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834 results on '"Yuspa, Stuart H."'

3. Murine models of HRAS-mediated cutaneous skeletal hypophosphatemia syndrome suggest bone as the FGF23 excess source

Author

Ovejero, Diana, Michel, Zachary, Cataisson, Christophe, Saikali, Amanda, Galisteo, Rebeca, Yuspa, Stuart H., Collins, Michael T., and de Castro, Luis F.

Subjects
Gene expression -- Health aspects, Fibroblast growth factors -- Health aspects, Hypophosphatemia -- Genetic aspects -- Development and progression -- Care and treatment, Health care industry
Abstract

Cutaneous skeletal hypophosphatemia syndrome (CSHS) is a mosaic RA Sopathy characterized by the association of dysplastic skeletal lesions, congenital skin nevi of epidermal and/or melanocytic origin, and FGF23-mediated hypophosphatemia. The primary physiological source of circulating FGF23 is bone cells. However, several reports have suggested skin lesions as the source of excess FGF23 in CSHS. Consequently, without convincing evidence of efficacy, many patients with CSHS have undergone painful removal of cutaneous lesions in an effort to normalize blood phosphate levels. This study aims to elucidate whether the source of FGF23 excess in CSHS is RAS mutation-bearing bone or skin lesions. Toward this end, we analyzed the expression and activity of Fgf23 in two mouse models expressing similar HRAS/Hras activating mutations in a mosaic-like fashion in either bone or epidermal tissue. We found that HRAS hyperactivity in bone, not skin, caused excess of bioactive intact FGF23, hypophosphatemia, and osteomalacia. Our findings support RAS- mutated dysplastic bone as the primary source of physiologically active FGF23 excess in patients with CSHS. This evidence informs the care of patients with CSHS, arguing against the practice of nevi removal to decrease circulating, physiologically active FGF23., Introduction Cutaneous skeletal hypophosphatemia syndrome (CSHS) is characterized by the association of dysplastic skeletal lesions, congenital skin nevi of epidermal and/or melanocytic origin (including epidermal nevi [EN], giant congenital melanocytic [...]

Published
2023
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4. Endogenous retroviruses promote homeostatic and inflammatory responses to the microbiota

Author

Lima-Junior, Djalma S., Krishnamurthy, Siddharth R., Bouladoux, Nicolas, Collins, Nicholas, Han, Seong-Ji, Chen, Erin Y., Constantinides, Michael G., Link, Verena M., Lim, Ai Ing, Enamorado, Michel, Cataisson, Christophe, Gil, Louis, Rao, Indira, Farley, Taylor K., Koroleva, Galina, Attig, Jan, Yuspa, Stuart H., Fischbach, Michael A., Kassiotis, George, and Belkaid, Yasmine

Published
2021
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11. Data from T-Cell Deletion of MyD88 Connects IL17 and IκBζ to RAS Oncogenesis

Author

Cataisson, Christophe, primary, Salcedo, Rosalba, primary, Michalowski, Aleksandra M., primary, Klosterman, Mary, primary, Naik, Shruti, primary, Li, Luowei, primary, Pan, Michelle J., primary, Sweet, Amalia, primary, Chen, Jin-Qiu, primary, Kostecka, Laurie G., primary, Karwan, Megan, primary, Smith, Loretta, primary, Dai, Ren-Ming, primary, Stewart, C. Andrew, primary, Lyakh, Lyudmila, primary, Hsieh, Wang-Ting, primary, Khan, Asra, primary, Yang, Howard, primary, Lee, Maxwell, primary, Trinchieri, Giorgio, primary, and Yuspa, Stuart H., primary

Published
2023
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12. Table S3 from T-Cell Deletion of MyD88 Connects IL17 and IκBζ to RAS Oncogenesis

Author

Cataisson, Christophe, primary, Salcedo, Rosalba, primary, Michalowski, Aleksandra M., primary, Klosterman, Mary, primary, Naik, Shruti, primary, Li, Luowei, primary, Pan, Michelle J., primary, Sweet, Amalia, primary, Chen, Jin-Qiu, primary, Kostecka, Laurie G., primary, Karwan, Megan, primary, Smith, Loretta, primary, Dai, Ren-Ming, primary, Stewart, C. Andrew, primary, Lyakh, Lyudmila, primary, Hsieh, Wang-Ting, primary, Khan, Asra, primary, Yang, Howard, primary, Lee, Maxwell, primary, Trinchieri, Giorgio, primary, and Yuspa, Stuart H., primary

