The Experts below are selected from a list of 210 Experts worldwide ranked by ideXlab platform

David Danielpour - One of the best experts on this subject based on the ideXlab platform.

  • Development and Characterization of DP-153, a Nontumorigenic Prostatic Cell Line That Undergoes Malignant Transformation by Expression of Dominant-negative Transforming Growth Factor β Receptor Type II
    Cancer research, 2003
    Co-Authors: Kyung Song, Susan C. Cornelius, David Danielpour
    Abstract:

    We have developed a nontumorigenic epithelial cell line, DP-153, from the dorsal prostate of a Lobund/Wistar Rat treated with N -methyl- N -nitrosourea and testosterone propionate. DP-153 cells express cytokeRatins 5 and 14, but not cytokeRatin 18, consistent with a basal epithelial cell phenotype. Similar to the nontumorigenic NRP-152 prostatic cell line, DP-153 cells do not form tumors in athymic mice and retain many of the properties of normal prostatic cells. They express prostatic acid phosphatase and androgen receptors and require several mitogens (epidermal growth factor, insulin, dexamethasone, and cholera toxin) for sustained growth in culture under serum-containing conditions. DP-153 cells are also growth-stimulated by keRatinocyte growth factor and basic fibroblast growth factor and growth-inhibited by all-trans- retinoic acid, 1,25-dihydroxyvitamin D3, and transforming growth factor (TGF)-β1. We demonstRate that expression of dominant-negative TGF-β receptor type II by retroviral transduction of DP-153 cells leads to complete loss of TGF-β1-induced growth inhibition. When transplanted s.c. in athymic mice, DP-153 cells expressing dominant-negative TGF-β receptor type II form tumors as early as 4 weeks, in contrast to the vector control and parental cell line, which do not form tumors even 8 months after transplantation, supporting the observation that TGF-β functions as a tumor suppressor in these cells. Our data further support that DP-153 is a suitable cell line for analysis of normal prostatic growth and carcinogenesis.

  • Regulation of trespin expression by modulators of cell growth, differentiation, and apoptosis in prostatic epithelial cells.
    Experimental cell research, 2003
    Co-Authors: Lamonica V. Stewart, Kyung Song, Andrew Y. Hsing, David Danielpour
    Abstract:

    We recently identified a novel Rat ov-serpin, Trespin, which inhibits the trypsin-like serine proteinase plasmin and is expressed in several tissues, including prostate. In this report Trespin expression was studied in prostatic cell lines, NRP-152, NRP-154, and DP-153, derived from the Lobund-Wistar Rat. Northern blots revealed Trespin mRNA is expressed in NRP-152 and DP-153 basal epithelial cell lines but not in the luminal line, NRP-154. Similarly, Trespin levels drop >30-fold following transdifferentiation of NRP-152 cells toward a luminal variant, further suggesting Trespin expression is specific for basal prostatic epithelial cells. Trespin expression in NRP-152 cells is up-regulated by dexamethasone (Dex) and insulin-like growth factor-I (IGF-I), each of which stimulate growth and prevent differentiation and apoptosis. However, Dex (alone) facilitates loss of Trespin by TGF-beta, yet enhances the ability of LR(3)-IGF-I to reverse such loss, similar to the pattern of apoptosis induced by TGF-beta. Likewise, several apoptosis inducers markedly decrease Trespin mRNA levels. HEK293 cells stably overexpressing Trespin display increased cell prolifeRation and partial resistance to growth inhibition and phosphorylation of c-Jun induced by the phorbol ester 12-O-tetradecanoylphorbol 13-acetate (TPA). Together these data strongly suggest that Trespin has critical functions tied to the regulation of growth, differentiation, and apoptosis of prostatic epithelial cells.

