Biomedical subjects

B Treiger

Publications and source records attributed to B Treiger.

6 recordsLinked to original sources

PubMed1995

Prostatic aperture resulting from visual laser ablation: classification system based on follow-up endoscopy.

To study the evolving prostatic aperture created by visual laser ablation (VLAP), we performed 38 video-endoscopies in 24 men with prostatism at various intervals 2 weeks to 1 year after treatment. Complete healing was generally observed within 3 to 4 months, never before 6 weeks; and in some patients, tissue sloughing was still apparent beyond 6 months. By review of the cystoscopic findings and video hard copies, three independent observers classified the healed prostatic apertures with great uniformity into one of four categories: (I) minimal change (lateral lobes still meet in midline throughout gland length) (N = 3); (II) minor aperture (opening less than 50% of cystoscopic field over less than 50% of gland length) (N = 5); (III) major aperture (opening more than 50% of cystoscopic field over more than 50% of gland length) (N = 11); and (IV) full ablation (nearly complete replacement of lobar configuration with a general concavity) (N = 5). Clinical outcomes (symptom scores, uroflow rates) matched with follow-up cystoscopic categories but not with any other readily identifiable measures. The four-category system proved to be simple, reproducible, and clinically relevant. If a standardized tissue aperture is the ultimate aim of new methods to ablate the prostate, the proposed system for classifying the aperture could have a considerable future application.

Aged↗

PubMed1995

Cloning and expression of an endothelin receptor subtype B from human prostate that mediates contraction.

Recent evidence suggests a role for endothelin (ET) in contraction of human prostate [J. Urol. 149:495-499 (1993)]. Although both ETA and ETB receptors have been shown to mediate contraction of smooth muscle, the molecular identity of the contractile ETB receptor is controversial. The aim of this study was to examine the receptor subtype that mediates ET-induced contraction in prostate from patients with benign prostatic hyperplasia. Saturation binding with 125I-ET-1 and 125I-ET-3 in prostate stromal cells (PSC) indicated the presence of receptors with subnanomolar affinity for these radioligands, with equivalent receptor densities. Inhibition of specific 125I-ET-1 or 125I-ET-3 binding in PSC revealed a rank order of potency of ET-1 - ET-3 = sarafotoxin S6c >> BQ-123. These data are consistent with a predominance of ETB receptors in PSC. The functional effects of ET stimulation of PSC were examined in a collagen gel contraction assay. ET-1 and ET-3 caused contraction of underlying collagen gel matrices with EC50 values of 0.4 +/- 0.04 and 0.7 +/- 0.2 nM, respectively. To determine the molecular nature of the contractile ETB receptor in PSC, reverse transcription-polymerase chain reactions were conducted with oligonucleotide primers to the 5' and 3' ends of the coding sequence of the full length human ETB receptor. DNA sequence analysis of the 1.3-kilobase DNA product showed 99% homology to other human ETB receptor cDNAs. The encoded protein has a deduced amino acid sequence identical to that of other human ETB receptors, with the exception of two conservative substitutions. Expression of the PSC ETB cDNA in COS-7 cells resulted in a binding profile similar to that observed in parent cells. Polymerase chain reaction analysis revealed the presence of prepro-ET-1 mRNA in PSC. Collectively, these data indicate that PSC from patients with benign prostatic hyperplasia express ETB receptors that mediate ET-induced contraction.

Amino Acid Sequence↗

PubMed1994

Morphometry of the prostate: I. Distribution of tissue components in hyperplastic glands.

OBJECTIVES: Morphometry, or quantitative image analysis, offers great promise in characterizing the various histologic types of benign prostatic hyperplasia (BPH), but to date, a systematic study of the tissue components is lacking. Thus we employed morphometry to examine the distribution of primary BPH tissues throughout whole human prostates. METHODS: The prostate glands of 20 men with BPH were removed for low-volume carcinoma and subjected to a uniform, comprehensive, systematic quantification of the primary BPH tissue components using the technique of digitization and point-count morphometry. RESULTS: We found the following average volumes among the 20 glands: epithelium, 19.9% (S.D. 5.1%, range 11.7% to 30.8%); fibromuscular stroma, 50.4% (S.D. 9.4%, range 32.2% to 74.4%); glandular lumina, 29.7% (S.D. 8.9%, range 11.9% to 47.5%). Within the individual prostates, we found symmetry in primary BPH tissue distribution, except that the outer prostate was on average 25% richer in epithelium than the inner prostate (p < 0.05). When tissue composition was determined in simulated biopsy specimens, corrected for radial (ie, inner vs outer gland) orientation, the correlation with whole-organ composition was statistically significant for "percentage epithelium" (r = 0.72, p < 0.01) and for "stromal/epithelial ratio" (r = 0.63, p < 0.01). CONCLUSIONS: Major differences in primary tissue composition may separate different hyperplastic prostates. Primary BPH tissues are rather symmetrically distributed within individual prostates. Quantitative histologic differences between prostates, potentially important in clinical decision-making may be accurately diagnosed by morphometry of radially oriented biopsy specimens.