Published
2023
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13. Supplemental Figures 1-3 from T-Cell Deletion of MyD88 Connects IL17 and IκBζ to RAS Oncogenesis

Author

Cataisson, Christophe, primary, Salcedo, Rosalba, primary, Michalowski, Aleksandra M., primary, Klosterman, Mary, primary, Naik, Shruti, primary, Li, Luowei, primary, Pan, Michelle J., primary, Sweet, Amalia, primary, Chen, Jin-Qiu, primary, Kostecka, Laurie G., primary, Karwan, Megan, primary, Smith, Loretta, primary, Dai, Ren-Ming, primary, Stewart, C. Andrew, primary, Lyakh, Lyudmila, primary, Hsieh, Wang-Ting, primary, Khan, Asra, primary, Yang, Howard, primary, Lee, Maxwell, primary, Trinchieri, Giorgio, primary, and Yuspa, Stuart H., primary

Published
2023
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17. Data from S100A7 Enhances Mammary Tumorigenesis through Upregulation of Inflammatory Pathways

Author

Nasser, Mohd W., primary, Qamri, Zahida, primary, Deol, Yadwinder S., primary, Ravi, Janani, primary, Powell, Catherine A., primary, Trikha, Prashant, primary, Schwendener, Reto A., primary, Bai, Xue-Feng, primary, Shilo, Konstantin, primary, Zou, Xianghong, primary, Leone, Gustavo, primary, Wolf, Ronald, primary, Yuspa, Stuart H., primary, and Ganju, Ramesh K., primary

Published
2023
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20. Supplementary Table 1 from S100A7 Enhances Mammary Tumorigenesis through Upregulation of Inflammatory Pathways

Author

Nasser, Mohd W., primary, Qamri, Zahida, primary, Deol, Yadwinder S., primary, Ravi, Janani, primary, Powell, Catherine A., primary, Trikha, Prashant, primary, Schwendener, Reto A., primary, Bai, Xue-Feng, primary, Shilo, Konstantin, primary, Zou, Xianghong, primary, Leone, Gustavo, primary, Wolf, Ronald, primary, Yuspa, Stuart H., primary, and Ganju, Ramesh K., primary

Published
2023
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26. Supplementary Figure 1 from S100A7 Enhances Mammary Tumorigenesis through Upregulation of Inflammatory Pathways

Author

Nasser, Mohd W., primary, Qamri, Zahida, primary, Deol, Yadwinder S., primary, Ravi, Janani, primary, Powell, Catherine A., primary, Trikha, Prashant, primary, Schwendener, Reto A., primary, Bai, Xue-Feng, primary, Shilo, Konstantin, primary, Zou, Xianghong, primary, Leone, Gustavo, primary, Wolf, Ronald, primary, Yuspa, Stuart H., primary, and Ganju, Ramesh K., primary

Published
2023
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28. Supplementary Legends for Tables 1-2, Figures 1-7, Methods from RasGRP3 Contributes to Formation and Maintenance of the Prostate Cancer Phenotype

Author

Yang, Dazhi, primary, Kedei, Noemi, primary, Li, Luowei, primary, Tao, Juan, primary, Velasquez, Julia F., primary, Michalowski, Aleksandra M., primary, Tóth, Balázs I., primary, Marincsák, Rita, primary, Varga, Attila, primary, Bíró, Tamás, primary, Yuspa, Stuart H., primary, and Blumberg, Peter M., primary

Published
2023
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49. Host CLIC4 expression in the tumor microenvironment is essential for breast cancer metastatic competence

Author

Sanchez, Vanesa C., primary, Yang, Howard H., additional, Craig-Lucas, Alayna, additional, Dubois, Wendy, additional, Carofino, Brandi L., additional, Lack, Justin, additional, Dwyer, Jennifer E., additional, Simpson, R. Mark, additional, Cataisson, Christophe, additional, Lee, Max P., additional, Luo, Ji, additional, Hunter, Kent W., additional, and Yuspa, Stuart H., additional

Published
2022
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