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PubMed1982

[Late urological complications of abdominopelvic radiotherapy. A personal series of 39 cases (author's transl)].

The authors study 39 cases of late genitourinary sequelae following abdominopelvic radiotherapy. Several points appear to be of interest: - the mean latent period was 3.5 years for bladder sequelae and 4 years for ureteric complications. Fistulae could develop on average 14 years after radiotherapy; - the possibility of ureteric complications in the form of stenosis after radiotherapy, exclusive of associated surgery; - all lesions were purely due to radiation, excluding recurrences of neoplasm; - bladder complications had striking symptoms with dysuria and haematuria. Ureteric stenosis was sometimes found by chance, being latent; - associated digestive tract radiation lesions were seen in 1 case in 4; - the frequent need for surgery, since this was required in 30 patients out of 39. The operations performed were often extensive; - the grave nature of surgical operations including a digestive phase in these patients who had received large doses of radiation. Peritonitis due to the breakdown of sutures was a notable source of mortality; - one of the great difficulties in investigating such patients is to be able to confirm the purely radiation aetiology of these complications, bearing in mind that amongst urological complications following the treatment of pelvic carcinomas, the majority are related not only to radiation but also to recurrence of neoplasm.

Abdominal Neoplasms↗
PubMed2001

Genomic imbalances in 61 renal cancers from the proximal tubulus detected by comparative genomic hybridization.

Comparative genomic hybridization (CGH) has been applied to characterize 61 primary renal cell carcinomas derived histogenetically from the proximal tubulus. The tumor samples comprised 46 clear-cell renal cell carcinomas (ccRCCs) and 15 papillary renal cell carcinomas (pRCCs). Changes in the copy number of entire chromosomes or subregions were detected in 56 tumors (92%). In ccRCCs, losses of chromosome 3 or 3p (63%); 14q (30%); 9 (26%); 1 and 6 or 6q (17% each); 4 and 8 or 8p (15% each); 22 (11%); 2 or 2q and 19 (9% each); 7q, 10, 16, 17p, 18, and Y (7% each); and 5, 11, 13, 15, and 21 (4% each) were detected. Most frequent genomic gains in ccRCC were found on chromosome 5 (63%); 7 (35%); 1 or 1q (33%); 2q (24%); 8 or 8q, 12, and 20 (20% each); 3q (17%); 16 (15%); 19 (13%); 6 and 17 or 17q (11% each); and 4, 10, 11, 21, and Y (9% each). In pRCCs, gains in the copy number of chromosomes 7 and 17 (7/15, each) and 16 and 20 (6/15, each) were frequent. One pRCC showed amplification of subchromosome regions 2q22-->q33, 16q, 17q and the entire X chromosome. In pRCC, losses were less frequently seen than gains. Losses of chromosomes 1, 14, 15, and Y (3/15 each) and 2, 4, 6, and 13 (2/15 each) were observed. In ccRCCs, statistical evaluation revealed significant correlations of chromosomal imbalances with tumor stage and grade, i.e., a gain in copy number of chromosome 5 correlated positively with low tumor grade, whereas a gain of chromosomes 10 and 17 correlated positively with high tumor grade. Furthermore, loss of chromosome 4 correlated positively with high tumor stage.

Adenocarcinoma, Clear Cell↗