  • Regulation of trespin expression by modulators of cell growth, differentiation, and apoptosis in prostatic epithelial cells.
    Experimental Cell Research, 2003
    Co-Authors: Lamonica V. Stewart, Kyung Song, Andrew Y. Hsing, David Danielpour
    Abstract:

    Abstract We recently identified a novel Rat ov-serpin, Trespin, which inhibits the trypsin-like serine proteinase plasmin and is expressed in several tissues, including prostate. In this report Trespin expression was studied in prostatic cell lines, NRP-152, NRP-154, and DP-153, derived from the Lobund-Wistar Rat. Northern blots revealed Trespin mRNA is expressed in NRP-152 and DP-153 basal epithelial cell lines but not in the luminal line, NRP-154. Similarly, Trespin levels drop >30-fold following transdifferentiation of NRP-152 cells toward a luminal variant, further suggesting Trespin expression is specific for basal prostatic epithelial cells. Trespin expression in NRP-152 cells is up-regulated by dexamethasone (Dex) and insulin-like growth factor-I (IGF-I), each of which stimulate growth and prevent differentiation and apoptosis. However, Dex (alone) facilitates loss of Trespin by TGF-β, yet enhances the ability of LR 3 -IGF-I to reverse such loss, similar to the pattern of apoptosis induced by TGF-β. Likewise, several apoptosis inducers markedly decrease Trespin mRNA levels. HEK293 cells stably overexpressing Trespin display increased cell prolifeRation and partial resistance to growth inhibition and phosphorylation of c-Jun induced by the phorbol ester 12- O -tetradecanoylphorbol 13-acetate (TPA). Together these data strongly suggest that Trespin has critical functions tied to the regulation of growth, differentiation, and apoptosis of prostatic epithelial cells.

Morris Pollard - One of the best experts on this subject based on the ideXlab platform.

  • Rat Prostate Tumors Express Cancer Procoagulant, an Activator of Coagulation Factor X
    Comparative medicine, 2008
    Co-Authors: Malgorzata M. Kamocka, Morris Pollard, Mark A. Suckow, Wojciech P. Mielicki, Elliot D. Rosen
    Abstract:

    Two common procoagulant activities associated with tumors are tissue factor and cancer procoagulant (CP), an activator of coagulation factor X. We have identified a convenient source of CP in transplanted Lobund–Wistar Rat PA3 prostate tumors. CP activity was purified from 5 independent transplanted prostate tumors by column chromatography. The protein activated factor X in the absence of TF and factor VII. An antihuman CP antibody recognized Rat CP in an ELISA and inactivated CP activity in a chromogenic assay. Lobund–Wistar prostate tumors may provide a convenient animal model useful in determining the role of CP in cancer development.

  • Vaccination against prostate cancer using a live tissue factor deficient cell line in Lobund–Wistar Rats
    Cancer Immunology Immunotherapy, 2007
    Co-Authors: Julie E. Heinrich, Morris Pollard, Elliot D. Rosen, William A. Wolter, Zhong Liang, Hui Song, Mark A. Suckow
    Abstract:

    Reducing expression of the tissue factor gene in prostate adenocarcinoma cells (PAIII) results in a cell line that, in vivo, mimics the growth of wildtype (wt) PAIII. However, instead of continuing to grow and metastasize as wt PAIII tumors do, tissue factor deficient PAIII (TFD PAIII) masses spontaneously regress after several weeks. Although whole cell vaccines are typically inactivated prior to administRation to prevent prolifeRation within the host, numerous studies have suggested that exposure to live, attenuated, whole tumor cells, and the extracellular microenvironment they recruit, increases immunotherapeutic potential. Here, we provide support for this notion, and a stRategy through which to implement it, by demonstRating that subcutaneous vaccinations with the TFD PAIII protect the Lobund–Wistar Rat against subsequent wt PAIII cell challenge. TFD PAIII immunized Rats suffered significantly less metastasis of wt PAIII challenge tumors compared to unvaccinated naïve controls Rats. These results offer the intriguing possibility that the TFD PAIII vaccine is an effective system for the prevention and, possibly, the treatment of prostate cancer.

  • Vaccination against prostate cancer using a live tissue factor deficient cell line in Lobund-Wistar Rats.
    Cancer immunology immunotherapy : CII, 2006
    Co-Authors: Julie E. Heinrich, Morris Pollard, Elliot D. Rosen, William A. Wolter, Zhong Liang, Hui Song, Mark A. Suckow
    Abstract:

    Reducing expression of the tissue factor gene in prostate adenocarcinoma cells (PAIII) results in a cell line that, in vivo, mimics the growth of wildtype (wt) PAIII. However, instead of continuing to grow and metastasize as wt PAIII tumors do, tissue factor deficient PAIII (TFD PAIII) masses spontaneously regress after several weeks. Although whole cell vaccines are typically inactivated prior to administRation to prevent prolifeRation within the host, numerous studies have suggested that exposure to live, attenuated, whole tumor cells, and the extracellular microenvironment they recruit, increases immunotherapeutic potential. Here, we provide support for this notion, and a stRategy through which to implement it, by demonstRating that subcutaneous vaccinations with the TFD PAIII protect the Lobund–Wistar Rat against subsequent wt PAIII cell challenge. TFD PAIII immunized Rats suffered significantly less metastasis of wt PAIII challenge tumors compared to unvaccinated naive controls Rats. These results offer the intriguing possibility that the TFD PAIII vaccine is an effective system for the prevention and, possibly, the treatment of prostate cancer.

  • Hormone-refractory prostate cancer in the Lobund-Wistar Rat.
    Experimental biology and medicine (Maywood N.J.), 2005
    Co-Authors: Morris Pollard, Mark A. Suckow
    Abstract:

    Research on cancer prevention and therapy must focus on the refractory disease, the fatal end-stage of cancer that develops in patients with organ-related solid tumors. Refractory cancers develop spontaneously in advanced-stage tumors or in relapsed cases after failed therapy. Because neither prevention nor therapy is currently feasible, refractory cancer is a major impediment to survival. There is a great need for an animal model of prostate cancer (PC), one that develops cancer from initial premalignant to the terminal refractory stages. We describe here a model of hormone-refractory prostate cancer (HRPC) that develops spontaneously through two stages by endogenous mechanisms in the Lobund-Wistar (LW) Rat. The early premalignant, testosterone (T)-dependent stage is promoted by high levels of endogenous T, and up to age 12 months is reversible by T deprivation; without this intervention, the tumorigenic process progresses to the refractory stage, which is highly aggressive and does not respond to T depr...

  • Increased Phospholipid Fatty Acid Remodeling in Human and Rat Prostatic Adenocarcinoma Tissues
    The Journal of urology, 1996
    Co-Authors: Fred H. Faas, Morris Pollard, An Q. Dang, Xiao-man Hong, Kang Fan, Phyllis H. Luckert, Michael Schutz
    Abstract:

    AbstractPurpose: To study the mechanism of diminished arachidonic acid levels in malignant prostatic tissues.Materials and Methods: Benign and malignant prostate tissues were obtained from human radical prostatectomy specimens and from Rats using Pollard's Lobund/Wistar Rat prostate cancer model. Fatty acid composition and a variety of enzyme activities involved in maintaining phospholipid fatty acid composition were compared in malignant and benign prostatic tissues.Results: Decreased arachidonic acid levels, previously reported in human prostate cancer, were present in malignant Rat as well as in human tissues. There were 21 percent and 26 percent decreases of arachidonic acid levels in the Rat and human malignant tissues compared with benign tissues. Fatty acid desaturase activity was undetectable. Fatty acyl-CoA hydrolase and synthetase activities were not altered in the malignant tissues. However, there was a 2-fold increase in phospholipase A2 activity and a 4- to 12-fold increase in fatty acyl-CoA ...

Kyung Song - One of the best experts on this subject based on the ideXlab platform.

  • Development and Characterization of DP-153, a Nontumorigenic Prostatic Cell Line That Undergoes Malignant Transformation by Expression of Dominant-negative Transforming Growth Factor β Receptor Type II
    Cancer research, 2003
    Co-Authors: Kyung Song, Susan C. Cornelius, David Danielpour
    Abstract:

