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Your search keyword '"Costa-Guda, Jessica"' showing total 29 results
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29 results on '"Costa-Guda, Jessica"'

3. Influence of Vitamin D Deficiency on Cyclin D1-Induced Parathyroid Tumorigenesis

Author

Costa-Guda, Jessica, primary, Corrado, Kristin, additional, Bellizzi, Justin, additional, Saria, Elizabeth, additional, Saucier, Kirsten, additional, Guemes-Aragon, Miriam, additional, Kakar, Guntas, additional, Rose, Madison, additional, Pascal, Melanie, additional, Alander, Cynthia, additional, Mallya, Sanjay M, additional, and Arnold, Andrew, additional

Published
2023
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8. List of Contributors

Author

Ackert-Bicknell, Cheryl, primary, Agarwal, Sunita K., additional, Albagha, Omar M.E., additional, Allen, Robyn S., additional, Arnold, Andrew, additional, Bassett, J.H. Duncan, additional, Bateman, John F., additional, Bellido, Teresita, additional, Bonewald, Lynda, additional, Boudin, Eveline, additional, Bouxsein, Mary L., additional, Boyce, Brendan F., additional, Brewer, Niambi S., additional, Brewster, Stephanie J., additional, Briggs, Mike, additional, Brown, Edward M., additional, Brown, Matthew A., additional, Bushinsky, David A., additional, Cabral, Wayne A., additional, Collins, Michael T., additional, Convente, Michael R., additional, Costa-Guda, Jessica, additional, Deng, Hong-Wen, additional, Devuyst, Olivier, additional, Drezner, Marc K., additional, Duncan, Emma L., additional, Egbuna, Ogo I., additional, Eisman, John A., additional, Farber, Charles R., additional, Feldman, David, additional, Ferreira, Carlos R., additional, Gahl, William A., additional, Gorvin, Caroline M., additional, Grol, Matthew W., additional, Guo, Yan, additional, Guse, Kilian, additional, Hannan, Fadil M., additional, Hao, Ruo-Han, additional, Holm, Ingrid A., additional, Igarashi, Takashi, additional, Jacobsen, Christina, additional, Johannesdottir, Fjola, additional, Jüppner, Harald, additional, Kaplan, Frederick S., additional, Karsenty, Gerard, additional, Kovacs, Christopher S., additional, Kuiper, John J., additional, Lee, Brendan H., additional, Loots, Gabriela G., additional, Lories, Rik J., additional, Luyten, Frank P., additional, Malloy, Peter J., additional, Mannstadt, Michael, additional, Marini, Joan C., additional, John Martin, T., additional, Miller, Walter L., additional, Moe, Orson W., additional, Newey, Paul J., additional, Nguyen, Tuan V., additional, Okamoto, Kazuo, additional, Pajevic, Paola D., additional, Papasian, Christopher J., additional, Piret, Siân E., additional, Ralston, Stuart H., additional, Rivadeneira, Fernando, additional, Robey, Pamela G., additional, Rosen, Clifford J., additional, Ruan, Merry Z.C., additional, Scheinman, Steven J., additional, Schurman, Scott J., additional, Sebastian, Aimy, additional, Shen, Yiping, additional, Shore, Eileen M., additional, Silve, Caroline, additional, Sims, Natalie A., additional, Stanley, Alexandra K., additional, Stone, Adrianne, additional, Takayanagi, Hiroshi, additional, Thakker, Rajesh V., additional, Towler, O. Will, additional, Uitterlinden, André G., additional, Valdes, Ana M., additional, van der Eerden, Bram C.J., additional, Van Hul, Wim, additional, Wei, Jianwen, additional, Wein, Marc N., additional, Weinstein, Lee S., additional, Whyte, Michael P., additional, Williams, Graham R., additional, Xing, Lianping, additional, Yang, Tie-Lin, additional, Zankl, Andreas, additional, Ziegler, Shira G., additional, and Zuscik, Michael J., additional

Published
2018
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10. GCM2 Variants in Familial and Multiglandular Primary Hyperparathyroidism

Author

Vincze, Sarah, primary, Peters, Nicholas V, additional, Kuo, Chia-Ling, additional, Brown, Taylor C, additional, Korah, Reju, additional, Murtha, Timothy D, additional, Bellizzi, Justin, additional, Riccardi, Aaliyah, additional, Parham, Kourosh, additional, Carling, Tobias, additional, Costa-Guda, Jessica, additional, and Arnold, Andrew, additional

Published
2021
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11. Parafibromin Abnormalities in Ossifying Fibroma

Author

Costa-Guda, Jessica, primary, Pandya, Chetanya, additional, Strahl, Maya, additional, Taik, Patricia, additional, Sebra, Robert, additional, Chen, Rong, additional, Uzilov, Andrew V, additional, and Arnold, Andrew, additional

Published
2021
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13. GCM2 Variants in Familial and Multiglandular Primary Hyperparathyroidism.

