The Experts below are selected from a list of 49806 Experts worldwide ranked by ideXlab platform
Robert M Hoffman - One of the best experts on this subject based on the ideXlab platform.
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selective methioninase induced trap of cancer Cells in s g2 phase visualized by fucci imaging confers chemosensitivity
Oncotarget, 2014Co-Authors: Shuya Yano, Qinghong Han, Yuying Tan, Michael Bouvet, Toshiyoshi Fujiwara, Robert M HoffmanAbstract:A major impediment to the response of tumors to chemotherapy is that the large majority of cancer Cells within a tumor are quiescent in G0/G1, where cancer Cells are resistant to chemotherapy. To attempt to solve this problem of quiescent Cells in a tumor, cancer Cells were treated with recombinant methioninase (rMETase), which selectively traps cancer Cells in S/G2. The Cell cycle phase of the cancer Cells was visualized with the fluorescence ubiquitination-based Cell cycle Indicator Cell cycle Indicator (FUCCI). At the time of rMETase-induced S/G2-phase blockage, identified by the cancer Cells' green fluorescence by FUCCI imaging, the cancer Cells were administered S/G2-dependent chemotherapy drugs, which interact with DNA or block DNA synthesis such as doxorubicin, cisplatin, or 5-fluorouracil. Treatment of cancer Cells with drugs only, without rMETase-induced S/G2 phase blockage, led to the majority of the cancer-Cell population being blocked in G0/G1 phase, identified by the cancer Cells becoming red fluorescent in the FUCCI system. The G0/G1 blocked Cells were resistant to the chemotherapy. In contrast, trapping of cancer Cells in S/G2 phase by rMETase treatment followed by FUCCI-imaging-guided chemotherapy was highly effective in killing the cancer Cells.
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selective methioninase induced trap of cancer Cells in s g2 phase visualized by fucci imaging confers chemosensitivity
Oncotarget, 2014Co-Authors: Shuya Yano, Qinghong Han, Yuying Tan, Michael Bouvet, Toshiyoshi Fujiwara, Robert M HoffmanAbstract:// Shuya Yano 1,2,3 , Shukuan Li 1 , Qinghong Han 1 , Yuying Tan 1 , Michael Bouvet 2 , Toshiyoshi Fujiwara 3 and Robert M. Hoffman 1,2 1 AntiCancer, Inc, San Diego, CA 2 Department of Surgery, University of California, San Diego, CA 3 Department of Gastroenterological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan Correspondence: Robert M. Hoffman, email: // Keywords : Cell cycle, FUCCI, imaging, S/G 2 phase block, recombinant methioninase, rMETase, chemotherapy, HeLa Cells, MCF-7 Cells Received : July 18, 2014 Accepted : August 18, 2014 Published : August 19, 2014 Abstract A major impediment to the response of tumors to chemotherapy is that the large majority of cancer Cells within a tumor are quiescent in G 0 /G 1 , where cancer Cells are resistant to chemotherapy. To attempt to solve this problem of quiescent Cells in a tumor, cancer Cells were treated with recombinant methioninase (rMETase), which selectively traps cancer Cells in S/G 2 . The Cell cycle phase of the cancer Cells was visualized with the fluorescence ubiquitination-based Cell cycle Indicator Cell cycle Indicator (FUCCI). At the time of rMETase-induced S/G 2 -phase blockage, identified by the cancer Cells’ green fluorescence by FUCCI imaging, the cancer Cells were administered S/G 2 -dependent chemotherapy drugs, which interact with DNA or block DNA synthesis such as doxorubicin, cisplatin, or 5-fluorouracil. Treatment of cancer Cells with drugs only, without rMETase-induced S/G 2 phase blockage, led to the majority of the cancer-Cell population being blocked in G 0 /G 1 phase, identified by the cancer Cells becoming red fluorescent in the FUCCI system. The G 0 /G 1 blocked Cells were resistant to the chemotherapy. In contrast, trapping of cancer Cells in S/G 2 phase by rMETase treatment followed by FUCCI-imaging-guided chemotherapy was highly effective in killing the cancer Cells.
Shuya Yano - One of the best experts on this subject based on the ideXlab platform.
