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J Couture

Publications and source records attributed to J Couture.

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

Malignant gastrointestinal stromal tumors of the small intestine: a review of 50 cases from a prospective database.

BACKGROUND: Malignant gastrointestinal stromal tumors (M-GIST) are rare mesenchymal tumors originating in the wall of the gastrointestinal (GI) tract. Previous studies have included limited numbers of patients, and most included malignant and benign cases from throughout the GI tract. We reviewed the experience of a single tertiary cancer care center with M-GIST of the small intestine only. METHODS: A prospective database identified all patients seen from 1989 to 1998. Clinical and pathological data, treatment, and outcome were analyzed. Overall median follow-up time was 24 months (range, 1-176 months). RESULTS: Fifty patients (31 male, 19 female) were identified. Mean age at diagnosis was 55 years. Disease was localized in 11 patients, locally advanced (invasion into adjacent organs/peritoneum) in 24 patients, perforated in 4 patients, multiple primary lesions in 2 patients, and distant metastases in 9 patients. All patients underwent resection, which was complete in 70%. Locoregional recurrence (LR) developed in 43% (median, 25 months), and distant metastases in 59% (median, 21 months) of patients at risk. At last follow-up, 14 patients were alive (6 disease-free), 2 had died disease-free, and 34 died with recurrent disease. Overall survival (OS) was similar for localized and locally advanced disease; OS also was similar for patients with multiple primaries and distant metastases at diagnosis. Patients were grouped into three stages: (I) patients with localized and locally advanced disease; (II) patients with perforated; and (III) patients with multiple primaries and distant metastases. Actuarial OS at 5 years was 41% (n = 50)--42% for those with complete resection and 8% for incomplete resection. Univariable analysis showed that earlier stage at diagnosis (P = .001) and completeness of resection (P = .004) predicted for longer OS. CONCLUSIONS: Most patients with M-GIST of the small intestine relapse following resection, but survival may be prolonged. In univariable analysis, stage at presentation and complete resection were significant prognostic variables for OS; grade was not significant. Localized and locally advanced M-GIST of the small intestine have a mean OS > 5 years. Complete resection should be the goal of initial surgical treatment.

Adult↗
PubMedDate not supplied

Molecular biology of colorectal cancer.

Colorectal cancer is a significant cause of morbidity and mortality in Western populations. This cancer develops as a result of the pathologic transformation of normal colonic epithelium to an adenomatous polyp and ultimately an invasive cancer. The multistep progression requires years and possibly decades and is accompanied by a number of recently characterized genetic alterations. Mutations in two classes of genes, tumor-suppressor genes and proto-oncogenes, are thought to impart a proliferative advantage to cells and contribute to development of the malignant phenotype. Inactivating mutations of both copies (alleles) of the adenomatous polyposis coli (APC) gene--a tumor-suppressor gene on chromosome 5q--mark one of the earliest events in colorectal carcinogenesis. Germline mutation of the APC gene and subsequent somatic mutation of the second APC allele cause the inherited familial adenomatous polyposis syndrome. This syndrome is characterized by the presence of hundreds to thousands of colonic adenomatous polyps. If these polyps are left untreated, colorectal cancer develops. Mutation leading to dysregulation of the K-ras protooncogene is also thought to be an early event in colon cancer formation. Conversely, loss of heterozygosity on the long arm of chromosome 18 (18q) occurs later in the sequence of development from adenoma to carcinoma, and this mutation may predict poor prognosis. Loss of the 18q region is thought to contribute to inactivation of the DCC tumor-suppressor gene. More recent evidence suggests that other tumor-suppressor genes--DPC4 and MADR2 of the transforming growth factor beta (TGF-beta) pathway--also may be inactivated by allelic loss on chromosome 18q. In addition, mutation of the tumor-suppressor gene p53 on chromosome 17p appears to be a late phenomenon in colorectal carcinogenesis. This mutation may allow the growing tumor with multiple genetic alterations to evade cell cycle arrest and apoptosis. Neoplastic progression is probably accompanied by additional, undiscovered genetic events, which are indicated by allelic loss on chromosomes 1q, 4p, 6p, 8p, 9q, and 22q in 25% to 50% of colorectal cancers. Recently, a third class of genes, DNA repair genes, has been implicated in tumorigenesis of colorectal cancer. Study findings suggest that DNA mismatch repair deficiency, due to germline mutation of the hMSH2, hMLH1, hPMS1, or hPMS2 genes, contributes to development of hereditary nonpolyposis colorectal cancer. The majority of tumors in patients with this disease and 10% to 15% of sporadic colon cancers display microsatellite instability, also know as the replication error positive (RER+) phenotype. This molecular marker of DNA mismatch repair deficiency may predict improved patient survival. Mismatch repair deficiency is thought to lead to mutation and inactivation of the genes for type II TGF-beta receptor and insulin-like growth-factor II receptor. Individuals from families at high risk for colorectal cancer (hereditary nonpolyposis colorectal cancer or familial adenomatous polyposis) should be offered genetic counseling, predictive molecular testing, and when indicated, endoscopic surveillance at appropriate intervals. Recent studies have examined colorectal carcinogenesis in the light of other genetic processes. Telomerase activity is present in almost all cancers, including colorectal cancer, but rarely in benign lesions such as adenomatous polyps or normal tissues. Furthermore, genetic alterations that allow transformed colorectal epithelial cells to escape cell cycle arrest or apoptosis also have been recognized. In addition, hypomethylation or hypermethylation of DNA sequences may alter gene expression without nucleic acid mutation.

