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G Guanti

Publications and source records attributed to G Guanti.

79 records · Page 5Linked to original sources
PubMedDate not supplied

Molecular genetics of hereditary non-polyposis colorectal cancer (HNPCC).

The story of the molecular genetics of HNPCC is one of astonishingly rapid achievements. In just 16 months, from May 1993 to September 1994, four different genes, namely hMSH2, hMLH1, hPMS1 and hPMS2 have been identified and demonstrated to be associated with the disease. Their cloning was facilitated by the finding that tumor cells in HNPCC patients display a hypermutability of DNA short tandem repeats (microsatellite instability). In fact, HNPCC associated genes are the human counterparts of genetic elements known to control the fidelity of DNA replication in lower organisms. So far, more than 50 germline mutations of hMSH2 and hMLH1 genes have been reported in HNPCC kindreds. In addition, somatic mutations have been documented in hereditary as well as sporadic cancers. Unfortunately, the molecular diagnosis of HNPCC is hampered by the lack of mutational "hot spots" and of clearly defined genotype-phenotype correlations and different screening methods are to be employed for the analysis of affected and at-risk individuals.

Colorectal Neoplasms, Hereditary Nonpolyposis↗
PubMedDate not supplied

Lack of effect by prostaglandin F2alpha on the proliferation of the HCT-8 and HT-29 human adenocarcinoma cell lines.

A variety of studies have supported the finding that regular intake of aspirin or non-steroidal anti-inflammatory drugs can affect colorectal cancer carcinogenesis by decreasing the synthesis of prostaglandins (PGs). We report that PG F2alpha, in the presence of indomethacin, did not stimulate the proliferation in HCT-8 and HT-29 human colon adenocarcinoma cells. Moreover, in both cell lines fluprostenol, a specific agonist of FP receptors, did not increase intracellular Ca2+ concentration, monitored with the fluorescent dye fura-2. These results indicate that in HCT-8 and HT-29 cells: i) proliferation is not sensitive to PG F2alpha; ii) functional FP receptors are absent. Therefore, either PG F2alpha is not necessarily involved in the proliferation of colorectal mucosa or cell lines other than HCT-8 and HT-29 should be used to assess the role played by PG F2alpha in promoting cell proliferation in colon cancer.

Adenocarcinoma↗