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Jamsheer J Talati - One of the best experts on this subject based on the ideXlab platform.

  • Original Articles Role of Estrogens in the Secondary Hormonal Manipulation of Hormone Refractory Prostate Cancer
    2015
    Co-Authors: Khurram Siddiqui, Farhat Abbas, Syed Raziuddin Biyabani, M. H. Ather, Jamsheer J Talati
    Abstract:

    Objective: To evaluate the role of Estrogens (Honvan) in the secondary hormonal manipulation of patients with hormone refractory prostate cancer (HRCP). Methods: Twelve patients diagnosed as hormone refractory prostate cancer received intravenous Estrogens for six days (Fosfestrol, a synthetic phosphorylated Estrogen Derivative), followed by a maintenance oral dose of 120 mg thrice daily as second line hormonal treatment. During the treatment they were given deep venous thrombo-sis prophylaxis. Their stage at initial presentation, primary treatment, mode of androgen ablation, prostate spe-cific antigen (PSA) level, duration of remission prior of HRPC status, PSA doubling time before and after estro-gen treatment were recorded. The morbidity and mortality of the treatment was also recorded. A drop in PSA of> 50 % was classified as major responder. The drop of < 50 % was defined as minor responders. Treatment fail-ure was defined as a rise in PSA> the level prior to the start of treatment. Results: The mean age at diagnosis of prostate cancer was 66.6 + 5.4 years (range 57-73). At the time of ini-tial diagnosis only 3 patients (25%) had localized disease and 9 (75%) had metastatic prostate cancer. Six patients each opted for surgical or medical castration (LHRH analogs) as the mode of androgen ablation. The mean initial PSA at diagnosis was 340 + 728.1 ng/ml (range 4.1-2375, Median 94). After development of HRPC, six patients (50%) had major response, four (33%) had minor response to Estrogen administration. Two patients (17%) did not respond to Estrogens. The mean PSA before receiving Fosfestrol was 60.5 + 82 ng/ml (range 0.013-246). The PSA (nadir) after treatment was 24.3 + 33.2 ng/ml (range 0.9-81.3). One patient developed gynaecomastia and one had congestive cardiac failure. Two patients died of non cancer related deaths and one patient died of cancer related death. Conclusion: Synthetic Estrogens are well tolerated, in-expensive agents and could be considered for palliative use against hormone resistant prostate cancer (JPMA 54:445;2004)

  • Original Articles Role of Estrogens in the Secondary Hormonal Manipulation of Hormone Refractory Prostate Cancer
    2004
    Co-Authors: Khurram M. Siddiqui, Khurram Siddiqui, Farhat Abbas, Syed Raziuddin Biyabani, Jamsheer J Talati, M. H. Ather, Hammad M Ather
    Abstract:

    Objective: To evaluate the role of Estrogens (Honvan) in the secondary hormonal manipulation of patients with hormone refractory prostate cancer (HRCP). Methods: Twelve patients diagnosed as hormone refractory prostate cancer received intravenous Estrogens for six days (Fosfestrol, a synthetic phosphorylated Estrogen Derivative), followed by a maintenance oral dose of 120 mg thrice daily as second line hormonal treatment. During the treatment they were given deep venous thrombo-sis prophylaxis. Their stage at initial presentation, primary treatment, mode of androgen ablation, prostate spe-cific antigen (PSA) level, duration of remission prior of HRPC status, PSA doubling time before and after estro-gen treatment were recorded. The morbidity and mortality of the treatment was also recorded. A drop in PSA of> 50 % was classified as major responder. The drop of < 50 % was defined as minor responders. Treatment fail-ure was defined as a rise in PSA> the level prior to the start of treatment. Results: The mean age at diagnosis of prostate cancer was 66.6 + 5.4 years (range 57-73). At the time of ini-tial diagnosis only 3 patients (25%) had localized disease and 9 (75%) had metastatic prostate cancer. Si

Marta M Fay - One of the best experts on this subject based on the ideXlab platform.

