Biomedical subjects

S Bierer

Publications and source records attributed to S Bierer.

5 recordsLinked to original sources

PubMed2005

[Bilateral renal angiomyolipomas with a thrombus in the inferior caval vein. Rare growth pattern of a benign tumor].

Renal angiomyolipomas are mesenchymal tumors that are composed of fat tissue, smooth muscle cells and vessels. These are benign tumors, but in rare cases they show a more aggressive growth pattern with invasion into the venous system but without revealing any signs of malignancy. We report a new case of bilateral renal angiomyolipomas with a caval thrombus in a 36 year old female patient with tuberous sclerosis, and give a brief review of the related literature.

Adult↗

PubMed2005

[Therapy of hormone refractory prostate cancer: new standards, new trends].

Hormone-refractory prostate cancer is diagnosed with increasing incidence and has become a growing challenge for urologists. The improved understanding of the tumor biological mechanisms of the hormone-refractory state has led to innovative therapeutic developments in the field of hormonal and cytotoxic therapies. Recently, two large randomized Phase III trials with docetaxel-based chemotherapy were able to show prolonged survival and a positive influence on pain and quality of life, establishing a new standard of care for these patients. Moreover, bisphosphonates seem to have positive influence on selected patients. In the growing field of molecular targeted therapy, first trials with compounds, such as tyrosine kinase inhibitors, anti-sense oligonucleotides, angiogenesis inhibitors and endothelin receptor antagonists, show promising results in the treatment of patients with hormone-refractory prostate cancer.

Angiogenesis Inhibitors↗

PubMed2005

[Expression of Her2/neu in locally advanced bladder cancer: implication for a molecular targeted therapy].

PURPOSE: The Her2/neu oncoprotein, belonging to the erbB-receptor family, is known to contribute to physiological mechanisms of cell proliferation by intrinsic tyrosine-kinase-activity. Overexpression has been shown for several tumors and is known to influence malignant cell proliferation, metastasis and angiogenesis. The clinical use of Her2-targeting agents has emerged in clinical research. In our study, we analyzed Her2/neu expression in urothelial tumors. MATERIALS AND METHODS: Her2/neu expression was evaluated immunohistochemically (IHC) in 127 patients undergoing radical cystectomy (DAKO- Herceptest). Additionally, fluorescent-in-situ-hybridisation (FISH) was carried out in all immunohistochemically "2+" cases (n = 41) to assess gene amplification. After grading the Her2/neu-overall status, Her2/neu expression was correlated with clinicopathological parameters and survival data. RESULTS: An immunohistochemical Her2/neu expression was found in 95 of 127 cases (74.8 %). Of all 41 cases with "2+" staining (32.2 %), 11 cases (26.8 %) showed positive amplification by FISH. Therefore, including the IHC 3+ cases, a Her2/neu overall status of 22 positive (17.3 %) tumors was assessed. Correlation with clinical data showed a relation to lymph node metastasis (P = 0.06), lymph vessel invasion (P = 0.07) and metastasis (P = 0.002). No further associations with other parameters nor with overall survival (P = 0.73) or disease-free survival (P = 0.63) were found. CONCLUSIONS: Her2/neu upregulation is found in invasive bladder cancer with significant differences in protein expression and gene amplification. The association with lymphogenic and distant metastases implicates a late event in carcinogenesis. Moreover, there was no further association with clinicopathological parameters and survival. The possible role of a molecular targeted therapy of advanced bladder cancer with Her2/neu targeting agents should be assessed in further clinical trials.

Adult↗

PubMed2005

[Obstructive uropathy in adults].

Urinary tract obstruction is a common clinical problem. The obstruction of the urinary flow may be acute or chronic, partial or complete, unilateral or bilateral, and may occur at any site of the urinary tract. The major causes of urinary tract obstruction vary with the age of the patient. Anatomic abnormalities, e. g. ureteropelvic junction obstruction, account for the majority of cases in children. In comparison, calculi are most common in young adults, while prostatic hyperplasia or carcinoma, retroperitoneal or pelvic neoplasms, and calculi are the primary causes in older patients. Urinary tract obstruction results in different pathophysiological changes causing various symptoms. In addition to the aetiology, pathophysiology and clinical presentation of obstructive uropathy in adults, modern diagnostic and therapeutic options are presented in this review.

Adult↗

PubMed2000

Heterogenous vascular effects of AP5A in different rat resistance arteries are due to heterogenous distribution of P2X and P2Y(1) purinoceptors.

In the accompanying article, we showed that AP5A displayed heterogenous vasoactive effects in rat resistance arteries. It induced a stable vasoconstriction in the superior epigastric artery (SEA) and a transient vasoconstriction in the mesenteric resistance artery (MrA). In the phenylephrine-precontracted MrA AP5A induced a marked vasorelaxation. In this study the noncompetitive inhibition of the AP5A-induced vasoconstriction with pyridoxal-phosphate-6-azophenyl-2',4'-disulphonic acid was found to be significantly stronger in MrA than in SEA. The nonselective P2 purinoceptor antagonist suramin inhibited AP5A-induced vasoconstriction in MrA only. The vasoconstriction by the P2X purinoceptor agonist alpha,beta-methylene ATP was inhibited by with pyridoxal-phosphate-6-azophenyl-2',4'-disulfonic acid and suramin similarly to that induced by AP5A. Thus, the AP5A-induced vasoconstriction is due to P2X receptor activation, but two different P2X receptors seem to be operational in the two different vessels. The AP5A-induced vasorelaxation of phenylephrine-precontracted MrA was inhibited by the P2Y(1) receptor antagonist ADP3'5'. The vasorelaxation induced by ADPbetaS (P2Y(1) agonist) also was inhibited by ADP3'5'. These findings suggest that AP5A-induced vasorelaxation of MrA is caused by P2Y(1) receptor activation. The P1 (A(2)) receptor antagonist 3, 7-dimethyl-1-propargylxanthine only slightly inhibited AP5A-induced vasorelaxation at high concentrations. Adenosine and the A(2) receptor agonist CGS21680 failed to produce significant vasorelaxation. Therefore, vasorelaxation in MrA does not involve A(2) purinoceptor activation. AP5A-induced vasorelaxation was not inhibited by Ca(2+)- or ATP-dependent K(+) channel blockade with clotrimazole, apamin, or glibenclamide. These data indicate that vasoconstriction in MrA and SEA by AP5A is due to different P2X receptors, and vasorelaxation in precontracted MrA is due to P2Y(1) receptor activation.

Animals↗