Alexander Kirschenbaum

Effect of the Addition of Estrogen to Medical Castration on Prostatic Size, Symptoms, Histology and Serum Prostate Specific Antigen in 4 Men with Benign Prostatic Hypertrophy

A total of 4 men with benign prostatic hypertrophy who underwent medical castration therapy with a long-acting gonadotropin-releasing hormone agonist (leuprolide) for more than 6 months elected to add an estrogen transdermal patch (0.05 mg. to the skin biweekly) to the leuprolide regimen. The average prostatic size (transrectal ultrasound), serum prostate specific antigen (PSA) levels and symptoms of prostatism were dramatically decreased with leuprolide alone. The addition of estrogen for 6 months did not result in any change in prostate size, symptoms or serum PSA levels over that seen with leuprolide alone. The development of squamous metaplasia was noted in 1 man with leuprolide alone and in 1 man after the addition of estrogen. Immunohistochemical staining with anticytokeratin 903 antibodies reveals that squamous metaplasia appears to arise from prostatic basal cells. We postulate that the target cell for estrogen action in the prostate is the prostatic basal cell. In the absence of androgen the only direct effect of estrogens is the induction of squamous metaplasia.

Primary renal carcinoid tumor

We report a case of primary renal carcinoid tumor. Only 13 prior cases are documented in the literature. The tumor fulfilled both histologic and immunochemical criteria for carcinoid. In addition, we employed new diagnostic modalities (i.e., magnetic resonance imaging and chromogranin-A levels) not used in prior published reports. A review of the literature is presented.

The effect of dihydrotestosterone and culture conditions on proliferation of the human prostatic cancer cell line LNCaP

Cell density, nutritional state, and serum factors modify the growth response of LNCaP human prostatic cancer cells to dihydrotestosterone. Evaluation of growth response to dihydrotestosterone requires logarithmic transformation of cell count or thymidine incorporation data. Under conditions of dose response, growth increases with cell density but no significant interaction of dihydrotestosterone with cell density was found under optimal culture conditions. The frequency of media change was a significant factor in modulating dose response. When cells from cultures maintained at different feeding periods were plated at different cell densities of (trypan blue) viable cells, significant effects of plating density on dihydrotestosterone response were found. Dihydrotestosterone protects cells under the adverse effects of media deprivation. Under the extreme adverse effects of serum deprivation, cells respond to dihydrotestosterone even under conditions of increasing cell loss. The effects of dihydrotestosterone on final cell density were significant. In the absence of serum, the elongated cells of LNCaP assume a round shape, but many remain adherent to the culture dish and can be restored to normal morphology by serum. A number of growth factors fail to restore normal morphology that was completely restored by a combination of fibronectin and dihydrotestosterone. We have not developed a practicable serum-free system for LNCaP.

Preclinical evaluation of PDS (polydioxanone) synthetic absorbable suture vs chromic surgical gut in urologic surgery

A variety of suture materials are available for use in urologic surgery. Urologists have relied on absorbable suture materials which provide transient strength in anticipation that healing will occur before the suture is absorbed. Absorbable sutures thus decrease the chance of stone formation, known to occur on suture material in direct contact with the urinary stream. This report compares the breaking strength retention of polydioxanone (PDS) suture and chronic surgical gut after in vivo residence in the urinary bladder and subcutaneous tissue of the dog.

Update on oncogenes and relevance in urology

Although the concept of an association between genes and cancer is not a new one, the precise mechanism by which genes are responsible for cancer development has remained elusive for decades. Recent developments in microbiology and genetic engineering possibly have put us on the brink of understanding these mechanisms. The identification and characterization of socalled “oncogenes,” genes presumably involved in the regulation of cell growth and in the loss of growth regulation, have refired intense study of genetic factors that may determine tumor development . The purpose of this article is to review recent evidence that has enhanced our understanding of the genetic basis of cancer development and to describe current directions in which such work is leading. We shall attempt to present this work in the context of tumors of the genitourinary tract. In so doing, we will also attempt to describe the clinical relevance of these exciting advances to urologic oncology and possibly also to our approach in the treatment of urologic neoplasia. Historical Perspectives The association between oncogenes and cancer is based on the recent convergence of several independent lines of investigation. It is important to understand that the observations underlying these associations occurred as isolated and often unrelated findings rather than in related sequence, and that their relevance to the genetic basis of cancer represents in many instances only a retrospective assessment.

Serum of patients with prostatic cancer or benign prostatic hypertrophy contains nonpolar testosterone.

We have previously described a nonpolar form of radioimmunoassayable serum testosterone (NPT) not measured by available antitestosterone antibodies. It is detected by mild alkaline hydrolysis of the petroleum ether extract of serum and subsequent radioimmunoassay. The properties of NPT are consistent with that of a fatty acid ester of testosterone or dihydrotestosterone. The serum of young males contains 1 to 3 ng/ml NPT, but it is not detected in female serum. We measured serum testosterone and NPT levels in 36 men between 58 and 87 years of age. Seventeen subjects with advanced prostatic cancer (NPT 1.70 +/- 1.44 ng/ml) were compared with a control group consisting of six patients with benign prostatic hypertrophy (BPH) and 13 patients with no prostatic disease (NPT 0.72 +/- 0.46, P = 0.017). There was no significant difference between BPH patients and patients with no prostatic disease; the results were pooled. The concentration of NPT in prostatic cancer patients but not in controls was inversely correlated with that of testosterone. Immunoassayable testosterone was present in the serum of two orchiectomized patients and, therefore, cannot derive solely from the testes.

Case Report: Biliary Obstruction Complicating Extracorporeal Shock Wave Lithotripsy

AbstractAn elderly woman with a solitary right kidney and unrecognized cholelithiasis underwent extracorporeal shock wave lithotripsy for renal calculi. Postoperatively, biliary obstruction developed that required emergency surgery. Pathological evaluation of the biliary calculi revealed superficial fragmentation. It is suggested that extracorporeal shock wave lithotripsy was responsible for the gallstone fragmentation and resultant bile duct obstruction.

Ureteroscopic management of ureteral cholesteatoma

Cholesteatoma of the upper urinary tract is a rare nonmalignant condition histologically characterized by keratinized desquamative squamous metaplasia. Most cases have been managed by extensive ablative surgery. We describe a new approach in the diagnosis and management of a patient with ureteral cholesteatoma using transurethral ureteroscopy and evacuation.

Oncocytoma and Metastatic Potential: Myth or Reality?

Oncocytomas, apparently benign renal tumors that have been described with increasing frequency in recent years, are discussed in terms of their place in the general pathways of tumor development in the kidney. In this context, the involvement of oncogenes, the origin of these lesions, is also considered.

Oncogenes and genitourinary neoplasia

The concept of an association between genes and cancer is not a new one. Over a century ago Broca observed a hereditary pattern of cancer among members of his wife’s family [1]. Although others also described a familial nature of certain conditions, this did not necessarily prove a genetic basis for disease. Indeed, the very concept of genes was unknown at the time. However, such observations stimulated intense interest in the causes of uncontrolled cell growth and the factors responsible for the formation of specific tumors.