The Experts below are selected from a list of 9270 Experts worldwide ranked by ideXlab platform
Bruce M Boman - One of the best experts on this subject based on the ideXlab platform.
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abstract 1136 decrease in maturation of stem cells along the neuroendocrine lineage contributes to stem cell Overpopulation that drives human crc development
Cancer Research, 2018Co-Authors: Bruce M Boman, Tao Zhang, Shirin R Modarai, Lynn Opdenacker, Fields JeremyAbstract:Stem cell (SC) Overpopulation is thought to drive tumor initiation and progression during colon cancer development, but it is unclear what causes the SC Overpopulation. Because most neuroendocrine (NE) cells (NECs) in normal colonic crypts reside within the SC niche at the crypt bottom, we thought that aberrant NECs might be linked to the SC Overpopulation. We hypothesized that (i) in normal crypts, SC and NEC populations are anatomically and functionally related, and (ii) during tumorigenesis, changes in these relationships quantitatively correlate with increased SC numbers. We tested this hypothesis - using quantitative immunohistochemical mapping - as a first step towards understanding how interactions between SC and NEC might become altered during colon tumorigenesis. In normal human colonic crypts, most (>80%) cells staining for ALDH1, a colonic SC marker, co-stained for chromogranin-A (CGA) and several other NE markers. Neither ALDH1+ nor CGA+ cells co-stained for MCM2, a marker for proliferating cells. These findings indicate that, in normal colonic crypts, many ALDH1+ cells have NE characteristics. In contrast, the proportion of ALDH1+ cells that co-stained for NE markers progressively decreased (to Citation Format: Bruce M. Boman, Tao Zhang, Shirin Modarai, Lynn Opdenacker, Fields Jeremy. Decrease in maturation of stem cells along the neuroendocrine lineage contributes to stem cell Overpopulation that drives human CRC development [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 1136.
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abstract 5195 progressive Overpopulation of colonic stem cells during tumorigenesis is linked to delayed licensing of cells for dna synthesis in the process of crypt cell maturation
Cancer Research, 2011Co-Authors: Bruce M Boman, Tao Zhang, Zenobia Cofer, Juan P Palazzo, Jeremy Z FieldsAbstract:Since cancer stem cell (SC) Overpopulation drives tumor growth, it is critical to identify mechanisms underlying SC Overpopulation. Our hypothesis that SC Overpopulation underlies development of colorectal cancer (CRC), which was based on our kinetic studies (Cancer Res 61: 3304-13, 2008), has since been supported by our biologic studies showing that ALDH1 is a specific marker for human colonic SC and can track SC Overpopulation during tumor development (Cancer Res 69:3382-9, 2009). We then asked: What cellular mechanisms that normally control SC population size in colonic crypts become dysregulated during colon tumorigenesis? Accordingly, we measured the orderly, sequential phenotypic transitions in human crypts that colonocyte subpopulations undergo during their maturatio– a process involving both proliferation and differentiation. Quantitative immunohistochemical mapping of crypt cell subpopulations was done using markers for SC (ALDH1), proliferating cells (DNA-synthesis-licensing proteins: CDT1/geminin/MCM2), cell-cycle arrest (P21), and apoptosis (M30/TUNEL). Staining indices were used to evaluate changes in maturation during the step-wise progression to colon cancer. The rate of crypt cell maturation was measured using clearance of BrdU from pre-labeled wildtype (C57BL/6) and premalignant (Apc Min/+ ) mouse intestine. In normal human colon, the proportion of cells expressing licensing proteins was low at crypt bottom (where SC reside), high in the lower crypt where proliferating cells reside, and nil in the upper crypt (where differentiated/apoptotic cells reside). In FAP and adenomatous human crypts, SC and proliferating cell populations expanded towards the crypt top while differentiated/apoptotic subpopulations in the upper crypt contracted. Apc Min/+ mouse crypts had slower BrdU clearance than controls. Colonocytes become licensed for DNA synthesis in the transition from SC to proliferating cells; licensing is delayed in premalignant crypts. Moreover, all transitions between cell phenotypes occur more slowly in premalignant human colonic crypts, indicating that crypt cell maturation becomes progressively delayed during colon tumorigenesis. Since crypt cell maturation regulates colonic SC population size, as maturation becomes progressively delayed, crypt SC Overpopulation will develop, leading to dysplasia and colon cancer. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 5195. doi:10.1158/1538-7445.AM2011-5195
Tao Zhang - One of the best experts on this subject based on the ideXlab platform.