    We have developed a nontumorigenic epithelial cell line, DP-153, from the dorsal prostate of a Lobund/Wistar Rat treated with N -methyl- N -nitrosourea and testosterone propionate. DP-153 cells express cytokeRatins 5 and 14, but not cytokeRatin 18, consistent with a basal epithelial cell phenotype. Similar to the nontumorigenic NRP-152 prostatic cell line, DP-153 cells do not form tumors in athymic mice and retain many of the properties of normal prostatic cells. They express prostatic acid phosphatase and androgen receptors and require several mitogens (epidermal growth factor, insulin, dexamethasone, and cholera toxin) for sustained growth in culture under serum-containing conditions. DP-153 cells are also growth-stimulated by keRatinocyte growth factor and basic fibroblast growth factor and growth-inhibited by all-trans- retinoic acid, 1,25-dihydroxyvitamin D3, and transforming growth factor (TGF)-β1. We demonstRate that expression of dominant-negative TGF-β receptor type II by retroviral transduction of DP-153 cells leads to complete loss of TGF-β1-induced growth inhibition. When transplanted s.c. in athymic mice, DP-153 cells expressing dominant-negative TGF-β receptor type II form tumors as early as 4 weeks, in contrast to the vector control and parental cell line, which do not form tumors even 8 months after transplantation, supporting the observation that TGF-β functions as a tumor suppressor in these cells. Our data further support that DP-153 is a suitable cell line for analysis of normal prostatic growth and carcinogenesis.

  • Regulation of trespin expression by modulators of cell growth, differentiation, and apoptosis in prostatic epithelial cells.
    Experimental cell research, 2003
    Co-Authors: Lamonica V. Stewart, Kyung Song, Andrew Y. Hsing, David Danielpour
    Abstract:

    We recently identified a novel Rat ov-serpin, Trespin, which inhibits the trypsin-like serine proteinase plasmin and is expressed in several tissues, including prostate. In this report Trespin expression was studied in prostatic cell lines, NRP-152, NRP-154, and DP-153, derived from the Lobund-Wistar Rat. Northern blots revealed Trespin mRNA is expressed in NRP-152 and DP-153 basal epithelial cell lines but not in the luminal line, NRP-154. Similarly, Trespin levels drop >30-fold following transdifferentiation of NRP-152 cells toward a luminal variant, further suggesting Trespin expression is specific for basal prostatic epithelial cells. Trespin expression in NRP-152 cells is up-regulated by dexamethasone (Dex) and insulin-like growth factor-I (IGF-I), each of which stimulate growth and prevent differentiation and apoptosis. However, Dex (alone) facilitates loss of Trespin by TGF-beta, yet enhances the ability of LR(3)-IGF-I to reverse such loss, similar to the pattern of apoptosis induced by TGF-beta. Likewise, several apoptosis inducers markedly decrease Trespin mRNA levels. HEK293 cells stably overexpressing Trespin display increased cell prolifeRation and partial resistance to growth inhibition and phosphorylation of c-Jun induced by the phorbol ester 12-O-tetradecanoylphorbol 13-acetate (TPA). Together these data strongly suggest that Trespin has critical functions tied to the regulation of growth, differentiation, and apoptosis of prostatic epithelial cells.

  • Regulation of trespin expression by modulators of cell growth, differentiation, and apoptosis in prostatic epithelial cells.
    Experimental Cell Research, 2003
    Co-Authors: Lamonica V. Stewart, Kyung Song, Andrew Y. Hsing, David Danielpour
    Abstract:

    Abstract We recently identified a novel Rat ov-serpin, Trespin, which inhibits the trypsin-like serine proteinase plasmin and is expressed in several tissues, including prostate. In this report Trespin expression was studied in prostatic cell lines, NRP-152, NRP-154, and DP-153, derived from the Lobund-Wistar Rat. Northern blots revealed Trespin mRNA is expressed in NRP-152 and DP-153 basal epithelial cell lines but not in the luminal line, NRP-154. Similarly, Trespin levels drop >30-fold following transdifferentiation of NRP-152 cells toward a luminal variant, further suggesting Trespin expression is specific for basal prostatic epithelial cells. Trespin expression in NRP-152 cells is up-regulated by dexamethasone (Dex) and insulin-like growth factor-I (IGF-I), each of which stimulate growth and prevent differentiation and apoptosis. However, Dex (alone) facilitates loss of Trespin by TGF-β, yet enhances the ability of LR 3 -IGF-I to reverse such loss, similar to the pattern of apoptosis induced by TGF-β. Likewise, several apoptosis inducers markedly decrease Trespin mRNA levels. HEK293 cells stably overexpressing Trespin display increased cell prolifeRation and partial resistance to growth inhibition and phosphorylation of c-Jun induced by the phorbol ester 12- O -tetradecanoylphorbol 13-acetate (TPA). Together these data strongly suggest that Trespin has critical functions tied to the regulation of growth, differentiation, and apoptosis of prostatic epithelial cells.

