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G Fournier

Publications and source records attributed to G Fournier.

At least 73 records · Page 4Linked to original sources
PubMed1996

[Familial forms of cancer of the urogenital tract: clinical and genetic features].

Familial forms of renal urinary tract and testicular cancers are rare (1 to 2%), in contrast with prostatic cancer (20%). Among these familial cancers, hereditary forms related to a genetic abnormality transmitted to the offspring are now better known and are of particular practical value for the clinician. Their diagnosis can modify the modalities of the patient's treatment in view of the multifocal nature of the tumours within the same organ and/or the frequent bilateral involvement of paired organs. The risk of transmission of the deleterious gene to the offspring requires information and close surveillance of relatives to allow early diagnosis and a better prognosis. When the predisposing gene is known, surveillance can be exclusively directed towards subjects possessing the deleterious gene in view of the increased cancer risk compared to the general population. This is the case for renal cancer in Von Lippel Lindau disease, and nephroblastoma and exceptional tumours of the urinary tract in Lynch syndrome. In the case of prostatic cancer, the most frequent familial cancer, in which hereditary forms represent 9% of cases, the predisposing gene has not been identified, which means that screening should be proposed to all male members of the family over the age of 40 years, due to the earlier age of development of these forms.

Humans↗
PubMed1996

[The PROGENE study, the French project of genetic analysis of familial prostatic cancer: recruitment and analysis].

OBJECTIVES: To initiate a genetic linkage study in order to localize one or several predisposition gene(s) for hereditary prostatic cancer (PC), as various epidemiological studies have demonstrated a possible family aggregation in about 25% of cases. A family segregation study [14] has also shown that a genetic predisposition, with autosomal dominant transmission and high penetrance (88% at 85 years) could be responsible for 9% of all PC. METHODS: A national collection of families with at least 2 cases of PC allowed: 1) identification of families with hereditary forms of PC, 2) creation of a constitutional DNA bank after collecting blood samples from subjects belonging to these families, and 3) a simulation study of genetic linkage analysis prior to microsatellite genotyping. RESULTS: From July 1994 to September 1995, we included 67 families (180 cases of PC). Another 45 families are currently being included. 24 of these 67 families (89 PC, 54 survivors) satisfied at least one of the criteria defined in the study by CARTER et al. for hereditary forms of familial PC. Two families were also included as the 3 patients with PC were second degree relatives. A total of 26 families therefore presented a hereditary form, 18 of which (73 PC, 46 survivors) were considered to be informative for a genetic linkage study (lod score = 4 for theta = 0.001 with an 8 allele marker). The constitutional DNA of 271 individuals of these informative families was extracted from circulating cells obtained from blood samples, immortalized lymphocytes, and the genotyping was initiated for 216 microsatellite markers distributed throughout the genome, an average of every 20 cM. CONCLUSION: Although the recruitment allowed us to identify many informative families for an inherited risk of PC, the predictive study suggested a high probability for localization of a predisposition gene by genetic linkage analysis. It would therefore be possible to identify, within the families concerned, the subjects carrying the genetic anomaly and consequently at high-risk of PC. Finally, the demonstration of the locus would allow cloning and identification of the gene (s) involved.

Female↗
PubMed1996

Differential chromosome allelic imbalance in the progression of human prostate cancer.

PURPOSE: It is widely accepted that an accumulation of genetic alterations plays an important role in the genesis of human cancers. We wished to obtain a comprehensive view of the role of genetic changes in prostate cancer. MATERIALS AND METHODS: We screened 42 primary prostate tumors for allelic imbalance (AI) on 8 autosomal chromosome arms of interest (5q, 7q, 8p, 10q, 13q, 16q, 17q, 18q) by using 2 DNA probes for restriction fragment length polymorphism (RFLP) and 19 microsatellite markers (CA repeats). RESULTS: The most frequent allelic imbalances were observed on 8p (58%) and 16q (53%). AI exceeding 20% was also observed at sites on chromosome arms 7q (46%), 10q (23%), 13q (26%), 17q (34%) and 18q (39%), whereas AI was infrequent on 5q (10%). CONCLUSIONS: The data indicate that a relatively large number of chromosome loci play a part in the etiology and progression of this tumor type. Moreover, our findings suggest that inactivation of a putative tumor suppressor gene on 7q and 13q is an early event in prostate tumorigenesis. In contrast, the close link between an invasive phenotype and AI on 10q and 18q suggests that these genetic alterations occur late in prostate tumorigenesis.

