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R Dahiya

Publications and source records attributed to R Dahiya.

At least 73 records · Page 4Linked to original sources
PubMed1998

Expression of TGF-beta-1 mRNA and ultrastructural alterations in pharmacologically induced prolonged penile erection in a canine model.

PURPOSE: Transforming growth factor beta (TGF-beta) is known to induce fibrosis. Our objective was to study the role of TGF-beta as a possible mediator of fibrosis that may follow prolonged penile erection. MATERIALS AND METHODS: Prolonged penile erection was induced in seven adult male mongrel dogs by intracavernosal injection of papaverine into one of the corpora cavernosa while the other was used as a control. Intracavernosal pressure measurements were carried out prior to administration of papaverine and at the end of the procedure. Penile tissue was collected from anesthetized animals prior to euthanasia for histological and electron microscopic (EM) studies. RT-PCR was carried out for detection of mRNA on same tissue samples. RESULTS: The light microscopy showed stasis of blood in the cavernosal sinusoids. EM studies revealed sporadic endothelial defects, loss of plasma membrane integrity and cytoplasmic condensation. There was expression of TGF-beta1 mRNA in 66.7% of the experimental group compared with 16.7% of the control group. CONCLUSIONS: Pharmacologically induced low flow prolonged penile erection in canine models is associated with histomorphological changes in relatively short periods of time, suggesting that early therapeutic intervention is desirable. The gene expression for TGF-beta1 may be a mediator of fibrosis; therefore the use of anti-TGF-beta agents presents a possible tool for therapeutic intervention.

Animals↗
PubMed1998

Multiple sites of loss of heterozygosity on chromosome 8 in human breast cancer has differential correlation with clinical parameters.

Recent studies have shown that chromosome 8p21-22 is the main site of frequent loss of heterozygosity (LOH) in breast cancers. However, the detailed molecular analysis of chromosome 8 so far in breast cancer has been variable. Most of the literature pertaining to LOH in breast cancer is mainly on short arm of chromosome 8. In the present study, we have examined LOH on both short and long arm of chromosome 8 using fifteen different polymorphic DNA markers in microdissected samples of normal breast epithelium and carcinoma from the same patients. For this purpose, DNA was extracted from the microdissected normal and tumor cells of 66 breast cancers, amplified by PCR and analyzed for LOH on chromosome 8 using fifteen different polymorphic DNA markers (D8S264, D8S298, D8S535, D8S255, D8S1098, D8S589, D8S567, D8S591, D8S285, D8S1102, D8S1763, D8S260, D8S530, D8S1772, and D8S1844). Expression of estrogen receptor, progesterone receptors, and p53 antigens was determined by immunohistochemistry using specific monoclonal antibodies. The results of this study suggest that LOH on chromosome 8 was identified in 40 of 66 cases (61%) with at least one marker. Three distinct regions of loss detected were: i) at 8p12, at loci between D8S535 and D8S255; ii) at 8p11, on loci D8S567, D8S591, D8S285, and D8S1102; iii) at 8q11-12, on loci D8S1763, D8S260 and D8S530. We found 45% (30 out of 66 informative cases) of the tumors showed LOH at 8p12; 52% (34 out of 66 informative cases) had LOH at 8p11; and 39% (26 out of 66 informative cases) had LOH at 8q11-12. Deletion at 8q11-12 was significantly correlated with the grade of the breast cancer specimens. Moderate to poorly differentiated specimens had higher incidence of LOH at 8q11-12 as compared to well differentiated specimens. Deletion at 8p12 and 8p11 was significantly higher in clinical stages III and IV of breast cancer tissues as compared to stage I and II cases. Tissues with lymph node involvement showed higher incidence of LOH at 8p12 as compared to the tissues with no lymph node involvement. There was no correlation of LOH at these loci with either the age of the patients, tumor size, BrdU labeling index, expression of estrogen receptor, progesterone receptor, and p53 in breast cancer specimens. These experiments, for the first time, report multiple sites of LOH on chromosome 8 in human breast cancer, and these deletions have differential correlation with clinical parameters of breast cancer samples.