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selective methioninase induced trap of cancer Cells in s g2 phase visualized by fucci imaging confers chemosensitivity
Oncotarget, 2014Co-Authors: Shuya Yano, Qinghong Han, Yuying Tan, Michael Bouvet, Toshiyoshi Fujiwara, Robert M HoffmanAbstract:A major impediment to the response of tumors to chemotherapy is that the large majority of cancer Cells within a tumor are quiescent in G0/G1, where cancer Cells are resistant to chemotherapy. To attempt to solve this problem of quiescent Cells in a tumor, cancer Cells were treated with recombinant methioninase (rMETase), which selectively traps cancer Cells in S/G2. The Cell cycle phase of the cancer Cells was visualized with the fluorescence ubiquitination-based Cell cycle Indicator Cell cycle Indicator (FUCCI). At the time of rMETase-induced S/G2-phase blockage, identified by the cancer Cells' green fluorescence by FUCCI imaging, the cancer Cells were administered S/G2-dependent chemotherapy drugs, which interact with DNA or block DNA synthesis such as doxorubicin, cisplatin, or 5-fluorouracil. Treatment of cancer Cells with drugs only, without rMETase-induced S/G2 phase blockage, led to the majority of the cancer-Cell population being blocked in G0/G1 phase, identified by the cancer Cells becoming red fluorescent in the FUCCI system. The G0/G1 blocked Cells were resistant to the chemotherapy. In contrast, trapping of cancer Cells in S/G2 phase by rMETase treatment followed by FUCCI-imaging-guided chemotherapy was highly effective in killing the cancer Cells.
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selective methioninase induced trap of cancer Cells in s g2 phase visualized by fucci imaging confers chemosensitivity
Oncotarget, 2014Co-Authors: Shuya Yano, Qinghong Han, Yuying Tan, Michael Bouvet, Toshiyoshi Fujiwara, Robert M HoffmanAbstract:// Shuya Yano 1,2,3 , Shukuan Li 1 , Qinghong Han 1 , Yuying Tan 1 , Michael Bouvet 2 , Toshiyoshi Fujiwara 3 and Robert M. Hoffman 1,2 1 AntiCancer, Inc, San Diego, CA 2 Department of Surgery, University of California, San Diego, CA 3 Department of Gastroenterological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan Correspondence: Robert M. Hoffman, email: // Keywords : Cell cycle, FUCCI, imaging, S/G 2 phase block, recombinant methioninase, rMETase, chemotherapy, HeLa Cells, MCF-7 Cells Received : July 18, 2014 Accepted : August 18, 2014 Published : August 19, 2014 Abstract A major impediment to the response of tumors to chemotherapy is that the large majority of cancer Cells within a tumor are quiescent in G 0 /G 1 , where cancer Cells are resistant to chemotherapy. To attempt to solve this problem of quiescent Cells in a tumor, cancer Cells were treated with recombinant methioninase (rMETase), which selectively traps cancer Cells in S/G 2 . The Cell cycle phase of the cancer Cells was visualized with the fluorescence ubiquitination-based Cell cycle Indicator Cell cycle Indicator (FUCCI). At the time of rMETase-induced S/G 2 -phase blockage, identified by the cancer Cells’ green fluorescence by FUCCI imaging, the cancer Cells were administered S/G 2 -dependent chemotherapy drugs, which interact with DNA or block DNA synthesis such as doxorubicin, cisplatin, or 5-fluorouracil. Treatment of cancer Cells with drugs only, without rMETase-induced S/G 2 phase blockage, led to the majority of the cancer-Cell population being blocked in G 0 /G 1 phase, identified by the cancer Cells becoming red fluorescent in the FUCCI system. The G 0 /G 1 blocked Cells were resistant to the chemotherapy. In contrast, trapping of cancer Cells in S/G 2 phase by rMETase treatment followed by FUCCI-imaging-guided chemotherapy was highly effective in killing the cancer Cells.
Mimi Ghosh - One of the best experts on this subject based on the ideXlab platform.