Alleles↗
PubMed1996

[Genetic aspects in cancers of the prostate].

The incidence of clinical prostate cancer varies across countries and ethnic groups. Genetic and epigenetic factors have been suggested as possible explanations to these variations, although no mesological factors with clearly significant effects have been identified. About 20% of patients with prostate cancer have a family history for this disease. Several studies have reported links between prostate cancer and breast cancer, suggesting that the same loci may predispose to both diseases. Identification of one or more inherited genes associated with an increased risk of prostate cancer in some families may be useful for identifying high-risk individuals. The value of this approach has been demonstrated in other familial cancers, such as colon and breast cancer. Current goals of research in this field are to localize the gene(s) that predispose to familial prostate cancer and to identify the molecular alterations related to tumor progression in sporadic and familial prostate cancer.

Humans↗
PubMed1996

[Nephrogenic metaplasia of the urinary tract].

Nephrogenic metaplasia or nephrogenic adenoma is a rare, benign disease arising in the urothelium, whose glandular structure resembles that of renal tubules. More than 350 cases have been reported in the literature, mostly in adults and with a male predominance. The mean age of onset is 31 years for women and 44 years for men (range: 3 weeks-83 years). The tumour can occur at any level of the urinary tract, but bladder involvement is predominant (72%) compared to ureteropelvic (19%) or urethral (9%) lesions. The pathogenesis remains unknown, but the hypothesis usually adopted is metaplastic transformation of urothelial cells in response to prior aggression of the urothelium (surgical operations, stones, trauma, etc.). This tumour is an incidental finding in 20% (bladder) to 90% of cases (urethral or ureteropelvic sites). In the other cases, the presenting symptoms and endoscopic appearance are nonspecific. Pathological examination is able to distinguish nephrogenic adenoma from other tumours (transitional cell carcinoma, adenocarcinoma), although these other tumour types may also be associated. The tumour must be treated conservatively, as there is no risk of malignant degeneration. The elimination of predisposing factors is essential in every case, but is not always able to prevent the recurrences observed in 37 to 60% of cases. In the particular context of renal transplant recipients, in whom this disease has been exceptionally reported, prolonged follow-up is necessary due to the absence of any data concerning the long-term course in this clinical context, and the possible carcinogenic risk of immunosuppressant therapy.

Adolescent↗
PubMed1996

[Endovascular treatment of traumatic and iatrogenic intrarenal arterial lesions by microcoil embolization].

Selective embolization is the best treatment for intrarenal arterial lesions due to trauma or percutaneous procedures with non-controlled or recurrent haematuria. Three male patients, aged 20-70 (mean 49 years), were recently treated in our institution by means of arterial embolization with microcoils. Two patients presented a pseudo-aneurysm and an arterio-venous fistula secondary to percutaneous nephrolithotomy and one patient presented an isolated pseudo-aneurysm due to trauma. In the 3 cases, haematuria (associated with retroperitoneal haemhorrage in one case) was not controlled and required repeated units of blood. Embolization allowed definitive treatment of these lesions. One of our patients with a solitary functional kidney presented rapidly increasing renal failure which completely resolved after arterial embolization. We think that microcoils are the embolic agents of choice to perform endovascular treatment in this indication.

Adult↗
PubMed1995

[Treatment of metastatic cancer of the prostate].