  • bisphenol a promotes stress granule assembly and modulates the integrated stress response
    Biology Open, 2021
    Co-Authors: Marta M Fay, Daniella Columbo, Cecelia Cotter, Chandler Friend, Shawna Henry, Megan Hoppe, Paulina Karabelas, Corbyn Lamy, Miranda Lawell
    Abstract:

    Bisphenol-A (BPA) is a ubiquitous precursor of polycarbonate plastics that is found in the blood and serum of >92% of Americans. While BPA has been well documented to act as a weak Estrogen receptor (ER) agonist, its effects on cellular stress are unclear. Here, we demonstrate that high-dose BPA causes stress granules (SGs) in human cells. A common Estrogen Derivative, β-estradiol, does not trigger SGs, indicating the mechanism of SG induction is not via the ER pathway. We also tested other structurally related environmental contaminants including the common BPA substitutes BPS and BPF, the industrial chemical 4-nonylphenol (4-NP) and structurally related compounds 4-EP and 4-VP, as well as the pesticide 2,4-dichlorophenoxyacetic acid (2,4-D). The variable results from these related compounds suggest that structural homology is not a reliable predictor of the capacity of a compound to cause SGs. Also, we demonstrate that BPA acts primarily through the PERK pathway to generate canonical SGs. Finally, we show that chronic exposure to a low physiologically relevant dose of BPA suppresses SG assembly upon subsequent acute stress. Interestingly, this SG inhibition does not affect phosphorylation of eIF2α or translation inhibition, thus uncoupling the physical assembly of SGs from translational control. Our work identifies additional effects of BPA beyond endocrine disruption that may have consequences for human health.

  • bisphenol a promotes stress granule assembly and modulates the integrated stress response
    bioRxiv, 2019
    Co-Authors: Marta M Fay, Daniella Columbo, Cecelia Cotter, Chandler Friend, Shawna Henry, Megan Hoppe, Paulina Karabelas, Corbyn Lamy
    Abstract:

    Abstract Bisphenol-A (BPA) is a ubiquitous precursor of polycarbonate plastics that is found in the blood and serum of >92% of Americans. While BPA has been well documented to act as a weak Estrogen receptor (ER) agonist, its effects on cellular stress are unclear. Here, we demonstrate that high-dose BPA causes stress granules (SGs) in human cells. A common Estrogen Derivative, β-estradiol, does not trigger SGs, indicating the mechanism of SG induction is not via the ER pathway. We also tested other structurally related environmental contaminants including the common BPA substitutes BPS and BPF, the industrial chemical 4-nonylphenol (4-NP) and structurally related compounds 4-EP and 4-VP, and the pesticide 2,4-dichlorophenoxyacetic acid (2,4-D). The variable results from these related compounds suggest that structural homology is not a reliable predictor of the capacity of a compound to cause SGs. Also, we demonstrate that BPA acts primarily through the PERK pathway to generate canonical SGs. Finally, we show that chronic exposure to a low physiologically relevant dose of BPA disrupts SG assembly by inhibiting SGs upon additional acute stress. Our work identifies additional effects of BPA beyond endocrine disruption that may have consequences for human health.

Dharminder Chauhan - One of the best experts on this subject based on the ideXlab platform.

  • NEOPLASIA Identification of genes regulated by 2-methoxyestradiol (2ME2) in multiple myeloma cells using oligonucleotide arrays
    2016
    Co-Authors: Dharminder Chauhan, Teru Hideshima, Klaus Podar, Daniel Auclair, Nicholas Mitsiades, Constantine Mitsiades, Paul Richardson, Ryung Suk Kim
    Abstract:

