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O Cussenot

Publications and source records attributed to O Cussenot.

At least 91 records · Page 5Linked to original sources

Laparoscopic fibrin glue ureteral anastomosis: experimental study in the porcine model.

Laparoscopic suturing is still difficult and time-consuming. The aim of this study, using the porcine model, was to evaluate the feasibility, safety, and efficacy of laparoscopic fibrin glue ureteral anastomosis without stay sutures for approximating the ureteral ends. In five pigs, after bilateral cystoscopic insertion of a 7F ureteral catheter, each upper ureter was laparoscopically dissected free and transected with scissors. The ureteral ends were then approximated with two atraumatic grasping forceps, and the fibrin glue was applied over the anastomotic site using a specially designed catheter (Duplocath). After waiting 5 minutes for the sealant to adhere, the forceps were removed, and the anastomotic site was examined for any early disruption. The ureteral stents were then pulled back to the distal ureter, and retrograde ureteropyelography was accomplished bilaterally in order to assess the immediate patency of the anastomoses. The animals were sacrificed and the ureteral anastomoses surgically removed for histologic examination. The operative time after insertion of the trocars averaged 15 minutes for each anastomosis, and no early disruption was observed after withdrawal of the grasping forceps. Immediate ureteral fluoroscopic patency was achieved in all 10 ureteral anastomoses, without leakage in 8 and with minimal leakage in 2. Histologic examination revealed a mild inflammatory reaction in the serosa with no modifications of the mucosa or the muscularis. Subsequently, two pigs were subjected to the same procedure bilaterally and not sacrificed. These two animals died with enormous urinomas on postoperative days 6 and 8. In each case, the anastomotic site was completely disrupted on one side, while the other side remained grossly patent. However, histologic examination of these latter anastomoses revealed no real coaptation of the ureteral ends, while demonstrating complete eversion of the mucosa. In conclusion, fibrin glue ureteroureterostomies, although easy to accomplish, are not safe enough to be used without stay sutures in laparoscopic surgery.

Anastomosis, Surgical↗

Argon laser induced autofluorescence may distinguish between normal and tumor human urothelial cells: a microspectrofluorimetric study.

PURPOSE: To assess the ability of argon laser-induced autofluorescence spectroscopy (LIAFS) to discriminate normal from tumor human urothelial cells. MATERIALS AND METHODS: Emission spectra of single living cells excited at 488 nm. have been studied with confocal microspectrofluorimeter. RESULTS: Cellular autofluorescence appeared as a broad band with a maximum in the same "green" spectral range, 550 to 560 nm., probably corresponding to oxidized flavoprotein emission. However, the maximum autofluorescence intensity of normal urothelial cells was much higher, 10 times (p<0.0001) that of any of the tumor cell types tested. CONCLUSIONS: These results, suggesting a significantly reduced oxidized flavoprotein concentration in tumor urothelial cells, should prompt us to evaluate argon LIAFS as a potential tool to detect occult urothelial severe dysplasia and carcinoma in situ.

Argon↗

Plasma neuroendocrine markers in patients with benign prostatic hyperplasia and prostatic carcinoma.

PURPOSE: Approximately 50% of all malignant prostatic tumors contain neuroendocrine cells, which cannot be attributed to small cell prostatic carcinoma or carcinoid-like tumors, and which represent only 1 to 2% of all prostatic malignancies. Only limited data are available concerning the plasma levels of neuroendocrine markers in patients with prostatic tumors. Therefore, we determine the incidence of high plasma levels of neuroendocrine markers in patients with benign and malignant prostatic disease. MATERIALS AND METHODS: The presence of elevated plasma neuropeptide levels was investigated in 135 patients with prostatic carcinoma and 28 with benign prostatic hyperplasia. Plasma chromogranin A, neurone-specific enolase, substance P, calcitonin, somatostatin, neurotensin and bombesin levels were analyzed by immunoassays, and were compared to clinical and pathological stages of disease. Plasma prostatic acid phosphatase and prostate specific antigen levels were also determined. All patients were followed for at least 2 years after inclusion in the study. RESULTS: Significantly elevated levels of chromogranin A were detected in 15% of patients with prostatic carcinoma before any treatment. During hormone resistant prostate cancer progression plasma chromogranin A and neuron-specific enolase levels were elevated in 55% and 30% of the patients, respectively. In patients with stage D3 disease survival curves were generated by the Kaplan-Meier method, and log rank analysis revealed a statistically significant difference between groups positive and negative for chromogranin A. Substance P and bombesin were also occasionally elevated in prostatic tumors. Determination of neuroendocrine differentiation by neuron-specific enolase or chromogranin A immunoassays was not helpful in the prediction of progressive localized prostatic carcinoma. CONCLUSIONS: Future studies of plasma neuropeptide levels should confirm whether these parameters can be used as prognostic markers during late progression of prostatic carcinoma or for the selection of patients suitable for evaluation of new antineoplastic drugs to be active against neuroendocrine tumors.