Breast Neoplasms↗
PubMed1998

Microsatellite instability in an animal model of mammary carcinogenesis.

Alterations in the length of simple repetitive genomic sequences (microsatellite instability, MSI) may characterize a distinct mechanism of mammary carcinogenesis. In order to investigate whether MSI is associated with chemically-induced mammary carcinogenesis in the rat, 30 microdissected mammary carcinomas were analyzed using 27 different microsatellite markers from chromosomes 1, 3, 5, 7 and 8. DNA was extracted from rat mammary cancer and adjoining microscopically normal tissues from the same slide, amplified by PCR, using different polymorphic DNA markers and the reaction products were analyzed for microsatellite instability. The results of this study indicate that 30% of cases (9 out of 30) showed microsatellite instability at a minimum of 1 locus. Three cases (out of 30) showed microsatellite instability at only three loci or less, called MSI-L (low frequency MSI). Six cases (out of 30) showed MSI at four loci or more, called MSI-H (high frequency MSI). Six cases showed MSI at D5Mit11 and D5Mgh3 loci, five cases showed MSI at D1Mit14, D1Mgh6, D5Mgh5 and D8Mgh10 loci, four cases had MSI at D1Mgh2, and D3Mgh7 loci, three cases had MSI at D3Mit3, D3Mgh5, D7Mgh1 loci, two cases had MSI at D7Mit11 locus and one case had MSI at D3Mgh9 locus. The results of these experiments suggest that MSI may be an important etiological event in the pathophysiology of mammary carcinogenesis.

Animals↗
PubMed1997

High frequency of genetic instability of microsatellites in human prostatic adenocarcinoma.

In order to investigate the genomic instability associated with prostate cancer, 36 microsatellite marker loci on chromosomes 1p, 3p, 5q, 8p, 8q, 9p, 11q and 13q were analyzed using microdissected samples from prostate cancer and adjoining microscopically normal tissues from the same slide. DNA was extracted from the normal and tumor cells of 40 microdissected prostate-cancer samples, amplified by PCR, and analyzed for microsatellite instability (MSI) using 36 different polymorphic DNA markers. In the present study, we have utilized a highly refined technique of PCR product separation on a sequencing gel, developed in our laboratory, which clearly shows high-quality results for the microsatellite instability in prostate cancer. The results of this study suggest that 45% (18 out of 40) showed genomic instability at a minimum of 1 locus; 4 cases each showed MSI at one and 2 loci, 4 cases had MSI at 3 loci, 3 cases showed MSI at 5 loci, while one case each showed MSI at 7, 8 and 15 loci. There was no significant correlation between the MSI and stage or grade of the tumors. This extensive study on genomic instability in prostate cancer found the occurrence of MSI to be very high, which suggests a role of MSI in the pathophysiology of prostate cancer.

Adenocarcinoma↗
PubMed1997

Deletion of chromosome 11p15, p12, q22, q23-24 loci in human prostate cancer.

Loss of heterozygosity (LOH) on chromosome 11 is frequently altered in various epithelial cancers. The present study was designed to investigate LOH on chromosome 11 in microdissected samples of normal prostatic epithelium and invasive carcinoma from the same patients. For this purpose, DNA was extracted from the microdissected normal and tumor cells of 38 prostate cancers, amplified by polymerase chain reaction PCR and analyzed for LOH on chromosome 11 using 9 different polymorphic DNA markers (D11S1307, D11S989, D11S1313, D11S898, D11S940, D11S1818, D11S924, D11S1336 and D11S912). LOH on chromosome 11 was identified in 30 of 38 cases (78%) with at least one marker. Four distinct regions of loss detected were: 1) at 11p15, at loci between D11S1307 and D11S989; 2) at 11p12, on locus D11S131 (11p12); 3) at 11q22, on loci D11S898, D11S940 and D11S1818; and 4) at 11q23-24, on loci between D11S1336 and D11S912. We found 25% of the tumors with LOH at 11p15; 39% had LOH at 11p12; 66% had LOH at 11q22; and 47% had LOH at 11q23-24. These deletions at 11p15, 11p12, 11q22 and 11q23-24 loci were not related to the stage or grade of the tumor.