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impact of chronic sexual abuse and depression on inflammation and wound healing in the female reproductive tract of hiv uninfected and hiv infected women
PLOS ONE, 2018Co-Authors: Mimi Ghosh, Jason Daniels, Maria Pyra, Monika Juzumaite, Mariel Jais, Kerry Murphy, Tonya N Taylor, Seble Kassaye, Lorie Benning, Mardge H CohenAbstract:Sexual violence is associated with increased risk of HIV acquisition/transmission in women. Forced sex can result in physical trauma to the reproductive tract as well as severe psychological distress. However, immuno-biological mechanisms linking sexual violence and HIV susceptibility are incompletely understood. Using the Women's Interagency HIV Study repository, a total of 77 women were selected to form 4 groups, stratified by HIV serostatus, in the following categories: 1) no sexual abuse history and low depressive symptom score (below clinically significant cut-off, scores <16) (Control); 2) no sexual abuse history but high depressive symptom score, ≥16 (Depression); 3) chronic sexual abuse exposure and low depressive symptom score (Abuse); 4) chronic sexual abuse exposure and high depressive symptom score (Abuse+Depression). Inflammation-associated cytokines/chemokines/proteases (TNF-α, IL-6, IL-1α, IL-1β, TGF-β MIP-3α, IP-10, MCP-1, Cathepsin B), anti-inflammatory/anti-HIV mediators (Secretory leukocyte protease inhibitor (SLPI), Elafin, beta defensin 2 (HBD2), alpha defensins (HNP 1-3), Thrombospondin (TSP-1), Serpin A1, A5, Cystatin A, B), and wound-healing mediators (Gro-α, VEGF, PDGF, EGF, FGF, IGF), were measured in cervical-vaginal lavage (CVL) using ELISA. Linear regression was used to model association of biomarkers with depression and abuse as predictor variables; the interaction between depression and abuse was also tested. Anti-HIV activity in CVL was tested using TZM-bl Indicator Cell line. In HIV-uninfected women, median levels of IL-6 (p = 0.04), IL-1α (p<0.01), TGF-β (p = 0.01), IP-10 (p = <0.01), PDGF (p<0.01) and FGF (p<0.01), differed significantly between groups. Specifically, an association was found between chronic sexual abuse and increased IL-1α (p<0.01), MIP-3α (p = 0.04), IP-10 (p<0.01), Serpin B1 (p = 0.01), FGF (p = 0.04) and decreased TGF-β (p<0.01), MCP-1 (p = 0.02), PDGF (p<0.01). Further, there was evidence of significant interactions between chronic sexual abuse and current depression for IL-1α, IP-10, Serpin A1, Cystatin B, and FGF. In HIV-infected women, median levels of TNF-α (p<0.01), IL-6 (p = 0.05), MIP-3α (p<0.01), and MCP-1 (p = 0.01), differed significantly between groups. Specifically, an association was found between chronic sexual abuse and increased MCP-1 (p = 0.03), Gro-α (p = 0.01) and decreased TNF-α (p<0.01), IL-1α (p = 0.02), MIP-3α (p<0.01) and Cathepsin B (p = 0.03). Current depressive symptoms were associated with significantly decreased MIP-3α (p<0.01). There was evidence of significant interactions between chronic sexual abuse and current depression for MCP-1 and FGF. No significant differences were observed in anti-HIV activity among all eight groups. Heat-map analyses revealed distinct immune network patterns, particularly in the Abuse groups for both HIV-infected and uninfected women. Our data indicates a complex relationship between chronic sexual abuse exposure, depressive symptoms, and FRT immune mediators that are also affected by HIV status. Association of chronic sexual abuse with increase in inflammation-associated cytokine/chemokine expression, along with impaired wound-healing associated growth-factors can create a microenvironment that can facilitate HIV infection. Evaluation of longitudinal changes in exposures and biomarkers are needed to untangle the immuno-biological mechanisms that may put women who endure life-long sexual abuse at increased risk for HIV.
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original article ccl20 mip3α is a novel anti hiv 1 molecule of the human female reproductive tract
American Journal of Reproductive Immunology, 2009Co-Authors: Mimi Ghosh, Zheng Shen, Todd M Schaefer, John V Fahey, Phalguni Gupta, Charles R WiraAbstract:Problem CCL20/MIP3α is a chemokine for immature dendritic Cells as well as an antibacterial against gram-positive and gram-negative bacteria. The role of CCL20/MIP3α as an antiviral is unknown. In this study, we have examined the production of CCL20/MIP3α by epithelial Cells from the upper female reproductive tract as well as its activity as an antiviral molecule. Method of study Primary uterine and Fallopian tube epithelial Cells were treated with Poly(I:C) and CCL20/MIP3α mRNA and protein was measured by Realtime RT-PCR and ELISA assays. Anti-HIV activity was determined using an Indicator Cell line TZM-bl and quantified by using a luminometer. Results Primary uterine and Fallopian tube epithelial Cells produce CCL20/MIP3α constitutively and the production is enhanced following stimulation with viral double-stranded RNA mimic Poly(I:C). Recombinant CCL20/MIP3α was able to inhibit both T-Cell-tropic X4/IIIB and macrophage-tropic R5/BaL HIV-1 when virus was directly incubated with CCL20/MIP3α but not when CCL20/MIP3α was added to Cells either prior to infection or post-infection. This suggests that the mechanism of inhibition is likely to be a direct interaction between HIV-1 and CCL20/MIP3α. Conclusion This study demonstrates that CCL20/MIP3α is an important endogenous anti-HIV-1 microbicide of the female reproductive tract.