    Our previous study demonstrated that 2-methoxyestradiol (2ME2), an Estrogen Derivative, induces apoptosis in multiple myeloma (MM) cells; however, the related transcriptional events are unclear. In the present study, we used oligonucleotide microarrays to identify genes altered dur-ing 2ME2-induced apoptosis in MM cells. 2ME2 triggers an early transient induc-tion of genes known to trigger cell death and repression of growth/survival-related genes. Many genes regulating cell de-fense/repair machinery also were tran-siently induced. Since 2ME2 also induces apoptosis in MM cells resistant to conven-tional therapies such as dexamethasone (Dex), we compared the gene profiles of 2ME2-treated and Dex-resistant MM cells. Our results suggest that 2ME2 over-comes Dex resistance by modulating genes that confer chemoresistance in MM cells. Microarray results were confirmed by Northern and Western blot analyses. A comparative analysis of selected genes from freshly isolated MM patient cells and 2ME2-treated MM.1S MM cells further pro-vides an in vivo relevance of our in vitro studies. Collectively, these findings sug-gest genetic events mediating anti-MM activity of 2ME2, as well as mechanisms whereby 2ME2 overcomes Dex resis-tance in MM cells. These studies may therefore allow improved therapeutic use of 2ME2, based upon targeting genes that regulate MM cell growth and survival

  • identification of genes regulated by 2 methoxyestradiol 2me2 in multiple myeloma cells using oligonucleotide arrays
    Blood, 2003
    Co-Authors: Dharminder Chauhan, Teru Hideshima, Paul G Richardson, Klaus Podar, Daniel Auclair, Nicholas Mitsiades, Constantine Mitsiades, Ryung Suk Kim, Nikhil C Munshi, Lan Bo Chen
    Abstract:

    Our previous study demonstrated that 2-methoxyestradiol (2ME2), an Estrogen Derivative, induces apoptosis in multiple myeloma (MM) cells; however, the related transcriptional events are unclear. In the present study, we used oligonucleotide microarrays to identify genes altered during 2ME2-induced apoptosis in MM cells. 2ME2 triggers an early transient induction of genes known to trigger cell death and repression of growth/survival-related genes. Many genes regulating cell defense/repair machinery also were transiently induced. Since 2ME2 also induces apoptosis in MM cells resistant to conventional therapies such as dexamethasone (Dex), we compared the gene profiles of 2ME2-treated and Dex-resistant MM cells. Our results suggest that 2ME2 overcomes Dex resistance by modulating genes that confer chemoresistance in MM cells. Microarray results were confirmed by Northern and Western blot analyses. A comparative analysis of selected genes from freshly isolated MM patient cells and 2ME2-treated MM.1S MM cells further provides an in vivo relevance of our in vitro studies. Collectively, these findings suggest genetic events mediating anti-MM activity of 2ME2, as well as mechanisms whereby 2ME2 overcomes Dex resistance in MM cells. These studies may therefore allow improved therapeutic use of 2ME2, based upon targeting genes that regulate MM cell growth and survival.

  • 2 methoxyestradiol overcomes drug resistance in multiple myeloma cells
    Blood, 2002
    Co-Authors: Dharminder Chauhan, Martin Sattler, Laurence Catley, Teru Hideshima, Richard Leblanc, Deepak K Gupta, Paul G Richardson, Robert L Schlossman, Klaus Podar, Edie Weller
    Abstract:

    2-Methoxyestradiol (2ME2) an Estrogen Derivative, induces growth arrest and apoptosis in leukemic cells and is also antiangiogenic. In this study, we demonstrate that 2ME2 inhibits growth and induces apoptosis in multiple myeloma (MM) cell lines and patient cells. Significantly, 2ME2 also inhibits growth and induces apoptosis in MM cells resistant to conventional therapies including melphalan (LR-5), doxorubicin (Dox-40 and Dox-6), and dexamethasone (MM.1R). In contrast to its effects on MM cells, 2ME2 does not reduce the survival of normal peripheral blood lymphocytes. Moreover, 2ME2 enhances Dex-induced apoptosis, and its effect is not blocked by interleukin-6 (IL-6). We next examined the effect of 2ME2 on MM cells in the bone marrow (BM) milieu. 2ME2 decreases survival of BM stromal cells (BMSCs), as well as secretion of vascular endothelial growth factor (VEGF), and IL-6 triggered by the adhesion of MM cells to BMSCs. We show that apoptosis induced by 2ME2 is mediated by the release of mitochondrial cytochrome-c (cyto-c) and Smac, followed by the activation of caspases-8, -9, and -3. Finally, 2ME2 inhibits MM cell growth, prolongs survival, and decreases angiogenesis in a murine model. These studies, therefore, demonstrate that 2ME2 mediates anti-MM activity directly on MM cells and in the BM microenvironment. They provide a framework for the use of 2ME2, either alone or in combination with Dex, to overcome drug resistance and to improve outcome in MM.