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abstract 1136 decrease in maturation of stem cells along the neuroendocrine lineage contributes to stem cell Overpopulation that drives human crc development
Cancer Research, 2018Co-Authors: Bruce M Boman, Tao Zhang, Shirin R Modarai, Lynn Opdenacker, Fields JeremyAbstract:Stem cell (SC) Overpopulation is thought to drive tumor initiation and progression during colon cancer development, but it is unclear what causes the SC Overpopulation. Because most neuroendocrine (NE) cells (NECs) in normal colonic crypts reside within the SC niche at the crypt bottom, we thought that aberrant NECs might be linked to the SC Overpopulation. We hypothesized that (i) in normal crypts, SC and NEC populations are anatomically and functionally related, and (ii) during tumorigenesis, changes in these relationships quantitatively correlate with increased SC numbers. We tested this hypothesis - using quantitative immunohistochemical mapping - as a first step towards understanding how interactions between SC and NEC might become altered during colon tumorigenesis. In normal human colonic crypts, most (>80%) cells staining for ALDH1, a colonic SC marker, co-stained for chromogranin-A (CGA) and several other NE markers. Neither ALDH1+ nor CGA+ cells co-stained for MCM2, a marker for proliferating cells. These findings indicate that, in normal colonic crypts, many ALDH1+ cells have NE characteristics. In contrast, the proportion of ALDH1+ cells that co-stained for NE markers progressively decreased (to Citation Format: Bruce M. Boman, Tao Zhang, Shirin Modarai, Lynn Opdenacker, Fields Jeremy. Decrease in maturation of stem cells along the neuroendocrine lineage contributes to stem cell Overpopulation that drives human CRC development [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 1136.
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abstract 5195 progressive Overpopulation of colonic stem cells during tumorigenesis is linked to delayed licensing of cells for dna synthesis in the process of crypt cell maturation
Cancer Research, 2011Co-Authors: Bruce M Boman, Tao Zhang, Zenobia Cofer, Juan P Palazzo, Jeremy Z FieldsAbstract:Since cancer stem cell (SC) Overpopulation drives tumor growth, it is critical to identify mechanisms underlying SC Overpopulation. Our hypothesis that SC Overpopulation underlies development of colorectal cancer (CRC), which was based on our kinetic studies (Cancer Res 61: 3304-13, 2008), has since been supported by our biologic studies showing that ALDH1 is a specific marker for human colonic SC and can track SC Overpopulation during tumor development (Cancer Res 69:3382-9, 2009). We then asked: What cellular mechanisms that normally control SC population size in colonic crypts become dysregulated during colon tumorigenesis? Accordingly, we measured the orderly, sequential phenotypic transitions in human crypts that colonocyte subpopulations undergo during their maturatio– a process involving both proliferation and differentiation. Quantitative immunohistochemical mapping of crypt cell subpopulations was done using markers for SC (ALDH1), proliferating cells (DNA-synthesis-licensing proteins: CDT1/geminin/MCM2), cell-cycle arrest (P21), and apoptosis (M30/TUNEL). Staining indices were used to evaluate changes in maturation during the step-wise progression to colon cancer. The rate of crypt cell maturation was measured using clearance of BrdU from pre-labeled wildtype (C57BL/6) and premalignant (Apc Min/+ ) mouse intestine. In normal human colon, the proportion of cells expressing licensing proteins was low at crypt bottom (where SC reside), high in the lower crypt where proliferating cells reside, and nil in the upper crypt (where differentiated/apoptotic cells reside). In FAP and adenomatous human crypts, SC and proliferating cell populations expanded towards the crypt top while differentiated/apoptotic subpopulations in the upper crypt contracted. Apc Min/+ mouse crypts had slower BrdU clearance than controls. Colonocytes become licensed for DNA synthesis in the transition from SC to proliferating cells; licensing is delayed in premalignant crypts. Moreover, all transitions between cell phenotypes occur more slowly in premalignant human colonic crypts, indicating that crypt cell maturation becomes progressively delayed during colon tumorigenesis. Since crypt cell maturation regulates colonic SC population size, as maturation becomes progressively delayed, crypt SC Overpopulation will develop, leading to dysplasia and colon cancer. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 5195. doi:10.1158/1538-7445.AM2011-5195
Fields Jeremy - One of the best experts on this subject based on the ideXlab platform.