Qinghong Han - One of the best experts on this subject based on the ideXlab platform.
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selective methioninase induced trap of cancer Cells in s g2 phase visualized by fucci imaging confers chemosensitivity
Oncotarget, 2014Co-Authors: Shuya Yano, Qinghong Han, Yuying Tan, Michael Bouvet, Toshiyoshi Fujiwara, Robert M HoffmanAbstract:A major impediment to the response of tumors to chemotherapy is that the large majority of cancer Cells within a tumor are quiescent in G0/G1, where cancer Cells are resistant to chemotherapy. To attempt to solve this problem of quiescent Cells in a tumor, cancer Cells were treated with recombinant methioninase (rMETase), which selectively traps cancer Cells in S/G2. The Cell cycle phase of the cancer Cells was visualized with the fluorescence ubiquitination-based Cell cycle Indicator Cell cycle Indicator (FUCCI). At the time of rMETase-induced S/G2-phase blockage, identified by the cancer Cells' green fluorescence by FUCCI imaging, the cancer Cells were administered S/G2-dependent chemotherapy drugs, which interact with DNA or block DNA synthesis such as doxorubicin, cisplatin, or 5-fluorouracil. Treatment of cancer Cells with drugs only, without rMETase-induced S/G2 phase blockage, led to the majority of the cancer-Cell population being blocked in G0/G1 phase, identified by the cancer Cells becoming red fluorescent in the FUCCI system. The G0/G1 blocked Cells were resistant to the chemotherapy. In contrast, trapping of cancer Cells in S/G2 phase by rMETase treatment followed by FUCCI-imaging-guided chemotherapy was highly effective in killing the cancer Cells.
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selective methioninase induced trap of cancer Cells in s g2 phase visualized by fucci imaging confers chemosensitivity
Oncotarget, 2014Co-Authors: Shuya Yano, Qinghong Han, Yuying Tan, Michael Bouvet, Toshiyoshi Fujiwara, Robert M HoffmanAbstract:// Shuya Yano 1,2,3 , Shukuan Li 1 , Qinghong Han 1 , Yuying Tan 1 , Michael Bouvet 2 , Toshiyoshi Fujiwara 3 and Robert M. Hoffman 1,2 1 AntiCancer, Inc, San Diego, CA 2 Department of Surgery, University of California, San Diego, CA 3 Department of Gastroenterological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan Correspondence: Robert M. Hoffman, email: // Keywords : Cell cycle, FUCCI, imaging, S/G 2 phase block, recombinant methioninase, rMETase, chemotherapy, HeLa Cells, MCF-7 Cells Received : July 18, 2014 Accepted : August 18, 2014 Published : August 19, 2014 Abstract A major impediment to the response of tumors to chemotherapy is that the large majority of cancer Cells within a tumor are quiescent in G 0 /G 1 , where cancer Cells are resistant to chemotherapy. To attempt to solve this problem of quiescent Cells in a tumor, cancer Cells were treated with recombinant methioninase (rMETase), which selectively traps cancer Cells in S/G 2 . The Cell cycle phase of the cancer Cells was visualized with the fluorescence ubiquitination-based Cell cycle Indicator Cell cycle Indicator (FUCCI). At the time of rMETase-induced S/G 2 -phase blockage, identified by the cancer Cells’ green fluorescence by FUCCI imaging, the cancer Cells were administered S/G 2 -dependent chemotherapy drugs, which interact with DNA or block DNA synthesis such as doxorubicin, cisplatin, or 5-fluorouracil. Treatment of cancer Cells with drugs only, without rMETase-induced S/G 2 phase blockage, led to the majority of the cancer-Cell population being blocked in G 0 /G 1 phase, identified by the cancer Cells becoming red fluorescent in the FUCCI system. The G 0 /G 1 blocked Cells were resistant to the chemotherapy. In contrast, trapping of cancer Cells in S/G 2 phase by rMETase treatment followed by FUCCI-imaging-guided chemotherapy was highly effective in killing the cancer Cells.