Acid Phosphatase↗

[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↗

[Sexually transmitted diseases in men].

Sexually transmitted diseases (STD) constitute a frequent presenting complaint. The epidemiology of human immunodeficiency virus (HIV) infection is identical to that of STD and must therefore be systematically investigated in the presence of any STD. Chlamydia trachomatis (CT) is involved in the majority of cases of urethritis and epididymitis in young subjects and is present in the urethra of 10% of subjects with a genital ulcer. Genital ulcers are due to either Treponema Pallidum, Haemophilus ducreyi, or Herpes simplex virus: there is little clinicobacteriological correlation and it is therefore essential to perform laboratory examinations in order to establish the diagnosis. The prevalence of venereal vegetations due to HPV viruses has increased markedly over recent years and require effective treatment and surveillance because of the risk of carcinoma induced by viral oncogenesis. Other viral diseases such as hepatitis B are also classified as STD. The main diagnostic techniques used at the present time for each STD are reviewed and the consensually accepted therapeutic protocols are also proposed.

Epididymitis↗

[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↗

Laser induced autofluorescence diagnosis of bladder tumors: dependence on the excitation wavelength.

PURPOSE: We assessed the ability of laser induced autofluorescence spectroscopy to distinguish neoplastic urothelial bladder lesions from normal or nonspecific inflammatory mucosa. MATERIALS AND METHODS: Three different pulsed laser excitation wavelengths were used successively: 308 nm. (xenium chloride excimer laser), 337 nm. (nitrogen laser) and 480 nm. (coumarin dye laser). The excitation light was delivered by a specially devised multifiber catheter connected to a 1 mm. core diameter silica monofiber introduced through the working channel of a standard cystoscope with saline irrigation. The captured fluorescence light was focused onto an optical multichannel analyzer detection system. Device performance was evaluated in 25 patients after obtaining consent and immediately before transurethral resection of a bladder tumor. Spectroscopic results were compared with histological findings. RESULTS: At 337 and 480 nm. excitation wavelengths the overall fluorescence intensity of bladder tumors was clearly decreased compared to normal urothelial mucosa regardless of tumor stage and grade. At the 308 nm. excitation wavelength the shape of the tumor spectra, including carcinoma in situ, was markedly different from that of normal or nonspecific inflammatory mucosa. No absolute intensity determinations were required in this situation, since a definite diagnosis could be established based on the fluorescence intensity ratio at 360 and 440 nm. CONCLUSIONS: This spectroscopic study could be particularly useful to design a simplified autofluorescence imaging device for detection of occult urothelial neoplasms.

Carcinoma in Situ↗

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↗

[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↗

Recurrent cytogenetic alterations of prostate carcinoma and amplification of c-myc or epidermal growth factor receptor in subclones of immortalized PNT1 human prostate epithelial cell line.