Alleles↗
PubMed1997

Expression and function of the complement membrane attack complex inhibitor protectin (CD59) in human prostate cancer.

Protectin (CD59) inhibits homologous complement-mediated cytolysis by preventing formation of the membrane attack complex at the point of insertion and polymerization of C9 into cell membranes. The present study investigated the expression and function of CD59 on human prostatic tumor cells in situ and on 5 human prostate cell lines in vitro originating from either metastatic tumors or benign prostate hypertrophy epithelial cells. Immunohistochemical staining of prostate carcinoma tissue with monoclonal antibody (MAb) MEM43 revealed weak to moderately strong expression of CD59 by prostate glandular epithelial cells. Flow cytometry with MEM43 demonstrated that the 5 prostate cell lines expressed different relative quantities of CD59. Indirect immunofluorescence analysis revealed uniform membrane staining of DU145 and PC3 cell lines with no membranous granularity in the staining pattern. Western immunoblots with MAb BRIC 229 showed that PC3 and DU145 cells express CD59 with a m.w. of 18-25 kDa. Treatment of DU 145 and PC3 cells with phosphatidylinositol-specific phospholipase C caused a significant decrease of CD59 expression indicating that the CD59 expressed by prostate cancer cells is anchored to the cell membrane via a glycosylphosphatidylinositol (GPI) linkage. PC3 and DU145 cells were completely resistant to human complement-mediated cytolysis but became sensitive to killing in the presence of the CD59-neutralizing MAb YTH53.1. We conclude that malignant and benign human prostate cells express CD59 that is GPI-linked to the cell surface and that CD59 may regulate the immunological response to cancerous prostate cells by protecting the cells from the cytolytic activity of complement.

Adenocarcinoma↗
PubMed1997

Effect of retinoic acid on prostatic development.

BACKGROUND AND METHODS: To assess the effect of retinoids on prostatic ductal branching morphogenesis, anterior prostates from newborn rats were cultured under serum-free conditions for 6 days in the presence of testosterone (10(-8) mM) plus 13-cis-retinoic acid (13-cis-RA), all-trans-retinoic acid (at-RA), or N-4-hydroxyphenyl-retinamide (4-HPR). Measures of morphologic complexity were computed and compared between specimens of different treatment groups. RESULTS: Prostatic ductal growth and branching were inhibited in a dose-dependent fashion by both 13-cis-RA and at-RA, but not by 4-HPR. This inhibitory effect of 13-cis-RA was reversible, as the prostatic ducts resumed branching and growth after removal of retinoic acid from the culture medium. Using reverse transcription polymerase chain reaction, we then investigated the expression of nuclear receptor genes for retinoic acid. CONCLUSIONS: This showed the presence of RAR-beta and RAR-gamma in the 0-day prostate, suggesting that the effects of these retinoids on ductal morphogenesis may be via these receptors.

Animals↗
PubMed1997

Chromosome 3p24-26 and 3p22-12 loss in human prostatic adenocarcinoma.

Identification of loss of heterozygosity on specific genetic loci is crucial for understanding the pathogenesis of prostate cancer at the molecular level. This is especially important because the deleted regions may contain putative tumor suppressor genes. Chromosome 3p loss appears to be frequently associated with various epithelial cancers. To our knowledge, there is no report on loss of heterozygosity (LOH) of chromosome 3 in human prostate cancer. The present study was designed to investigate the LOH on chromosome 3p in microdissected samples of delineated regions of normal and invasive carcinoma areas of prostatic epithelium from the same tumor sections. For this purpose, DNA was extracted from microdissected normal and tumor cells of 38 prostate cancers, amplified by PCR and analyzed for LOH on chromosome 3p using 6 different polymorphic DNA markers (D3S1560, THRB, D3S647, D3S1298, D3S1228 and D3S1296). Our results suggest that LOH was identified in 34 of 38 cases (89%) with at least one marker. Twelve of 30 informative cases showed LOH at D3S1560; 18 of 22 informative cases showed loss at THRB; 20 of 38 informative cases showed deletion at D3S647; 16 of 38 informative cases showed loss at D3S1298; 12 of 34 informative cases showed LOH at D3S1228; and 6 of 34 informative cases showed LOH at D3S1296 regions. Our results suggest that the LOH is on the 3p24-26 and 3p22-12 regions of the short arm of chromosome 3, indicating 2 discrete areas of deletion on chromosome 3p. The deletion at 3p24-26 and 3p22-12 was not related to the stage or grade of the tumor.