Yuying Tan - One of the best experts on this subject based on the ideXlab platform.
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selective methioninase induced trap of cancer Cells in s g2 phase visualized by fucci imaging confers chemosensitivity
Oncotarget, 2014Co-Authors: Shuya Yano, Qinghong Han, Yuying Tan, Michael Bouvet, Toshiyoshi Fujiwara, Robert M HoffmanAbstract:A major impediment to the response of tumors to chemotherapy is that the large majority of cancer Cells within a tumor are quiescent in G0/G1, where cancer Cells are resistant to chemotherapy. To attempt to solve this problem of quiescent Cells in a tumor, cancer Cells were treated with recombinant methioninase (rMETase), which selectively traps cancer Cells in S/G2. The Cell cycle phase of the cancer Cells was visualized with the fluorescence ubiquitination-based Cell cycle Indicator Cell cycle Indicator (FUCCI). At the time of rMETase-induced S/G2-phase blockage, identified by the cancer Cells' green fluorescence by FUCCI imaging, the cancer Cells were administered S/G2-dependent chemotherapy drugs, which interact with DNA or block DNA synthesis such as doxorubicin, cisplatin, or 5-fluorouracil. Treatment of cancer Cells with drugs only, without rMETase-induced S/G2 phase blockage, led to the majority of the cancer-Cell population being blocked in G0/G1 phase, identified by the cancer Cells becoming red fluorescent in the FUCCI system. The G0/G1 blocked Cells were resistant to the chemotherapy. In contrast, trapping of cancer Cells in S/G2 phase by rMETase treatment followed by FUCCI-imaging-guided chemotherapy was highly effective in killing the cancer Cells.
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selective methioninase induced trap of cancer Cells in s g2 phase visualized by fucci imaging confers chemosensitivity
Oncotarget, 2014Co-Authors: Shuya Yano, Qinghong Han, Yuying Tan, Michael Bouvet, Toshiyoshi Fujiwara, Robert M HoffmanAbstract:// Shuya Yano 1,2,3 , Shukuan Li 1 , Qinghong Han 1 , Yuying Tan 1 , Michael Bouvet 2 , Toshiyoshi Fujiwara 3 and Robert M. Hoffman 1,2 1 AntiCancer, Inc, San Diego, CA 2 Department of Surgery, University of California, San Diego, CA 3 Department of Gastroenterological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan Correspondence: Robert M. Hoffman, email: // Keywords : Cell cycle, FUCCI, imaging, S/G 2 phase block, recombinant methioninase, rMETase, chemotherapy, HeLa Cells, MCF-7 Cells Received : July 18, 2014 Accepted : August 18, 2014 Published : August 19, 2014 Abstract A major impediment to the response of tumors to chemotherapy is that the large majority of cancer Cells within a tumor are quiescent in G 0 /G 1 , where cancer Cells are resistant to chemotherapy. To attempt to solve this problem of quiescent Cells in a tumor, cancer Cells were treated with recombinant methioninase (rMETase), which selectively traps cancer Cells in S/G 2 . The Cell cycle phase of the cancer Cells was visualized with the fluorescence ubiquitination-based Cell cycle Indicator Cell cycle Indicator (FUCCI). At the time of rMETase-induced S/G 2 -phase blockage, identified by the cancer Cells’ green fluorescence by FUCCI imaging, the cancer Cells were administered S/G 2 -dependent chemotherapy drugs, which interact with DNA or block DNA synthesis such as doxorubicin, cisplatin, or 5-fluorouracil. Treatment of cancer Cells with drugs only, without rMETase-induced S/G 2 phase blockage, led to the majority of the cancer-Cell population being blocked in G 0 /G 1 phase, identified by the cancer Cells becoming red fluorescent in the FUCCI system. The G 0 /G 1 blocked Cells were resistant to the chemotherapy. In contrast, trapping of cancer Cells in S/G 2 phase by rMETase treatment followed by FUCCI-imaging-guided chemotherapy was highly effective in killing the cancer Cells.