Lamonica V. Stewart - One of the best experts on this subject based on the ideXlab platform.

  • Regulation of trespin expression by modulators of cell growth, differentiation, and apoptosis in prostatic epithelial cells.
    Experimental cell research, 2003
    Co-Authors: Lamonica V. Stewart, Kyung Song, Andrew Y. Hsing, David Danielpour
    Abstract:

    We recently identified a novel Rat ov-serpin, Trespin, which inhibits the trypsin-like serine proteinase plasmin and is expressed in several tissues, including prostate. In this report Trespin expression was studied in prostatic cell lines, NRP-152, NRP-154, and DP-153, derived from the Lobund-Wistar Rat. Northern blots revealed Trespin mRNA is expressed in NRP-152 and DP-153 basal epithelial cell lines but not in the luminal line, NRP-154. Similarly, Trespin levels drop >30-fold following transdifferentiation of NRP-152 cells toward a luminal variant, further suggesting Trespin expression is specific for basal prostatic epithelial cells. Trespin expression in NRP-152 cells is up-regulated by dexamethasone (Dex) and insulin-like growth factor-I (IGF-I), each of which stimulate growth and prevent differentiation and apoptosis. However, Dex (alone) facilitates loss of Trespin by TGF-beta, yet enhances the ability of LR(3)-IGF-I to reverse such loss, similar to the pattern of apoptosis induced by TGF-beta. Likewise, several apoptosis inducers markedly decrease Trespin mRNA levels. HEK293 cells stably overexpressing Trespin display increased cell prolifeRation and partial resistance to growth inhibition and phosphorylation of c-Jun induced by the phorbol ester 12-O-tetradecanoylphorbol 13-acetate (TPA). Together these data strongly suggest that Trespin has critical functions tied to the regulation of growth, differentiation, and apoptosis of prostatic epithelial cells.

  • Regulation of trespin expression by modulators of cell growth, differentiation, and apoptosis in prostatic epithelial cells.
    Experimental Cell Research, 2003
    Co-Authors: Lamonica V. Stewart, Kyung Song, Andrew Y. Hsing, David Danielpour
    Abstract:

    Abstract We recently identified a novel Rat ov-serpin, Trespin, which inhibits the trypsin-like serine proteinase plasmin and is expressed in several tissues, including prostate. In this report Trespin expression was studied in prostatic cell lines, NRP-152, NRP-154, and DP-153, derived from the Lobund-Wistar Rat. Northern blots revealed Trespin mRNA is expressed in NRP-152 and DP-153 basal epithelial cell lines but not in the luminal line, NRP-154. Similarly, Trespin levels drop >30-fold following transdifferentiation of NRP-152 cells toward a luminal variant, further suggesting Trespin expression is specific for basal prostatic epithelial cells. Trespin expression in NRP-152 cells is up-regulated by dexamethasone (Dex) and insulin-like growth factor-I (IGF-I), each of which stimulate growth and prevent differentiation and apoptosis. However, Dex (alone) facilitates loss of Trespin by TGF-β, yet enhances the ability of LR 3 -IGF-I to reverse such loss, similar to the pattern of apoptosis induced by TGF-β. Likewise, several apoptosis inducers markedly decrease Trespin mRNA levels. HEK293 cells stably overexpressing Trespin display increased cell prolifeRation and partial resistance to growth inhibition and phosphorylation of c-Jun induced by the phorbol ester 12- O -tetradecanoylphorbol 13-acetate (TPA). Together these data strongly suggest that Trespin has critical functions tied to the regulation of growth, differentiation, and apoptosis of prostatic epithelial cells.

Mark A. Suckow - One of the best experts on this subject based on the ideXlab platform.

  • Rat Prostate Tumors Express Cancer Procoagulant, an Activator of Coagulation Factor X
    Comparative medicine, 2008
    Co-Authors: Malgorzata M. Kamocka, Morris Pollard, Mark A. Suckow, Wojciech P. Mielicki, Elliot D. Rosen
    Abstract:

    Two common procoagulant activities associated with tumors are tissue factor and cancer procoagulant (CP), an activator of coagulation factor X. We have identified a convenient source of CP in transplanted Lobund–Wistar Rat PA3 prostate tumors. CP activity was purified from 5 independent transplanted prostate tumors by column chromatography. The protein activated factor X in the absence of TF and factor VII. An antihuman CP antibody recognized Rat CP in an ELISA and inactivated CP activity in a chromogenic assay. Lobund–Wistar prostate tumors may provide a convenient animal model useful in determining the role of CP in cancer development.