Adenocarcinoma↗
PubMed1997

An animal model of Peyronie's-like condition associated with an increase of transforming growth factor beta mRNA and protein expression.

PURPOSE: Transforming growth factor beta (TGF-beta) is involved in numerous vital processes including tissue fibrosis. Our objective was to study the role of TGF-beta in the induction of a Peyronie's-like condition and to produce an animal model for the further study of Peyronie's disease. MATERIALS AND METHODS: Twenty-four adult male Sprague-Dawley rats were divided into two groups. Different concentrations of cytomodulin, a synthetic heptopeptide with TGF-beta-like activity, were injected into the tunica of each rat from the first group (n = 18). Rats in the second group (n = 6) received saline injections as a control. The tunical tissues were taken after 3 days, 2 weeks, and 6 weeks and were examined using Hart and Trichrome stains. In the same tissue samples, TGF-beta mRNA and protein expression were studied. RESULTS: Histological alterations were observed in 15 out of 18 cytomodulin-injected rats, especially in tissue examined after 6 weeks. The most prominent changes were chronic cellular infiltration, focal and diffuse elastosis, thickening, disorganization and clumping of the collagen bundles. Results from immunoblot revealed remarkable TGF-beta1 protein expression in all the cytomodulin-injected rats only after 2 and 6 weeks. No remarkable TGF-beta2 or TGF-beta3 protein expression was observed. TGF-beta1 mRNA expression in the cytomodulin-injected rats was noticed in rats injected with higher concentrations after 3 days, while it was expressed in all rats after 2 weeks. There was no expression in the control group after either 3 days or 2 weeks. CONCLUSIONS: Cytomodulin can induce Peyronie's-like condition in the rat penis, which may explain the role of TGF-beta in the pathogenesis of Peyronie's disease.

Animals↗
PubMed1997

Free ureteral replacement in rats: regeneration of ureteral wall components in the acellular matrix graft.

OBJECTIVES: To evaluate ureteral replacement by a free homologous graft of acellular matrix in a rat model. METHODS: In 30 male Sprague-Dawley rats, a 0.3 to 0.8-cm midsegment of the left ureter was resected and replaced with an acellular matrix graft of equal length placed on a polyethylene stent. The animals were killed at varying intervals, and the grafted specimens were prepared for light and electron microscopy. RESULTS: In all animals, the acellular matrix graft remained in its original position without evidence of incrustation or infection, and histologic examination showed complete epithelialization and progressive infiltration by vessels. At 10 weeks, smooth muscle fibers were observed; at 12 weeks, nerve fibers were first detected; at 4 months, smooth muscle cells had assumed regular configuration. CONCLUSIONS: The ureteral acellular matrix graft appears to promote the regeneration of all ureteral wall components.

Animals↗
PubMed1997

Mucins secreted by cell lines derived from colorectal mucinous carcinoma and adenocarcinoma.

