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Biomedical subjects

J Sheinfeld

Publications and source records attributed to J Sheinfeld.

62 records · Page 4Linked to original sources

Direct fibrinolytic therapy for renal vein thrombosis: radiographic followup.

Renal vein thrombosis is a rare entity whose true incidence is unknown. The disease occurs most frequently in patients with the nephrotic syndrome but it also can occur in the presence of other hypercoagulable states. Previous modes of therapy have been limited to systemic anticoagulation or surgery. We report a case of successful dissolution of acute renal vein thrombosis using direct fibrinolytic therapy, which was documented radiographically during treatment and at 3-month followup.

Female↗

Ultrafiltration evidence of ion binding by macromolecules in urine.

In an effort to rationalize the difference between computed estimates of urinary calcium oxalate supersaturation and estimates obtained by equilibrating urine with solid calcium oxalate, we examined ultrasfiltered urine for the binding of urinary ions. Urine was passed through a filter with a nominal passage cutoff of 1000 Daltons. The average reduction in concentration of the ultrafiltrate was 12.7 per cent for oxalate, 11.9 per cent for phosphate, 9.4 percent for calcium, 7.6 per cent for magnesium, and 6.9 per cent for sodium. From these results we conclude that calculations of urinary ion equilibrium will give better estimates if the composition of ultrafiltered urine is used.

Calcium↗

Genetic studies and molecular markers of bladder cancer.

Target genes implicated in cellular transformation and tumor progression have been divided into two categories: proto-oncogenes which, when activated, become dominant events characterized by the gain of function, and tumor suppressor genes which become recessive events characterized by the loss of function. Alterations in proto-oncogenes and tumor suppressor genes seem equally prevalent among human cancers. Multiple mutations appear to be required to conform the malignant phenotype. Proto-oncogenes are activated mainly by point mutations; however, amplification and translocation events are also common. Tumor suppressor genes are inactivated by an allelic loss followed by a point mutation of the remaining allele. The prototype suppressor genes are the retinoblastoma (RB) gene and the TP53 (also known as p53) genes. Recent studies have shown that inactivation of TP53 and RB occur in bladder tumors that have a more aggressive clinical outcome and poor prognosis. We will review the molecular abnormalities associated with both oncogenes and tumor suppressor genes in bladder tumors, and also discuss the potential clinical use of their detection. The implementation of objective predictive assays to identify these alterations in clinical material will enhance our ability to assess tumor biological activities and to design effective treatment regimes.

Alleles↗

Cell surface differentiation antigens of normal urothelium and bladder tumors.

Bladder cancer ranks as the third most common malignancy among men and tenth among women. Superficial transitional cell carcinomas (stage Ta, Tis, and T1) account for approximately 70-80% of these tumors, while the remaining 20-30% are invasive (T2, T3, and T4). Approximately 70% of superficial tumors will have one or more recurrences, with 25% of these expressing a higher histologic grade and 10-15% subsequently developing invasive and/or metastatic disease. The detection and prediction of tumor recurrence and/or tumor progression is crucially important if timely and appropriate therapy is to be instituted. Conventional histopathologic evaluation usually provides definitive diagnosis upon which therapeutic planning is based. However, at present there are no more reliable morphologic indicator to identify which individuals will have recurrent disease or who will progress to invasive and/or metastatic cancer. Recent advances in tumor biology have identified markers that are good candidates for clinical applications in early tumor detection, as well as for the stratification of patients with like-appearing morphological lesions with different biological and clinical behavior. The ultimate goal is to develop predictive assays that would segregate patients with high probability of failures versus patients who would be cured by localized modes of therapy.

Antibodies, Monoclonal↗

Expression of blood group antigens in bladder cancer: current concepts.

Blood group antigens are a group of carbohydrate structures bound to membrane lipids or proteins of erythrocytes and certain epithelial tissues including urothelium. The Lewis antigens are structures that are genetically and biochemically related to the ABO blood group. The ABO and Lewis blood group systems are differentially expressed in the normal urothelium of "secretors" versus "nonsector" individuals. The normal urothelium of "secretors" is rich ABH, Leb, and Ley antigens while the urothelium of "nonsecretors" does not express these antigens. Therefore, deletion of ABH antigens, commonly noted in TCC, can only be reliably ascertained in "secretor" individuals. Neoexpression of the Lewis X antigen (which is absent in normal urothelium) is noted in over 85% of TCC regardless of tumor stage and grade. Immunocytological detection of the Lewis X antigen on exfoliated bladder epithelial cells enhances the detection of urothelial tumor cells, particularly from low grade and low stage neoplasms.

ABO Blood-Group System↗

Enhanced detection of bladder cancer in urine cytology with Lewis X, M344 and 19A211 antigens.

Lewis X, M344 and 19A211, all glycoprotein antigens associated with bladder tumors, were evaluated in urine cytologic specimens from 52 patients with transitional cell bladder neoplasms and from 12 controls. Forty-three of 52 patients had a tumor on a concurrent bladder biopsy, while 9 of 52 patients had a negative biopsy. Of the 43, 27 (62.8%) had positive or suspicious cytology, 35 (81.4%) had positive immunocytochemical reactions with at least one antibody, and 36 (83.7%) had either cytologic or immunocytochemical abnormalities. Of the 15 patients with a low grade tumor (papilloma or grade 1 transitional cell carcinoma), 14 (93.3%) had positive immunohistochemical findings, while 6 (40%) had recognizable abnormal cells on routine cytology. Of 28 patients with a high grade tumor, 21 (75%) had positive immunohistochemical findings, while 21 (75%) had abnormal cytology. Staining of rare epithelial cells was seen in 2 of 12 control cases (specificity, 83.3%). Immunocytochemistry with antibodies to tumor-associated antigens can enhance the cytologic detection of exfoliated low grade bladder epithelial tumor cells.

Antibodies, Monoclonal↗

Tobacco smoking, occupation, and p53 nuclear overexpression in early stage bladder cancer.

Epidemiological studies show an increased risk of bladder cancer associated with tobacco smoking and occupational exposures. Certain carcinogens in tobacco and occupational exposures cause DNA damage and may produce specific mutations. TP53 is considered a common target for carcinogenic agents, and mutations of this gene are reported to be the most frequent nuclear abnormalities in human cancer. In order to investigate the relationship between tobacco smoking, occupations, and altered patterns of p53 expression, we have analyzed a group of 109 incident patients with superficial transitional cell carcinoma of the bladder. We assessed p53 nuclear overexpression by the use of anti-p53 antibody PAb1801 and immunohistochemistry, and identified 45 of 109 patients (41%) displaying p53-positive phenotype. We observed a significant association between the number of cigarettes smoked per day and p53 nuclear overexpression (p = 0.02). The odds ratios were 2.3 for those smoking 1-2 packs per day and 8.4 for smoking more than 2 packs per day. Similar estimates were obtained after controlling for age, sex, and race. Elevated odds ratios were also observed for dye-/ink-related (odds ratio = 2.0; 95% CI, 0.4-9.4) and cooking-related occupations (1.8, 0.6-5.0), although those were not statistically significant. These data support the hypothesis that certain carcinogens derived from cigarette smoking and occupations may induce TP53 mutations, which in turn are involved in early steps of bladder carcinogenesis.

Aged↗