We hypothesize that expression of proangiogenic genes correlates with the metastatic potential of prostate cancer cells. LNCaP, DU-145, and PC-3 are prostate cancer cell lines with low, moderate, and high metastatic potential, respectively, as we demonstrated by their capacity to invade an extracellular matrix, an established tumor invasion assay. The constitutive gene expression of the proangiogenic factors, vascular endothelial growth factor, intercellular adhesion molecule-1, interleukin-8, and transforming growth factor-beta2, was significantly greater in the more metastatic DU-145 and PC-3 cells as compared with LNCaP cells. Matrix metalloproteinase (MMP)-9 is thought to contribute to the invasive phenotype of tumor cells. PC-3 cells showed increased expression of MMP-9 and membrane type 4-MMP as compared with LNCaP and DU-145. Tissue inhibitors of metalloproteinase 1 and 4 gene expression were elevated in DU-145 and PC-3 cells, but paradoxically, LNCaP cells had undetectable levels of these genes. We transfected and overexpressed MMP-9 in poorly metastatic LNCaP cells and measured their invasive activity. Transient expression of human MMP-9 in LNCaP cells produced a 3-5-fold increase in MMP-9 activity with a comparable increase in invasiveness. Antisense ablation of the expression of MMP-9 in DU-145 and PC-3 cells produced concomitant inhibition of the gene expression of the proangiogenic factors, vascular endothelial growth factor, and intercellular adhesion molecule-1 (ICAM-1). Treatment of DU-145 and PC-3 cells with a selective chemical inhibitor of MMP-9 proteinase activity also inhibited their invasive activity. These results support our hypothesis that metastatic potential of prostate cancer cells correlates with expression of proangiogenic factors.

In renal carcinoma, the inappropriate, unscheduled, or aberrant production of hormones and other serologic markers and the resulting clinical or biochemical syndromes are unique manifestations of this tumor. The elaboration of biologically active factors by renal adenocarcinoma may add a metabolic burden to an already compromised host, and thus affect therapy and prognosis; they should be considered before ascribing symptoms to metastasis or dissemination. Similarly it has been suggested that the elaboration of biologically-inactive peptides and proteins is a very common concomitant of neoplasia and the identification of such factors may facilitate earlier diagnosis and novel therapies in patients with renal carcinoma.

The Constant Composition (CC) kinetics method has been used for studying the mineralization of calcium oxalate monohydrate (COM) at sustained supersaturations in the presence of pre-bladder urine and macromolecules isolated from normal urine and kidney and bladder stones. The method is especially sensitive for investigating the inhibitory activities of these urinary macromolecular components (UMMC) and matrix macromolecular components (MMMC) with a coefficient of variation in growth rate of approximately 2%. Significant COM mineral inhibition was observed in a wide molecular weight region of urine components. Urine removed directly from the kidney showed appreciable inhibitory activity towards COM crystallization. Normal urinary proteins and the dissolved precipitate resulting from urine centrifugation were fractionated by gel filtration. The resulting solutions were mostly COM mineralization inhibitors. Electrodialysis was utilized to isolate the MMMC (greater than 7000 d) of renal and bladder calculi. While these solutions inhibited COM crystallization, they were also found to be calcium binders as measured by the calcium electrode.

Additional histopathological and immunocytological studies were completed on the serially transplanted Warren rat pheochromocytoma. Special efforts were made to characterize features of the primary tumor common to pheochromocytomas, as well as features of the primary tumor commonly found in neuroblastoma. In summary this study found evidence for a composite primary tumor exhibiting a dual differentiative expression of both pheochromocytoma and neuroblastoma. We feel this reflects a possibility that this primary tumor arose from a common progenitor cell in the neural crest.

No AccessJournal of UrologySpecial Article1 Jun 1986Training Grants for the Urological Scientist (Report of Joint Meeting of National Institutes of Health Staff and Concerned Program Directors*) Frank Hinman, Gary E. Striker, and Gerald Sufrin Frank HinmanFrank Hinman , Gary E. StrikerGary E. Striker , and Gerald SufrinGerald Sufrin View All Author Informationhttps://doi.org/10.1016/S0022-5347(17)46014-9AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookLinked InTwitterEmail "Training Grants for the Urological Scientist (Report of Joint Meeting of National Institutes of Health Staff and Concerned Program Directors*)." The Journal of Urology, 135(6), pp. 1125–1126 © 1986 by The American Urological Association Education and Research, Inc.FiguresReferencesRelatedDetails Volume 135Issue 6June 1986Page: 1125-1126 Advertisement Copyright & Permissions© 1986 by The American Urological Association Education and Research, Inc.Metrics Author Information Frank Hinman More articles by this author Gary E. Striker More articles by this author Gerald Sufrin More articles by this author Expand All Advertisement PDF downloadLoading ...