Mucinous (colloid) carcinoma and well- to moderately-differentiated adenocarcinoma of the colon differ in the pattern and the amount of mucin secretion and perhaps in their behaviour and clinical outcome. To ascertain why these differences exist and to elucidate the mechanisms of tumour progression, we examined two model human cell lines derived from colorectal mucinous carcinoma (C1a) and moderately differentiated adenocarcinoma (HM3) which show typical pathological and mucin staining patterns of the respective type of carcinomas to nude mouse tumour xenografts. Specifically, we sought to determine if there were quantitative and qualitative differences in mucin synthesis, in mucin gene expression and in biological properties between the two model cell lines. Northern blot analysis showed that MUC2 mRNA levels were significantly higher in C1a cells compared with HM3 cells, while those of MUC3, -5 and -6 mRNA were lower. C1a cells secreted approximately five times more radiolabelled apomucin and 1.5 times more glycosylated apomucin than HM3 cells. When the carbohydrate side-chain length of secreted mucins by these cell lines were examined by beta-elimination followed by P4 column chromatography, C1a mucins had mostly short carbohydrate side-chains, while HM3 cells had predominantly longer side-chains. Western blot analysis of the cell homogenate showed higher expression of MUC2 apomucin and mucin-associated carbohydrate antigens, such as T, Tn and sialyl Tn, with decreased sialyl Le(x) expression in C1a cells compared with HM3. Immunohistochemical analysis of 35 colorectal adenocarcinoma and 25 mucinous colorectal carcinoma tissues also demonstrated increased MUC2 apomucin, T, Tn and sialyl Tn antigens in the mucinous cancer specimens. Examination of the biological properties of these cell lines showed that C1a cells had significantly higher in vitro invasive activity in assays of invasion and collagenase activity and significantly lower E-selectin binding and liver colonisation activities in nude mice. These results indicate that colorectal mucinous carcinoma cells differ considerably from colorectal adenocarcinoma cells, both qualitatively and quantitatively, in the pattern of mucin gene expression and in the synthesis and secretion of mucin. In addition, biological studies showed that mucinous carcinoma cells have a greater degree of invasiveness, but less liver colonising activity. These results suggest that the biological and mucin characteristics of mucinous carcinoma cells contribute to extensive local invasion through tissue stroma as the predominant mechanism of tumour progression, while the biological and mucin characteristics of well- to moderately-differentiated colorectal adenocarcinoma contribute to progression via distant metastasis formation.

Adenocarcinoma↗
PubMed1997

Induction of cyclo-oxygenase-2 mRNA by prostaglandin E2 in human prostatic carcinoma cells.

Prostaglandins are synthesized from arachidonic acid by the enzyme cyclo-oxygenase. There are two isoforms of cyclooxygenases: COX-1 (a constitutive form) and COX-2 (an inducible form). COX-2 has recently been categorized as an immediate-early gene and is associated with cellular growth and differentiation. The purpose of this study was to investigate the effects of exogenous dimethylprostaglandin E2 (dmPGE2) on prostate cancer cell growth. Results of these experiments demonstrate that administration of dmPGE2 to growing PC-3 cells significantly increased cellular proliferation (as measured by the cell number), total DNA content and endogenous PGE2 concentration. DmPGE2 also increased the steady-state mRNA levels of its own inducible synthesizing enzyme, COX-2, as well as cellular growth to levels similar to those seen with fetal calf serum and phorbol ester. The same results were observed in other human cancer cell types, such as the androgen-dependent LNCaP cells, breast cancer MDA-MB-134 cells and human colorectal carcinoma DiFi cells. In PC-3 cells, the dmPGE2 regulation of the COX-2 mRNA levels was both time dependent, with maximum stimulation seen 2 h after addition, and dose dependent on dmPGE2 concentration, with maximum stimulation seen at 5 microg ml(-1). The non-steroidal anti-inflammatory drug flurbiprofen (5 microM), in the presence of exogenous dmPGE2, inhibited the up-regulation of COX-2 mRNA and PC-3 cell growth. Taken together, these data suggest that PGE2 has a specific role in the maintenance of human cancer cell growth and that the activation of COX-2 expression depends primarily upon newly synthesized PGE2, perhaps resulting from changes in local cellular PGE2 concentrations.

16,16-Dimethylprostaglandin E2↗
PubMed1997

Reproduction of functional smooth muscle tissue and partial bladder replacement.

