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Biomedical subjects

G Bevilacqua

Publications and source records attributed to G Bevilacqua.

233 records · Page 13Linked to original sources
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[Nosological limits of wet lung syndrome. Clinical and radiological investigations (author's transl)].

41 hyaline membrane diseases (H.M.D.), 39 fetal aspiration syndromes (F.A.S.) and 81 wet lung syndromes (W.L.S.) observed during the last four years have been critically examined by the Authors. Anamnestic, clinic and radiological findings have revealed how it is difficult to make a differential diagnosis between W.L.S. and the two other neonatal respiratory disorders and therefore how it is difficult to classify the W.L.S. as an autonomous nosological entity. Therefore the AA. think that the neonatal respiratory disorders can be divided in only two groups: H.M.D. and F.A.S., and suggest the hypothesis that W.L.S. is not an autonomous nosological entity but may be only a milder clinic and radiological aspect of the two other syndromes.

Diagnosis, Differential↗
PubMedDate not supplied

Genomic PCR-SSCP analysis of the metastasis associated NM23-H1 (NME1) gene: a study on colorectal cancer.

To facilitate further mutational analysis of NM13-H1, a human metastasis suppressor gene, we have established its genomic organization. NM23-H1 is composed of five exons, spanning a genomic DNA fragment of 10 kb. Using oligonucleotide primers flanking each exon, PCR-SSCP analysis was performed on genomic DNAs of healthy individuals. A common polymorphism, a C to T transition, was detected 30 nucleotides upstream from the 5' splice site flanking exon 1. As NM23-H1 allele loss and altered expression have been reported in colorectal cancer, genomic DNAs of 20 colorectal tumors were analyzed for the presence of gene-specific mutations by PCR-SSCP: no abnormal sequences were detected within the coding and splice site regions of the NM23-H1 gene. This finding suggests that NM23-H1 mutations are rare events in human colorectal cancer.

Base Sequence↗
PubMedDate not supplied

Preoperative serum antibodies against the p53 protein in patients with ovarian and endometrial cancer.

Antibodies against the p53 protein were measured with a sandwich-type enzyme-linked immunosorbent assay in blood samples preoperatively collected from 30 patients with ovarian cancer and 30 patients with endometrial cancer. Anti-p53 antibodies were detected in 33.3% of patients with ovarian cancer, comprising 22.2% of the 9 patients with stage I-II disease, 30.8% of the 13 patients with stage III disease, and 50.0% of the 8 patients with stage IV disease. Anti-p53 antibodies were found in none of the 4 patients with well differentiated tumors and in 38.5% of the 26 patients with moderately or poorly differentiated tumors. Among the 21 patients with stage III-IV disease, a complete clinical response to front-line platinum-based chemotherapy was obtained by 46.2% of the 13 patients without anti-p53 antibodies and 25.0% of the 8 patients with anti-p53 antibodies. Antibodies against the p53 protein were detected in only 6.7% of patients with endometrial cancer. The low incidence of anti-p53 antibodies in patients with endometrial cancer seems to suggest that the serum assay of these autoantibodies has a limited clinical relevance in the management of this malignancy. On the other hand in patients with ovarian cancer the incidence of serum anti-p53 antibodies is relatively high, and, moreover, it seems to increase with tumor stage and grade and seems to be associated with a lower response rate to chemotherapy. However, the small number of patients did not allow us to obtain statistically significant differences.

Adult↗
PubMedDate not supplied

Genetic instability, p53 and nm23 mutation and clinicopathological features in rectal carcinoma.

Defective DNA mismatch repair proteins fail to correct replication errors (RERs). These defects may lead to secondary, mutation of oncogenes and tumor suppressor genes. Microsatellite instability might be a marker of such replication errors. Eighteen rectal tumors were examined to evaluate genetic instability, in sporadic rectal cancer by PCR. RERs were observed in 27.8% of the cases. No significant difference was noticed between RER+ and RER- patients as far as prognosis, clinicopathological features and p53 gene mutation are concerned. The incidence of nm23 gene mutation was the only statistically significant difference between the 2 groups. Three patients with only one altered microsatellite showed advanced tumor and nm23 gene mutation. Two cases with 5 altered microsatellites and nm23 gene mutated are disease-free: in one of them the p53 gene was also mutated. Probably more than one altered microsatellite is necessary to protect from the effects of secondary mutations.

Adult↗
PubMedDate not supplied

Determination of angiogenesis in human neoplasms: current prognostic and therapeutic implications.

The growth of solid tumours beyond a certain mass is strictly dependent on the formation of a vascular bed from a pre-existing host vasculature. This process has been termed OangiogenesisO and its importance in the process of tumour growth and metastasis has recently gained wide acceptance. Studies have been reported in several kinds of human cancers in which the number of microvessels in the most intense areas of neo-vascularisation (Ohot spotsO) have been shown to be strictly related to the development and progression of the tumour. In the majority of these studies highly vascularised tumours showed a poor prognosis and the influence of tumour angiogenesis proved to be independent of conventional prognostic indicators. The evaluation of tumour angiogenesis by quantitative pathology may represent an important prognostic indicator in human cancers and will be increasingly important in the investigation of new therapies directed to inhibiting angiogenesis or targeting tumour vasculature. This review will briefly summarise the current knowledge on the prognostic impact of tumour angiogenesis in human cancers with a final reference to angiogenesis inhibitors which are currently used in phase I/II and III clinical trials.

Antineoplastic Agents↗
PubMedDate not supplied

Multidrug resistance related genes and p53 expression in human non small cell lung cancer.

BACKGROUND: Many genes (mdr1, mrp, DNA topoisomerases II) are known to be involved in the resistance to unrelated drugs (the MDR phenomenon), but the mechanisms of their activation have to be further investigated. MATERIALS AND METHODS: Because several authors showed that p53 mutated gene was able to induce mdr1 overexpression, we evaluated in 51 non small cell lung cancer samples, already tested for p53 mutations, the expression of mdr1, mrp, DNA topoisomerase II alpha and beta mRNAs by qualitative RT-PCR assays. RESULTS: Mutations of p53 were found in 56% of cases. Mdr1 expression was detected in 27%, mrp in 100%, topoisomerase alpha in 82% and beta in 94% of the samples. CONCLUSIONS: It was not possible to detect any relationship between the expression of the MDR-related genes and tumor histological type, stage or lymph node involvement. Nevertheless, a close association between p53 alterations and either mdr1 gene (p = 0.001) or DNA topoisomerase II alpha (p = 0.003) expression was found.

ATP Binding Cassette Transporter, Subfamily B, Mem↗