Rising incidence, resulting from diagnosis together with the increasing age in the population, and high mortality combine to make cancer of the prostate a leading cause of death in men. Despite early, and unfortunately overly optimistic, hopes placed in oestrogen therapy, management of patients with metastatic cancer of the prostate remains one of the major challenges facing urologists. For stage D1 (invasion of the iliac nodes), systemic treatment is required, based on androgen deprivation, with five years disease free survival ranging from 55% to 95%. Radical prostatectomy is not indicated in cases of pathologically confirmed macroscopic nodal involvement, but the question remains controversial for patients with microscopic metastases. Pelvic radiotherapy at "curative doses" is not indicated because of the lack of any improvement over hormone therapy alone. Controversies still exist about timing of androgen deprivation (early or deferred endocrine treatment) either for stage D1 or stage D2 asymptomatic patients, but controlled studies are ongoing. Immediate endocrine therapy is however clearly indicated in stage D2 symptomatic disease and leads to improvement of symptoms (mainly bone pain) in up to 80% of patients. When there is spinal cord compression adding corticosteroids can be useful; surgery or radiotherapy are indicated particularly in cases of vertebral instability or neurological involvement. Current protocols are based on maximal androgen deprivation combining medical or surgical castration and anti-androgens. Prognosis is very poor at relapse despite hormone therapy (stage D3). Survival rate at 1 year is only 50%. It is essential that anti-androgens be withdrawn at this time since clinical improvement can be observed in some patients (anti-androgen withdrawal syndrome). None of the second line treatments (hormonal or chemotherapy) have led to any improvement in survival time. Treatments only alleviate patient discomfort and improve quality of life. The lack of progress over the last 50 years in the treatment of advanced stage cancer of the prostate means that the only way to cure future patients will be conditioned by early diagnosis and treatment during the less advanced stages.

Androgen Antagonists↗
PubMed1995

Gene amplifications in advanced-stage human prostate cancer.

Gene amplification is a model of proto-oncogene alterations occasionally observed in human tumors. This amplification can, in some cases, have prognostic value (N-myc in neuroblastoma, c-erbB2 and int-2 in breast cancer, etc.). Amplifications of the proto-oncogenes c-myc, c-erbB2 and int-2 have not yet been report in prostate adenocarcinoma, which, like breast cancer, is hormone dependent. We sought amplifications of these three proto-oncogenes by means of Southern blotting in 15 human prostate adenocarcinoma specimens, most of which were advanced (7 stage C and 6 stage D1 or D2). We confirmed the lack of c-myc and c-erbB2 amplification, regardless of the stage, in contrast to the case of breast cancer. Int-2 amplification was observed in one advanced tumor with bone metastases, out of a total of six stage D tumors. The precise frequency of int-2 amplification and its role in prostate carcinogenesis remain to be determined.

Adenocarcinoma↗
PubMed1995

Impact of prostate size on the outcome of transurethral laser evaporation of the prostate for benign prostatic hyperplasia.

OBJECTIVES: The aim of this study was to evaluate efficacy and safety of transurethral evaporation of the prostate (TUEP) using neodymium:yttrium-aluminum-garnet (Nd:YAG) laser in prostate glands of various sizes. METHODS: One hundred consecutive patients with benign prostatic hyperplasia (BPH) and prostate volumes less than 40 cc (group I, n = 41), 41 to 80 cc (group II, n = 39), and more than 80 cc (group III, n = 20), who had preoperative prostate volume estimation by transrectal ultrasound and had completed a minimum of 3 months' follow-up, underwent TUEP. At baseline, and at 3 and 6 months, American Urological Association (AUA) score, peak flow rate (PFR), postvoid residual urine (PVR), and complications, if any, were documented. RESULTS: There were no significant differences in failure rates, complications, or ability to improve symptom score, PFR, and PVR between patients with prostate glands of various sizes. The mean improvement in PFR at 6 months was: group I, 9.9 cc/s (116%); group II, 7.4 cc/s (81%); and group III, 9.2 cc/s (107%). Reduction in AUA score was: group I, 14.6 (63%); group II, 17.7 (71%); and group III, 16.2 (70%). PVR was: group I, 62.5 cc (51%); group II, 31.4 cc (16%), and group III, 71 cc (83%) (differences not significant). The patients in urinary retention were separately analyzed (group I, 9, group II, 12, and group III, 5) and mean PFR at 6 months was: group I, 18.5 cc/s, group II, 15 cc/s, and group III, 17.1 cc/s. Mean AUA score at 6 months was: group I, 25.8; group II, 21; and group III, 23.6. Mean PVR score was: group I, 370 cc, group II, 439 cc; and group III, 400 cc (differences not significant). Mean postoperative catheterization time was higher in patients with glands larger than 80 cc (2.2 versus 2.9 versus 4.7 days in groups I, II, and III, respectively, P < 0.009 between groups II and III). Incidence of urinary tract infection (10 versus 0%) was greater in patients receiving only 48-hour as opposed to 10-day postoperative antibiotics. CONCLUSIONS: TUEP appears to be a safe and effective treatment for relief of symptoms of BPH and improvement of PFR in patients with all sizes of prostate glands.