OBJECTIVE: To find a means of bladder augmentation that would avoid the complications encountered with the use of bowel segments, using a newly developed acellular biomaterial, the bladder acellular matrix graft (BAMG), as a homologous graft. MATERIALS AND METHODS: Thirty-four rats underwent a partial cystectomy (40-50%) and grafting with a BAMG of equal size. Eleven rats died within the first 72 h. probably from urinary leakage caused by obstruction of the bladder neck with stones or coagula; the surviving 23 were killed at varying intervals after cystectomy and examined. RESULTS: After providing initial bladder enlargement, the graft was progressively infiltrated by the vessels and smooth muscle cells of the host: furthermore, the mucosal lining was complete within 10 days. After 4 weeks, all bladder wall components were evident histologically in the graft. The ingrowth was complete after 8 weeks, except for neural regeneration, which was only partial. At 12 weeks, the bladder wall muscle structure in the graft was so well developed that it was difficult to delineate the junction between host bladder and BAMG. Neural regeneration continued to improve. Normal bladder capacities were maintained throughout the study. CONCLUSION: The BAMG appears to serve, without rejection, as a framework of collagen and elastin for the ingrowth of all bladder wall components. The reason for the better acceptance of the BAMG than of other bladder augmentation grafts requires further investigation.

Animals↗
PubMed1997

mRNA and protein expression of nitric oxide synthase and adrenoceptor alpha 1 in young and old rat penile tissues.

OBJECTIVE: To investigate alterations of neuronal structure and the mRNA expression of nitric oxide synthase (NOS) and adrenoceptor alpha 1 in young and old rat penile tissues, and assess the importance of these factors in erectile dysfunction (ED) associated with ageing. MATERIALS AND METHODS: NOS was determined in the pelvic ganglia of 32 rats using nicotinamide adenine dinucleotide phosphate (NADPH)-diaphorase staining. Adrenergic neurons were identified by histofluorescence staining. The gene expression for NOS and for adrenoceptor alpha 1 was investigated in corporal tissue by differential reverse transcriptase-polymerase chain reaction (RT-PCR) using specific oligonucleotide primers. b-actin was used as an internal standard in each tube to quantify the baseline gene expression. RESULTS: The following changes occurred in old rats: (i) an increase of lipofuscin and a decrease in both bNOS-containing neurons and fluorescent adrenergic neurons in the pelvic ganglia; (ii) significantly less expression of NOS mRNA than in young rat penile tissues; and (iii) no significant alteration in adrenoreceptor alpha 1 mRNA expression. CONCLUSIONS: The fewer adrenergic and NOS-containing neurons and neurotransmitters in pelvic ganglia from old rats may explain the enhanced penile smooth muscle tone previously reported in older impotent men. Furthermore, lower mRNA expression of NOS may be associated with structural and functional changes associated with ageing penile tissue.

Age Factors↗
PubMed1997

Peyronie's disease is associated with an increase in transforming growth factor-beta protein expression.

PURPOSE: Transforming growth factor-beta (TGF-beta) has been implicated in many chronic fibrotic conditions such as pulmonary and hepatic fibrosis. We postulated that TGF-beta may play a role in the pathogenesis of Peyronie's disease. MATERIALS AND METHODS: Tissues from the tunica albuginea of 30 Peyronie's disease patients (study group) and from 6 patients without Peyronie's disease, who had undergone penile prosthesis surgery for organic impotence (control group), were subjected to histological examination using Hart and trichrome stains and Western blotting for the detection of TGF-beta protein expression. RESULTS: The results of these experiments demonstrate that all tissue from Peyronie's disease patients showed a variety of histological changes of the tunica, ranging from chronic inflammatory cellular infiltration to complete calcification and ossification of the tissues. The most prominent changes observed in the majority of patients were focal or diffused elastosis, fenestration and disorganization of the collagen bundles. TGF-beta1 protein expression was detected in 26 patients (86%), while only 7 (23%) and 5 (17%) patients showed TGF-beta2 and TGF-beta3 protein expression, respectively. One patient in the control group showed fibrosis of the tunica albuginea and protein expression of TGF-beta1 and TGF-beta2. This patient had undergone surgery for the revision of his prosthesis twice. Five patients from the control group showed normal histological patterns of the tunica albuginea and no protein expression for TGF-beta1, TGF-beta2 and TGF-beta3. CONCLUSIONS: TGF-beta1 protein expression is significantly associated with Peyronie's disease, which may provide a new insight and the potential for the prevention and treatment of this disease.