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abstract 1136 decrease in maturation of stem cells along the neuroendocrine lineage contributes to stem cell Overpopulation that drives human crc development
Cancer Research, 2018Co-Authors: Bruce M Boman, Tao Zhang, Shirin R Modarai, Lynn Opdenacker, Fields JeremyAbstract:Stem cell (SC) Overpopulation is thought to drive tumor initiation and progression during colon cancer development, but it is unclear what causes the SC Overpopulation. Because most neuroendocrine (NE) cells (NECs) in normal colonic crypts reside within the SC niche at the crypt bottom, we thought that aberrant NECs might be linked to the SC Overpopulation. We hypothesized that (i) in normal crypts, SC and NEC populations are anatomically and functionally related, and (ii) during tumorigenesis, changes in these relationships quantitatively correlate with increased SC numbers. We tested this hypothesis - using quantitative immunohistochemical mapping - as a first step towards understanding how interactions between SC and NEC might become altered during colon tumorigenesis. In normal human colonic crypts, most (>80%) cells staining for ALDH1, a colonic SC marker, co-stained for chromogranin-A (CGA) and several other NE markers. Neither ALDH1+ nor CGA+ cells co-stained for MCM2, a marker for proliferating cells. These findings indicate that, in normal colonic crypts, many ALDH1+ cells have NE characteristics. In contrast, the proportion of ALDH1+ cells that co-stained for NE markers progressively decreased (to Citation Format: Bruce M. Boman, Tao Zhang, Shirin Modarai, Lynn Opdenacker, Fields Jeremy. Decrease in maturation of stem cells along the neuroendocrine lineage contributes to stem cell Overpopulation that drives human CRC development [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 1136.
Jeremy Z Fields - One of the best experts on this subject based on the ideXlab platform.
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abstract 5195 progressive Overpopulation of colonic stem cells during tumorigenesis is linked to delayed licensing of cells for dna synthesis in the process of crypt cell maturation
Cancer Research, 2011Co-Authors: Bruce M Boman, Tao Zhang, Zenobia Cofer, Juan P Palazzo, Jeremy Z FieldsAbstract:Since cancer stem cell (SC) Overpopulation drives tumor growth, it is critical to identify mechanisms underlying SC Overpopulation. Our hypothesis that SC Overpopulation underlies development of colorectal cancer (CRC), which was based on our kinetic studies (Cancer Res 61: 3304-13, 2008), has since been supported by our biologic studies showing that ALDH1 is a specific marker for human colonic SC and can track SC Overpopulation during tumor development (Cancer Res 69:3382-9, 2009). We then asked: What cellular mechanisms that normally control SC population size in colonic crypts become dysregulated during colon tumorigenesis? Accordingly, we measured the orderly, sequential phenotypic transitions in human crypts that colonocyte subpopulations undergo during their maturatio– a process involving both proliferation and differentiation. Quantitative immunohistochemical mapping of crypt cell subpopulations was done using markers for SC (ALDH1), proliferating cells (DNA-synthesis-licensing proteins: CDT1/geminin/MCM2), cell-cycle arrest (P21), and apoptosis (M30/TUNEL). Staining indices were used to evaluate changes in maturation during the step-wise progression to colon cancer. The rate of crypt cell maturation was measured using clearance of BrdU from pre-labeled wildtype (C57BL/6) and premalignant (Apc Min/+ ) mouse intestine. In normal human colon, the proportion of cells expressing licensing proteins was low at crypt bottom (where SC reside), high in the lower crypt where proliferating cells reside, and nil in the upper crypt (where differentiated/apoptotic cells reside). In FAP and adenomatous human crypts, SC and proliferating cell populations expanded towards the crypt top while differentiated/apoptotic subpopulations in the upper crypt contracted. Apc Min/+ mouse crypts had slower BrdU clearance than controls. Colonocytes become licensed for DNA synthesis in the transition from SC to proliferating cells; licensing is delayed in premalignant crypts. Moreover, all transitions between cell phenotypes occur more slowly in premalignant human colonic crypts, indicating that crypt cell maturation becomes progressively delayed during colon tumorigenesis. Since crypt cell maturation regulates colonic SC population size, as maturation becomes progressively delayed, crypt SC Overpopulation will develop, leading to dysplasia and colon cancer. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 5195. doi:10.1158/1538-7445.AM2011-5195
J. Palazzo - One of the best experts on this subject based on the ideXlab platform.
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Key mechanisms underlying cancer stem cell Overpopulation in colon carcinomas: Implications for anticancer therapy.
Journal of Clinical Oncology, 2011Co-Authors: B. M. Boman, T. Zhang, J. PalazzoAbstract:e13548 Background: Since cancer stem cell (SC) Overpopulation appears to drive tumor growth in the colon (Boman and Huang, JCO 26:2828-38, 2008), effective or even curative treatments will likely require targeting mechanisms that underlie SC Overpopulation. To identify such mechanisms, the organization and distribution of colonocyte cell subpopulations in human colon tissues were investigated as a way to evaluate crypt cell maturation. We hypothesized that maturation of these subpopulations becomes dysregulated during colon tumorigenesis. Methods: Quantitative immunohistochemical mapping of crypt cell subpopulations was done using markers for SC (ALDH1), proliferating cells (DNA-synthesis-licensing proteins: CDT1/geminin/MCM2), cell-cycle arrest (P21), and apoptosis (M30/TUNEL). Staining indices were used to evaluate changes in maturation during the step-wise progression to colon cancer. The rate of crypt cell maturation was measured using clearance of BrdU from pre-labeled wildtype (C57BL/6) and premalig...
