected in malignancies of high grade, high stage, and large size, this molecular event seems to play a role in the progression rather than in the induction of cervical adenocarcinoma. In our series, patients with HPV-negative tumors and patients with mutated neoplasms, irrespective of HPV infection, had a shorter survival. Yet the absence of HPV infection and presence of p53 mutations are not independent risk factors for tumor-related death after adjustment for clinicopathological confounders. The only significant and independent predictors of survival are age of patient, stage of disease, tumor grade, and presence of lymph node metastases.

Latent human papillomavirus infection in pregnant women at term: a case-control study.

Cervicovaginal lavages from 752 pregnant women at term were investigated by polymerase chain reaction to evaluate human papillomavirus (HPV) infection prevalences and were compared with cervicovaginal samples from two series of nonpregnant subjects (504 healthy women attending a family planning service and 560 symptomatic patients attending a vaginitis outpatient service). The odds ratios (ORs) of HPV infection were computed by conditional logistic regression analysis on age-matched sets. In pregnant women, the overall risk of HPV infection was about the same as in nonpregnant healthy subjects (adjusted OR, 0.90; 95% confidence interval [CI], 0.51-1.58) and was 50% less than in patients with symptomatic vaginitis (adjusted OR, 0.48; 95% CI, 0.30-0.76). Moreover, the prevalence of oncogenic HPV types 16 or 18 (or both) was lower in pregnant women (P = .015 and P = .0018 respectively).

Human papillomavirus types 16 and 18 infection in infiltrating adenocarcinoma of the cervix: PCR analysis of 138 cases and correlation with histologic type and grade.

The authors investigated by PCR 138 infiltrating cervical adenocarcinoma (27 grade 1, 76 grade 2, and 35 grade 3) for the presence of human papillomavirus (HPV) 16 and 18 infection. They included 95 (68.8%) mucinous and 43(31.2%) non-mucinous tumors. The overall prevalence of HPV infection was 84.8%; 28.3% of the cases were positive for HPV 16, 29.7% for HPV 18, and 26.8% for both HPVs. Amplification of HPV 16 and 18 negative cases with consensus primers MY09/MY11 failed to yield any additional tumors with HPV DNA sequences. Patients with HPV infection were younger than the patients who were HPV-negative (P = .001). The type of HPV was unrelated to age. Human papillomavirus infection was found in 95.8% mucinous and in 60.5% non-mucinous tumors (P < .001), with even distribution among grade 1, 2 and 3 adenocarcinoma. Our findings confirm the key role of HPV 16 and 18 in the development of cervical adenocarcinoma, particularly in mucinous histotypes. The absence of HPV infection, the old age of patients and the non-mucinous differentiation may identify a subset of cervical adenocarcinoma with different etiopathogenesis.