Aged↗
PubMed1995

[Severe acute buflomedil poisoning].

The severity of the acute intoxication from buflomedil, a vasodilator with papaverinic and alpha-adrenolytic effects, remains generally underestimated. We report the case of a 18-year-old girl who ingested a high amount of buflomedil. Two hours later, she developed seizures and ventricular arrhythmias. On admission to the ICU, she was in circulatory arrest followed by deep coma with mydriasis (GCS = 3). Buflomedil blood concentration, 2 hours after admission, was 97.3 mg.L-1. Toxicological screening for other drugs was negative. Therapy included external chest compressions tracheal intubation, mechanical ventilation, epinephrine and gastric lavage. The haemodynamic status improved within the first 24 h, although she remained comatose until the fifth day. She was discharged the eight day after her admission. This observation demonstrates that the potential severity of buflomedil poisoning is mainly due to early cardiac complications. Treatment remains purely supportive.

Acute Disease↗
PubMed1995

Epididymo-orchitis after cryoablation of prostate for prostate cancer.

We report two cases of acute epididymo-orchitis developing 4 to 6 weeks after cryoablation for prostate cancer. One patient required a simple orchiectomy for epididymal abscess; the other responded to treatment with antibiotics. Since the occurrence of these two cases, we routinely perform bilateral vasectomy prior to prostate cryoablation. We suggest that an extended course of prophylactic antibiotics may also be needed in order to avoid this complication.

Abscess↗
PubMed1995

[Genetic alterations in localized cancers of the prostate: identification of a common region of deletion on the chromosome 18q].

Prostate cancer is one of the most common malignancies in men. Few authors have attempted to identify consistent genetic alterations at the molecular level in adenocarcinoma of the prostate, but those most frequently reported are loss of heterozygosity (LOH) involving chromosome arms 8p, 10q, 16q, and 18q and inactivation of the TP53 tumor suppressor gene. In order to determine if alterations frequently found in other adenocarcinomas (breast, ovarian, colorectal), including losses of genetic material from chromosome arms 1p, 3p, 7q, 8p, 11p, 17p, 17q, and 18q, are also involved in prostate cancer, we examined 20 localized early-stage prostate tumors. We detected no mutations of the TP53 gene. Allelic losses were found from 7q (33%), 8p (50%), 10q (20%), and 18q (33%). Furthermore, as the first step toward isolating tumor suppressor genes on 18q, we used six polymorphic markers and identified a small common deleted region between the chromosome 18 centromere and the D18S19 locus.

Aged↗
PubMed1995

[Compared diagnostic performances of CKMB measurements by immuno-inhibition and three immunoenzyme methods for the early diagnosis of myocardial infarction].

In 98 patients consecutively admitted in a medical intensive care unit, an aliquot taken from the blood sample withdrawn for the cardiac enzyme admission request has been frozen. After thawing of these 98 aliquots total CK and the creatine kinase MB isoenzyme were measured on the same day. For this last determination, four methods were used and compared: an immunoinhibition method (Merck) and three immunoenzymatic assays (Abbott on IMX; Baxter on Stratus II; Hybritech on single use Icon cylinder). In 19 out of the 98 patients studied the diagnosis of myocardial infarction was made retrospectively by a cardiologist. This diagnosis was established according to the criteria defined by the WHO. The clinical performances (sensitivity, specificity, positive predictive value, negative predictive value) have been calculated for each test according to the following criteria: on the one hand, a cut-off of 8% (reference range of our laboratory) for the immunoinhibition technique; on the other hand, a cut-off defined by the manufacturer together with a cut-off obtained from the ROC curves for the three immunoenzymatic assays. Our results clearly demonstrate that the clinical performances of the three immunoenzymatic CKMB assays are very comparable and appear to be much better than the immunoinhibition method which should be abandoned.

Adult↗
PubMed1995

[Metastasis of renal adenocarcinoma to the spermatic cord and the epididymis: 2 cases].