Endometrial carcinoma of the prostate is a unique lesion which contrasts markedly to the more ubiquitous prostatic acinar carcinoma with regard to morphology, clinical manifestations, localization stage at diagnosis, and possibly prognosis. Although endometrial carcinoma of the prostate may occur more commonly than previously recognized, wider recognition and study are essential for further delineation of this lesion. Finally, the inherent limits of endoscopic or of enucleative surgery and the propensity of endometrial carcinoma to present at a low stage suggest in appropriately selected cases that radical prostatectomy or possible external radiotherapy may offer the best opportunity for cure.

In the Wistar/Furth rat, twenty-four hours after unilateral nephrectomy, the remaining contralateral kidney produces maximum amounts of renotropic growth factors. These factors stimulate tumor growth in recipient rats with s.c. Wilms tumor, but have no effect on kidney weight. In tumor-free recipients, kidney hypotrophy results when the factors are administered.

In assessing the inhibitory activity of urine, seeded COM mineralization experiments are usually made in the presence of high urine dilutions (typically 100-fold) but there is some question as to whether these results can be extrapolated to in vivo conditions1,2. In our laboratory, by using a calcium-specific ion electrode protected from the poisoning effects of urinary macromolecules by means of a dialysis membrane, it is now possible to measure rates of mineralization and demineralization of stone components in whole urines with a precision hitherto unattainable.

Torsion of the testis is a common urological emergency. Blunt scrotal trauma also may precipitate an emergency. We recently treated 2 adolescent boys in whom blunt scrotal trauma induced testicular torsion. A retrospective review of the charts of 138 patients explored for acute scrotal pain at our hospital revealed a history of scrotal trauma in 3 of 57 patients (5 per cent) with testicular torsion and 7 of 73 (10 per cent) with torsion of the testicular appendages. The possibility of torsion must be considered in cases of scrotal trauma.

Carcinoma of the urinary bladder is among the more frequent neoplasms in the United States, with an estimated 37,100 new cases diagnosed in 1982, 27,000 in males and 10,100 in females.' In addition, more than 2,000 new cases of carcinoma of the renal pelvis and ureter would be expected during the same one-year period. 1.2 The urethra is less often the site of the presenting carcinoma, but carcinoma in situ of the urethra may coexist with invasive bladder carcinoma, and subsequently become invasive after treatment of the bladder carcinoma. 5 Both stage and histologic grade? influence the course of the disease and response to therapy. The proliferative rate of urothelial carcinoma could be another determinant of prognosis. Prior studies have shown that normal epithelium and carcinomas of the urinary bladder can be labeled in vitro with tritiated thymidine and S-phase cells thereby detected.v Veenema, Fingerhut, and Craff! and Hainau and Dornbernowsky? reported that carcinomas of high histologic grade had a;high thymidine labeling index (TLI) compared with low-grade carcinomas. Histologically low-grade carcinomas with high TLI tended to have rapid clinical courses. 10 Flat transitional cell carcinomas were

No AccessJournal of UrologyEditorial1 Aug 1984Cellular Markers of Renal Adenocarcinoma Gerald Sufrin Gerald SufrinGerald Sufrin More articles by this author View All Author Informationhttps://doi.org/10.1016/S0022-5347(17)49610-8AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookLinked InTwitterEmail "Cellular Markers of Renal Adenocarcinoma." The Journal of Urology, 132(2), p. 322 © 1984 by The American Urological Association Education and Research, Inc.FiguresReferencesRelatedDetails Volume 132Issue 2August 1984Page: 322 Advertisement Copyright & Permissions© 1984 by The American Urological Association Education and Research, Inc.MetricsAuthor Information Gerald Sufrin More articles by this author Expand All Advertisement PDF DownloadLoading ...