Aged↗

PubMed1988

Early cell motility changes associated with an increase in metastatic ability in rat prostatic cancer cells transfected with the v-Harvey-ras oncogene.

The development of metastatic ability by cancer cells is a multifactorial process whose temporal events are complex and poorly understood. One step in the metastatic process may involve cell motility. Previous studies reported correlations between motility and metastatic ability. Whether this correlation, seen in cancer cells maintained for long periods of time, is an epiphenomenon developing late in the growth of the cancer as a selection artifact of continuous passage, or is critically required for the acquisition of metastatic ability is unknown. To investigate the relationship between cell motility and the acquisition of metastatic ability, advantage was taken of recently developed DNA transfection methods for inducing high metastatic ability in initially low metastatic cancer cells. The Dunning AT2.1 cell line, a clonal rat prostatic cancer cell line with low metastatic ability, was transfected with a plasmid containing the neomycin resistance gene alone or in combination with the v-Harvey-ras oncogene. A series of the transfected cells was isolated by limiting dilution. After the first in vitro passage following transfection, cells were inoculated into rats to characterize their metastatic ability. The same transfectants were simultaneously studied using our visual grading system of cell motility to study the early motility changes associated with newly acquired metastatic ability. The data demonstrate increased membrane ruffling, pseudopodal extension, and cell translation (translocation) in the v-H-ras-transfected cell lines with high metastatic potential.

Animals↗

PubMed1988

Down modulation of fibronectin messenger RNA in metastasizing rat prostatic cancer cells revealed by differential hybridization analysis.

To identify genes whose expression is down modulated in the process of metastasis, gene expression was analyzed in cell lines derived from Dunning R-3327 rat prostatic tumor sublines. A complementary DNA (cDNA) library from the anaplastic nonmetastasizing subline AT-1 was used for a differential hybridization analysis, using probes derived from mRNAs of the AT-1 and the metastasizing MAT-LyLu subline. In this way 14 cDNA clones were isolated representing 6 differentially expressed genes. The expression levels in a panel of tumor sublines measured with these cDNA clones were tested for correlation with the anaplastic non-metastasizing phenotype. One cDNA clone, designated pSE-1, whose expression was high in all tested sublines with that phenotype, appeared to represent the gene for fibronectin. To further investigate the down modulation of this gene, we studied its expression in AT-2 (anaplastic, nonmetastasizing tumor) and lines derived therefrom that exhibited a high metastatic potential after transfection with the v-Ha-ras oncogene. In the genetically manipulated metastasizing tumor sublines, fibronectin mRNA levels were approximately 4- to 8-fold lowered compared to the nonmetastasizing parental AT-2 line.

Animals↗

PubMed1988

Expression of a transfected v-Harvey-ras oncogene in a Dunning rat prostate adenocarcinoma and the development of high metastatic ability.

To investigate the role of oncogenes in the development of metastatic ability by prostatic cancer, the viral-Harvey-ras (v-H-ras) oncogene was introduced into the Dunning rat prostate adenocarcinoma cell line, AT2.1 by means of DNA transfection. The AT2.1 cell line is a cloned cell line that is anaplastic, rapidly growing, and has low metastatic potential; after subcutaneous (s.c.) inoculation in syngeneic rats, fewer than 10% of inoculated rats develop distant metastases. Calcium phosphate mediated DNA transfections of AT2.1 cells were performed with the v-H-ras oncogene or with control DNA. The in vitro growth rate of cloned transfectants, which contain and express the v-H-ras oncogene is similar to that of untransfected AT2.1 cells and of control transfectants. After s.c. inoculation in syngeneic rats, all transfectants produced rapidly growing tumors with similar growth rates. While control transfectants had low metastatic ability comparable to untransfected AT2.1 cells, the H-ras expressing transfectants metastasized in over 80% of inoculated rats. While the mechanism by which nonmetastatic Dunning tumor sublines spontaneously develop high metastatic ability in vivo during serial s.c. passage has not been addressed in the present studies, these studies do demonstrate that expression of an activated H-ras oncogene can reproducibly convert a tumorigenic nonmetastatic prostatic cell line to a highly metastatic state.

Adenocarcinoma↗