Humans↗
PubMed1996

Effect of thermal variables on frozen human primary prostatic adenocarcinoma cells.

OBJECTIVES: Recent advances in imaging technology and cryotechnology have rekindled interest in prostate cryosurgery. Cryosurgery, however, cannot be applied precisely without knowing how the thermal variables used during the procedure affect tissue destruction. The goal of this article is to provide quantitative values for the relationship between thermal variables during freezing and the destruction of human primary prostatic adenocarcinoma cells. METHODS: Human primary prostatic adenocarcinoma cells were frozen with controlled thermal parameters, using a directional solidification apparatus. Cell viability was determined after thawing, using trypan blue and a two-dye fluorescent test and correlated to the thermal variables used during freezing. RESULTS: Human primary prostatic adenocarcinoma cells are damaged by intracellular chemical damage when frozen with cooling rates lower than 5 degrees C/min and by intracellular ice formation when frozen with cooling rates higher than 25 degrees C/min. A double freeze/thaw cycle is required to ensure complete cell destruction at high subzero temperatures, which must be lower than -40 degrees C for the low cooling rates and lower than -19 degrees C for the higher cooling rate. CONCLUSIONS: Haphazard freezing does not necessarily destroy tissue during cryosurgery; however, quantitative data on the relation between thermal variables and frozen cell destruction can provide the means for performing cryosurgery more precisely and with greater control over the outcome of the procedure.

Adenocarcinoma↗
PubMed1996

Differential gene expression of transforming growth factors alpha and beta, epidermal growth factor, keratinocyte growth factor, and their receptors in fetal and adult human prostatic tissues and cancer cell lines.

OBJECTIVES: Recent studies have shown that growth factors may play a role in the etiology of benign prostatic hyperplasia (BPH) and prostatic carcinoma. Several growth factors have been reported to be expressed by prostatic tissues, but these growth factors have never been examined in human fetal prostate and compared with adult prostates and cancer cell lines. The present study was designed to investigate the messenger ribonucleic acid (mRNA) expression of transforming growth factor (TGF)-alpha, TGF-beta 1, TGF-beta 2, TGF- beta 3, keratinocyte growth factor (KGF), epidermal growth factor (EGF), EGF receptor (EGF-R), and KGF receptor (KGF-R) in human fetal and adult prostatic tissues and cancer cell lines by reverse-transcriptase-polymerase chain reaction-(RT-PCR) using specific oligonucleotide primers. METHODS: Total RNA was extracted from human fetal and adult prostates (BPH tissues) and cancer cell lines. The gene expression of these growth factors and their receptors was determined by RT-PCR using specific oligonucleotide primers. RESULTS: The results of these experiments suggest that: (1) human fetal prostate expressed mRNA transcripts for TGF-alpha, TGF-beta 1, TGF-beta 2, TGF-beta 3, and EGF. However, KGF, KGF-R, and EGF-R mRNA were not expressed by human fetal prostate; (2) human adult prostate (BPH tissues) showed mRNA transcripts for all growth factors and their receptors except KGF-R; (3) human BPH-1 cell lines expressed mRNA transcripts for TGF-alpha, TGF-beta 1, TGF-beta 2, TGF-beta 3, EGF, and KGF-R, but not for EGF-R and KGF growth factors; (4) human primary prostate cancer cell line (ND-1) showed mRNA transcripts for all growth factors except EGF and KGF; and (5) human prostate cancer cell lines (LNCaP, DU-145, PC-3) expressed mRNA transcripts for all growth factors except KGF, which was absent in all cell lines. However, KGF-R mRNA was absent in the PC-3 prostate cancer cell line. CONCLUSIONS: These results suggest that the differential gene expression for various growth factors and their receptors in human fetal and adult prostatic tissues and cancer cell lines may be important in understanding the role of these factors in the pathophysiology of prostatic diseases.

Adult↗