Syed Raziuddin Biyabani - One of the best experts on this subject based on the ideXlab platform.

  • Original Articles Role of Estrogens in the Secondary Hormonal Manipulation of Hormone Refractory Prostate Cancer
    2015
    Co-Authors: Khurram Siddiqui, Farhat Abbas, Syed Raziuddin Biyabani, M. H. Ather, Jamsheer J Talati
    Abstract:

    Objective: To evaluate the role of Estrogens (Honvan) in the secondary hormonal manipulation of patients with hormone refractory prostate cancer (HRCP). Methods: Twelve patients diagnosed as hormone refractory prostate cancer received intravenous Estrogens for six days (Fosfestrol, a synthetic phosphorylated Estrogen Derivative), followed by a maintenance oral dose of 120 mg thrice daily as second line hormonal treatment. During the treatment they were given deep venous thrombo-sis prophylaxis. Their stage at initial presentation, primary treatment, mode of androgen ablation, prostate spe-cific antigen (PSA) level, duration of remission prior of HRPC status, PSA doubling time before and after estro-gen treatment were recorded. The morbidity and mortality of the treatment was also recorded. A drop in PSA of> 50 % was classified as major responder. The drop of < 50 % was defined as minor responders. Treatment fail-ure was defined as a rise in PSA> the level prior to the start of treatment. Results: The mean age at diagnosis of prostate cancer was 66.6 + 5.4 years (range 57-73). At the time of ini-tial diagnosis only 3 patients (25%) had localized disease and 9 (75%) had metastatic prostate cancer. Six patients each opted for surgical or medical castration (LHRH analogs) as the mode of androgen ablation. The mean initial PSA at diagnosis was 340 + 728.1 ng/ml (range 4.1-2375, Median 94). After development of HRPC, six patients (50%) had major response, four (33%) had minor response to Estrogen administration. Two patients (17%) did not respond to Estrogens. The mean PSA before receiving Fosfestrol was 60.5 + 82 ng/ml (range 0.013-246). The PSA (nadir) after treatment was 24.3 + 33.2 ng/ml (range 0.9-81.3). One patient developed gynaecomastia and one had congestive cardiac failure. Two patients died of non cancer related deaths and one patient died of cancer related death. Conclusion: Synthetic Estrogens are well tolerated, in-expensive agents and could be considered for palliative use against hormone resistant prostate cancer (JPMA 54:445;2004)

  • Original Articles Role of Estrogens in the Secondary Hormonal Manipulation of Hormone Refractory Prostate Cancer
    2004
    Co-Authors: Khurram M. Siddiqui, Khurram Siddiqui, Farhat Abbas, Syed Raziuddin Biyabani, Jamsheer J Talati, M. H. Ather, Hammad M Ather
    Abstract:

    Objective: To evaluate the role of Estrogens (Honvan) in the secondary hormonal manipulation of patients with hormone refractory prostate cancer (HRCP). Methods: Twelve patients diagnosed as hormone refractory prostate cancer received intravenous Estrogens for six days (Fosfestrol, a synthetic phosphorylated Estrogen Derivative), followed by a maintenance oral dose of 120 mg thrice daily as second line hormonal treatment. During the treatment they were given deep venous thrombo-sis prophylaxis. Their stage at initial presentation, primary treatment, mode of androgen ablation, prostate spe-cific antigen (PSA) level, duration of remission prior of HRPC status, PSA doubling time before and after estro-gen treatment were recorded. The morbidity and mortality of the treatment was also recorded. A drop in PSA of> 50 % was classified as major responder. The drop of < 50 % was defined as minor responders. Treatment fail-ure was defined as a rise in PSA> the level prior to the start of treatment. Results: The mean age at diagnosis of prostate cancer was 66.6 + 5.4 years (range 57-73). At the time of ini-tial diagnosis only 3 patients (25%) had localized disease and 9 (75%) had metastatic prostate cancer. Si

Farhat Abbas - One of the best experts on this subject based on the ideXlab platform.