To develop an experimental prostate cancer model, we immortalized normal human prostate adult epithelial cells with SV40 large-T antigen. Two sublines were derived in culture, namely PNT1A and PNT1B. They retained the characteristics of prostate epithelial cells, but did not clone in soft agarose. PNT1A occasionally formed undifferentiated adenocarcinoma tumors in nude mice, but only in the presence of matrigel. PNT1A and PNT1B displayed common cytogenetic alterations: a 10q arm deletion, which is a recurrent alteration in prostate carcinoma, chromosome losses and a translocation involving chromosome 5. An extensive study of oncogenic alterations occurring in these cells showed that PNT1A displayed c-myc gene amplification, forming an hsr on chromosome 4, as well as gene amplification, forming an hsr on chromosome 4, as well as c-myc mRNA overexpression, with a faster doubling time (25 hr); moreover, it seemed less sensitive to EGF than PNT1B. PNT1B had a doubling time identical to that of normal cells (48 hr) but displayed EGF receptor gene amplification accompanied by an increased number of EGF binding sites and sensitivity to EGF. Because both cell lines displayed cytogenetic and oncogenic alterations found in prostate cancer, as well as differing malignant potentials, they represent an interesting model for studying the progression of prostate tumors.

Adult↗

A microdissection approach to detect molecular markers during progression of prostate cancer.

To investigate the underlying mechanisms of carcinogenesis, we have developed a technique to determine the frequency of genetic changes in prostatic carcinoma tissue. We have demonstrated that at a ratio of between 1:4 and 1:9 mutant-normal alleles, the signal from a mutant TP53 allele is not apparent after polymerase chain reaction (PCR) amplification and further direct sequencing or single-strand conformation polymorphism (SSCP) analysis. To bypass this problem, which is inherent in the heterogeneity of the prostate tissue and of the tumour, we selected areas of graded prostate tumours (Gleason score) from cryosectioned preparations and microdissected these cells (20-100 cells). After anionic resin removal of proteins, PCR amplification of TP53 gene exons 5/6 and SSCP analysis, an abnormal SSCP band shift was observed in suspected tumour cells, compared with microdissected stromal cells used as an internal control, while (1) a crude preparation of tissue DNA carrying the tumour did not show any abnormality and (2) immunostaining by a set of monoclonal antibodies against TP53 protein remained negative. Nucleotide sequence analysis of the different bands confirmed the presence of a mutation in the TP53 gene exon 6 position 13,336 in an abnormal band for one specimen, while no mutation was detected in the normal SSCP band. By targeting recognised tumour cells we can find DNA mutations which are undetectable using the standard technique of whole-tissue DNA extraction, particularly in a heterogeneous tumour such as carcinoma of the prostate.

Base Sequence↗

Subcutaneous urinary diversions for palliative treatment of pelvic malignancies.

PURPOSE: We developed 2 subcutaneous urinary diversion techniques, pyelovesical bypass and anterior cutaneous nephrostomy, to improve the quality of life of patients undergoing permanent palliative percutaneous nephrostomy. MATERIALS AND METHODS: A total of 21 patients underwent either pyelovesical bypass (19) or anterior cutaneous nephrostomy (13). Technically, the percutaneous nephrostomy tube is replaced by a self-retaining expanded polytetrafluoroethylene-silicone tube tunneled underneath the skin. The distal extremity can be either introduced into the bladder, creating a pyelovesical bypass, or brought out directly through a cutaneous orifice, creating an anterior cutaneous nephrostomy. RESULTS: No tube was dislodged and none became obstructed due to incrustation or angulation. Standard percutaneous nephrostomy was necessary in 1 patient in each group. Improvement in the quality of life was stressed by all patients. Pyelovesical bypass eliminates external drainage and anterior cutaneous nephrostomy performed when the bladder is no longer functional allows for the creation of a single, easily dressed anterior stoma. CONCLUSIONS: Pyelovesical bypass and anterior cutaneous nephrostomy constitute valuable alternatives to standard permanent palliative percutaneous nephrostomy.

Aged↗

Tumour-associated trypsin inhibitor and renal cell carcinoma.