  • Vaccination against prostate cancer using a live tissue factor deficient cell line in Lobund–Wistar Rats
    Cancer Immunology Immunotherapy, 2007
    Co-Authors: Julie E. Heinrich, Morris Pollard, Elliot D. Rosen, William A. Wolter, Zhong Liang, Hui Song, Mark A. Suckow
    Abstract:

    Reducing expression of the tissue factor gene in prostate adenocarcinoma cells (PAIII) results in a cell line that, in vivo, mimics the growth of wildtype (wt) PAIII. However, instead of continuing to grow and metastasize as wt PAIII tumors do, tissue factor deficient PAIII (TFD PAIII) masses spontaneously regress after several weeks. Although whole cell vaccines are typically inactivated prior to administRation to prevent prolifeRation within the host, numerous studies have suggested that exposure to live, attenuated, whole tumor cells, and the extracellular microenvironment they recruit, increases immunotherapeutic potential. Here, we provide support for this notion, and a stRategy through which to implement it, by demonstRating that subcutaneous vaccinations with the TFD PAIII protect the Lobund–Wistar Rat against subsequent wt PAIII cell challenge. TFD PAIII immunized Rats suffered significantly less metastasis of wt PAIII challenge tumors compared to unvaccinated naïve controls Rats. These results offer the intriguing possibility that the TFD PAIII vaccine is an effective system for the prevention and, possibly, the treatment of prostate cancer.

  • Vaccination against prostate cancer using a live tissue factor deficient cell line in Lobund-Wistar Rats.
    Cancer immunology immunotherapy : CII, 2006
    Co-Authors: Julie E. Heinrich, Morris Pollard, Elliot D. Rosen, William A. Wolter, Zhong Liang, Hui Song, Mark A. Suckow
    Abstract:

    Reducing expression of the tissue factor gene in prostate adenocarcinoma cells (PAIII) results in a cell line that, in vivo, mimics the growth of wildtype (wt) PAIII. However, instead of continuing to grow and metastasize as wt PAIII tumors do, tissue factor deficient PAIII (TFD PAIII) masses spontaneously regress after several weeks. Although whole cell vaccines are typically inactivated prior to administRation to prevent prolifeRation within the host, numerous studies have suggested that exposure to live, attenuated, whole tumor cells, and the extracellular microenvironment they recruit, increases immunotherapeutic potential. Here, we provide support for this notion, and a stRategy through which to implement it, by demonstRating that subcutaneous vaccinations with the TFD PAIII protect the Lobund–Wistar Rat against subsequent wt PAIII cell challenge. TFD PAIII immunized Rats suffered significantly less metastasis of wt PAIII challenge tumors compared to unvaccinated naive controls Rats. These results offer the intriguing possibility that the TFD PAIII vaccine is an effective system for the prevention and, possibly, the treatment of prostate cancer.

  • Hormone-refractory prostate cancer in the Lobund-Wistar Rat.
    Experimental biology and medicine (Maywood N.J.), 2005
    Co-Authors: Morris Pollard, Mark A. Suckow
    Abstract:

    Research on cancer prevention and therapy must focus on the refractory disease, the fatal end-stage of cancer that develops in patients with organ-related solid tumors. Refractory cancers develop spontaneously in advanced-stage tumors or in relapsed cases after failed therapy. Because neither prevention nor therapy is currently feasible, refractory cancer is a major impediment to survival. There is a great need for an animal model of prostate cancer (PC), one that develops cancer from initial premalignant to the terminal refractory stages. We describe here a model of hormone-refractory prostate cancer (HRPC) that develops spontaneously through two stages by endogenous mechanisms in the Lobund-Wistar (LW) Rat. The early premalignant, testosterone (T)-dependent stage is promoted by high levels of endogenous T, and up to age 12 months is reversible by T deprivation; without this intervention, the tumorigenic process progresses to the refractory stage, which is highly aggressive and does not respond to T depr...