Colorectal Neoplasms↗
PubMedDate not supplied

Chemically processed bovine heterografts of the second generation as arterial substitutes: a comparative evaluation of three commercial prostheses.

The use of chemically processed bovine heterografts is primarily confined to the construction of arterio-venous blood accesses in those patients requiring hemodialysis, plasmapheresis or chemotherapy. The grafts of the first generation i.e. Artegraft and Solcograft are now being supplanted by those of the second generation i.e. Reinforced Artegraft, Solco P and NCGT. We have investigated these three types of arterial prostheses as a biomaterial in terms of sterility, inflammatory response and cytocompatibility and as a blood conduit in dogs in terms of patency and healing. For each type of graft, two implantations were carried out for durations of 4 hours, 24 hours, 48 hours, one week, two weeks, one month, three months, and six months. Therefore a total of 48 grafts were implanted. All grafts but five were patent at sacrifice: thromboses were observed in two Reinforced Artegraft (after two weeks and after one month) and in three NCGT (after 24 hours, after 48 hours, and after one month). Therefore the following patencies were observed: Reinforced Artegraft 14/16, Solco P 16/16 and NCGT 13/16. In all the patent grafts, the healing was reduced to the formation of a pannus along both anastomoses; thrombotic accumulations were observed on the surface defects of the grafts, particularly the NCGT graft. The Reinforced Artegraft presents only minor advantages over the previous Artegraft; the Solco P, somewhat more acceptable is no longer commercially available since the manufacturer withdrew it after early clinical failures. The improvements noted in the bovine heterografts of the second generation appear to be marginal as compared to those of the first generation.

Anastomosis, Surgical↗
PubMedDate not supplied

New frontiers of vascular grafting.

Vascular grafting can be a very rewarding surgical technique: following surgery, most patients will maintain their autonomy and, in many cases, will be able to return to work. Should small diameter calibre substitutes be required, the autologous saphenous vein is the gold standard. If not available, the expanded PTFE is probably the best choice. For medium and large diameters, the polyesters (Dacron) are recommended provided they have a structure adapted to the needs of patients. However, progress in the last few years is not related to improvements in the grafts themselves. The only breakthrough has come with the success of graft seeding. This is the reason why other approaches have been proposed to restore or improve blood flow in atherosclerotic arteries: medication, sympathectomy, dilatation, laser endarterectomy, stent and spinal cord stimulation. All those approaches have more and more precise indications: they can supplement vascular grafting.

Arterial Occlusive Diseases↗