Metastases of renal cell carcinoma are exceptional in the spermatic cord and epididymis (17 cases reported in the literature). The authors report two cases of metastases occurring 30 and 44 months after radical nephrectomy, respectively. Both patients are alive without metastases after surgical resection, with a follow-up of 4 and 8 years after the diagnosis of renal cancer, respectively. The mechanism of development, usually retrograde venous spread, and the particular features of these metastatic sites are discussed.

Adenocarcinoma↗
PubMed1995

[Gangrene of the external genitalia].

The term gangrene of the male external genital organs is applied to two different entities : Primary gangrene of the external genital organs (5% of cases), also called Fournier's disease, first described in 1883 : gangrene of the integument of the external genital organs in the absence of a local cause, according to an unknown mechanism and with inevitable progression towards a specific distribution of necrosis, regardless of treatment. "Secondary" gangrene of the external genital organs (95% of cases) related to a local, cutaneous, urogenital or gastrointestinal cause, whose course can be modified by early application of appropriate treatment. An early diagnosis is essential : in true Fournier's disease to avoid the systemic complications of this necrosis, and in secondary gangrene to limit the local extension and to prevent systemic complications. In view of the galloping course of the disease and in order to very rapidly reach the diagnosis, many authors recommend : local aspiration, biopsy or search for subcutaneous gas by ultrasound or radiology. Treatment consists of : Antibiotic therapy using two or three antibiotics to cover the usually mixed bacterial flora (Gram positive cocci, Gram negative bacilly and anaerobes). Surgical debridement as required, possibly repeated to excise necrotic zones, to drain collections and for irrigation of cavities. Hyperbaric oxygen therapy. Urinary diversion (cystostomy) or gastrointestinal diversion (colostomy) may be required when either of these two tracts are responsible for the infection, or when diversion facilitates management. Surgical reconstruction (grafts or flaps) as required. The mortality is high, of the order of 20% : < 10% in young patients with a good general condition who are correctly treated after an early diagnosis; > 50% in elderly patients with other concomitant diseases, when diagnosis and treatment are delayed.

Diagnosis, Differential↗
PubMed1995

Loss of heterozygosity at 7q31 is a frequent and early event in prostate cancer.

It is widely accepted that an accumulation of genetic alterations plays an important role in the genesis of human cancers, but little is known about prostate cancer in this respect. Recent studies have identified regions on chromosome arms 8p, 10q, 16q, and 18q that are frequently deleted in human prostate cancer. We have previously described a loss of heterozygosity (LOH) at the Met locus on chromosome band 7q31 in a study of 20 localized prostate tumors. To determine whether a region on the 7q arm is important in the initiation and/or progression of prostate cancer, prostate tissue from 13 patients with confined prostate tumors, 17 with local extracapsular extension, and 13 with metastatic forms were analyzed for LOH, using a DNA probe for RFLP (pMetH) and 8 CA microsatellite repeats (7 on 7q21-q33 and 1 on 7p). Twenty (47%) of the 43 cases studied showed LOH at one or more 7q loci. The most frequently deleted region was chromosome 7q31.1-7q31.2, whereas the centromeric locus on 7q21 was generally conserved. The percentage of LOH was normally distributed around the D7S480 locus. Moreover, the rate of LOH in the 7q31 region was lower in metastatic tumors than in localized tumors. These results strongly suggest the presence of a tumor suppressor gene on the chromosome band 7q31 with an important role in the early stages of prostate cancer.

Chromosomes, Human, Pair 7↗
PubMed1994

Oncogene amplifications in early-stage human prostate carcinomas.

Oncogene amplifications are frequently found in solid tumours and are often associated with more aggressively growing forms of human cancer. The proto-oncogenes c-myc, c-erbB2/neu and the 11q13 band are the most frequently amplified regions in adenocarcinomas of various origins. The present study was undertaken to define whether c-myc, int2/FGF3 (11q13 region) and c-erbB2/neu genes are involved in prostate tumorigenesis. Tumours and peripheral lymphocyte DNA from 21 localized early-stage prostatic carcinomas were analysed by Southern-blot electrophoresis for amplification of the c-myc and c-erbB2/neu genes and the 11q13 region (int2/FGF3). We detected no amplification of these 3 oncogenes in our panel.

Biomarkers, Tumor↗