In the absence of a specific marker for renal cell carcinoma (RCC), we evaluated the tumour-associated trypsin inhibitor (TATI) in patients with RCC. Between November 1990 and November 1993, 63 patients with RCC and 23 patients with benign renal disease underwent a competitive radioimmunoassay of TATI. The cutoff value was defined on a series of serum samples of 96 healthy subjects (normal n < 20 micrograms/l, then 25 micrograms/l after April 1993). We related the value of TATI to the tumour stage and compared the sensitivities of TATI and other markers (CEA, CA 15-3, CA 125, CA 19-9, ferritin). In 24 patients the TATI assay was repeated 3-12 months after radical nephrectomy. 15 patients with benign disease had a normal value of TATI (specificity: 65%). 44 of the 63 patients had a value of TATI above the cutoff point (sensitivity: 69%). Sensitivities of CEA, CA 15-3, CA 125, CA 19-9 and ferritin were 5, 10, 13, 5, 35%, respectively. The TATI value was correlated with the stage of the disease. Among the 15 patients without metastasis, the mean preoperative value was 112 micrograms/l (14-760) versus 46 micrograms/l (24-180) postoperatively. In the 9 patients with metastasis, the preoperative mean value was 100 micrograms/l (20-434) versus 240 micrograms/l (22-544) postoperatively. TATI showed a better sensitivity than other markers for RCC but its specificity is limited. Nevertheless it can be useful for a postoperative follow-up. TATI remains one of the best serum markers for RCC.

Biomarkers, Tumor↗

[The role of the laser in urology].

There is currently a renewed interest in laser in the field of urology, essentially for the treatment of benign prostatic hypertrophy, as a result of recent developments in the field of fibres. Laser is light coherent in time and space emitted continuously or in pulses. Only its thermal and photochemical properties are used in urology. Endoscopic coagulation of superficial bladder tumours by Nd YAG laser does not seem to be better than classical endoscopic resection, at the present time, as although it is less haemorrhagic, it does not decrease the recurrence rate. Photochemotherapy of bladder carcinoma in situ still constitutes a complex treatment protocol reserved for specialized centres. Lastly, upper urinary tract tumours can be treated by Nd YAG laser coagulation, in rare indications which are the same as those of ureteroscopic or percutaneous resection. The recent development of lateral firing laser fibres and contact tip fibres has led to a renewed interest in laser in benign prostatic hypertrophy. Two different techniques have been proposed: Nd YAG laser coagulation under direct visual or ultrasound control (TULIP), which gives delayed objective results (two or three months) and contact tissue vaporization (Nd YAG, diode), whose effects are more immediate. In both cases, intraoperative bleeding is minimal and the length of hospital stay is decreased, but the duration of urine drainage remains to be defined. Endoscopic pulsed laser urinary lithotripsy (dye, Ho YAG), although effective and atraumatic, is not justified at the present time because of its high cost compared to mechanical percussion lithotripters. Lastly, laser treatment for urethral stricture has not been found to be superior to classical scalpel urethrotomy and laser tissue welding is still in the experimental stages. In conclusion, laser technology, especially fibers, has currently reached an important phase of development with applications for urological disease, essentially in the treatment of benign prostatic hypertrophy in order to reduce the morbidity of classical endoscopic resection. However, other urological applications of laser could be validated in the near future due to the development of less expensive lasers (diode) and/or with multiple functions (Ho YAG).

Humans↗

[Carcinoma of Bellini's tubules].

Carcinoma of the papillary ducts of Bellini is a rare form of renal cancer. Patients are usually asymptomatic middle-aged men who frequently have metastatic disease at the time of diagnosis. The diagnosis is based on histological examination of the nephrectomy specimen with a precise immunohistochemical examination. Radical nephrectomy is the first-line treatment and adjuvant chemotherapy, recommended by certain authors, does not appear to improve the usually poor prognosis of these tumours.

Adenocarcinoma↗

[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↗

[Functional properties of a new line of immortalized human endothelial cells].

An immortalized human endothelial cell line was obtained by transfecting umbilical vein endothelial cells in primary culture with plasmid pMK16 containing SV40 replicated origin defective gene. The essential functional properties demonstrated in these immortalized human endothelial cells also retaining the classical phenotypical characteristics of endothelial cells in primary culture are: (1) endothelin-1 secretion; (2) capacity to convert big endothelin-1 into endothelin-1; (3) the capacity to secrete IL1 beta and IL6 interleukins both spontaneously and after lipopolysaccharide (LPS) stimulation; (4) arginine transfer from the extracellular to the intracellular medium. Such stable cell line could facilitate studies of regulation of endothelin-1 production; (5) No-synthase activity; (6) binding and metabolisation of acetylated low-density lipoproteins.

Arginine↗

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↗