  • Original Articles Role of Estrogens in the Secondary Hormonal Manipulation of Hormone Refractory Prostate Cancer
    2015
    Co-Authors: Khurram Siddiqui, Farhat Abbas, Syed Raziuddin Biyabani, M. H. Ather, Jamsheer J Talati
    Abstract:

    Objective: To evaluate the role of Estrogens (Honvan) in the secondary hormonal manipulation of patients with hormone refractory prostate cancer (HRCP). Methods: Twelve patients diagnosed as hormone refractory prostate cancer received intravenous Estrogens for six days (Fosfestrol, a synthetic phosphorylated Estrogen Derivative), followed by a maintenance oral dose of 120 mg thrice daily as second line hormonal treatment. During the treatment they were given deep venous thrombo-sis prophylaxis. Their stage at initial presentation, primary treatment, mode of androgen ablation, prostate spe-cific antigen (PSA) level, duration of remission prior of HRPC status, PSA doubling time before and after estro-gen treatment were recorded. The morbidity and mortality of the treatment was also recorded. A drop in PSA of> 50 % was classified as major responder. The drop of < 50 % was defined as minor responders. Treatment fail-ure was defined as a rise in PSA> the level prior to the start of treatment. Results: The mean age at diagnosis of prostate cancer was 66.6 + 5.4 years (range 57-73). At the time of ini-tial diagnosis only 3 patients (25%) had localized disease and 9 (75%) had metastatic prostate cancer. Six patients each opted for surgical or medical castration (LHRH analogs) as the mode of androgen ablation. The mean initial PSA at diagnosis was 340 + 728.1 ng/ml (range 4.1-2375, Median 94). After development of HRPC, six patients (50%) had major response, four (33%) had minor response to Estrogen administration. Two patients (17%) did not respond to Estrogens. The mean PSA before receiving Fosfestrol was 60.5 + 82 ng/ml (range 0.013-246). The PSA (nadir) after treatment was 24.3 + 33.2 ng/ml (range 0.9-81.3). One patient developed gynaecomastia and one had congestive cardiac failure. Two patients died of non cancer related deaths and one patient died of cancer related death. Conclusion: Synthetic Estrogens are well tolerated, in-expensive agents and could be considered for palliative use against hormone resistant prostate cancer (JPMA 54:445;2004)

  • Original Articles Role of Estrogens in the Secondary Hormonal Manipulation of Hormone Refractory Prostate Cancer
    2004
    Co-Authors: Khurram M. Siddiqui, Khurram Siddiqui, Farhat Abbas, Syed Raziuddin Biyabani, Jamsheer J Talati, M. H. Ather, Hammad M Ather
    Abstract:

    Objective: To evaluate the role of Estrogens (Honvan) in the secondary hormonal manipulation of patients with hormone refractory prostate cancer (HRCP). Methods: Twelve patients diagnosed as hormone refractory prostate cancer received intravenous Estrogens for six days (Fosfestrol, a synthetic phosphorylated Estrogen Derivative), followed by a maintenance oral dose of 120 mg thrice daily as second line hormonal treatment. During the treatment they were given deep venous thrombo-sis prophylaxis. Their stage at initial presentation, primary treatment, mode of androgen ablation, prostate spe-cific antigen (PSA) level, duration of remission prior of HRPC status, PSA doubling time before and after estro-gen treatment were recorded. The morbidity and mortality of the treatment was also recorded. A drop in PSA of> 50 % was classified as major responder. The drop of < 50 % was defined as minor responders. Treatment fail-ure was defined as a rise in PSA> the level prior to the start of treatment. Results: The mean age at diagnosis of prostate cancer was 66.6 + 5.4 years (range 57-73). At the time of ini-tial diagnosis only 3 patients (25%) had localized disease and 9 (75%) had metastatic prostate cancer. Si