Author

Vincze, Sarah, Peters, Nicholas V., Chia-Ling Kuo, Brown, Taylor C., Korah, Reju, Murtha, Timothy D., Bellizzi, Justin, Riccardi, Aaliyah, Parham, Kourosh, Carling, Tobias, Costa-Guda, Jessica, and Arnold, Andrew

Subjects
HYPERPARATHYROIDISM, POLYMERASE chain reaction
Abstract

Context: Multiglandular and familial parathyroid disease constitute important fractions of primary hyperparathyroidism (PHPT). Germline missense variants of GCM2, a regulator of parathyroid development, were observed in familial isolated hyperparathyroidism and sporadic PHPT. However, as these previously reported GCM2 variants occur at relatively high frequencies in the population, understanding their potential clinical utility will require both additional penetrance data and functional evidence relevant to tumorigenicity. Objective: Determine the frequency of GCM2 variants of interest among patients with sporadic multigland or familial parathyroid disease and assess their penetrance. Design and Patients: DNA-encoding PHPT-associated GCM2 germline variants were polymerase chain reaction–amplified and sequenced from 107 patients with either sporadic multigland or suspected/confirmed familial parathyroid tumors. Results: GCM2 variants were observed in 9 of 107 cases (8.4%): Y282D in 4 patients (6.3%) with sporadic multigland disease; Y394S in 2 patients (11.1%) with familial PHPT and 3 (4.8%) with sporadic multigland disease. Compared with the general population, Y282D was enriched 5.9-fold in multigland disease, but its penetrance was very low (0.02%). Y394S was enriched 79-fold in sporadic multigland disease and 93-fold in familial PHPT, but its penetrance was low (1.33% and 1.04%, respectively). Conclusions: Observed in vitro–activating GCM2 variant alleles are significantly over-represented in PHPT patients with multiglandular or familial disease compared to the general population, yet penetrance values are very low; that is, most individuals with these variants in the population have a very low risk of developing PHPT. The potential clinical utility of detecting these GCM2 variants requires further investigation, including assessing their possible role as pathogenic/low-penetrance alleles. [ABSTRACT FROM AUTHOR]

Published
2022
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16. PIK3CA Mutational Analysis of Parathyroid Adenomas

Author

Riccardi, Aaliyah, primary, Lemos, Carolina, additional, Ramos, Ryan, additional, Bellizzi, Justin, additional, Parham, Kourosh, additional, Brown, Taylor C., additional, Korah, Reju, additional, Carling, Tobias, additional, Costa‐Guda, Jessica, additional, and Arnold, Andrew, additional

Published
2020
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21. Analysis of Activating GCM2 Sequence Variants in Sporadic Parathyroid Adenomas

Author

Riccardi, Aaliyah, primary, Aspir, Tori, additional, Shen, Lilia, additional, Kuo, Chia-Ling, additional, Brown, Taylor C, additional, Korah, Reju, additional, Murtha, Timothy D, additional, Bellizzi, Justin, additional, Parham, Kourosh, additional, Carling, Tobias, additional, Costa-Guda, Jessica, additional, and Arnold, Andrew, additional

Published
2019
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22. New and future perspectives for parathyroid carcinoma.

Author

Perrier, Nancy D., Arnold, Andrew, Costa-Guda, Jessica, Busaidy, Naifa L., Ha Nguyen, Chuang, Hubert H., and Brandi, Maria Luisa

Subjects
FORUMS, CARCINOMA, HISTORICAL literature, BALANCE of payments, EXPERT evidence
Abstract

This report summarizes published data on parathyroid cancer, with the inclusion of topics discussed at MEN2019: 16th International Workshop on Multiple Endocrine Neoplasia, 27-29 March 2019, Houston, TX, USA. An expert panel on parathyroid cancer was constituted by the Steering Committee to address key questions in the field. The objectives were to recap open forum discussion of interested parties from multiple disciplines. The expert panel met in a closed session to consul t on the data to be highlighted on the evidence-based results and on the future directions. Preceding the Conference, members of the expert panel conducted an extensive literature search. All presentations were based upon the best peer-reviewed information taking into account the historical and current literature. Questions were developed by the expert panel on parathyroid carcinoma. A comprehensive literature search for relevant studies was undertaken. This report represents the expert panel's synthesis of the conference material placed in a context designed to be relevant to clinici ans and those engaged in cutting-edge studies of parathyroid carcinoma. This document not only provides a summary of our current knowledge but also places recent advances in its management into a context that should enhance future advances in our under standing of parathyroid carcinoma. [ABSTRACT FROM AUTHOR]

Published
2020
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24. Molecular analysis of cyclin D1 modulators PRKNand FBX4as candidate tumor suppressors in sporadic parathyroid adenomas

Author

Brewer, Kelly, Nip, Isabel, Bellizzi, Justin, Costa-Guda, Jessica, and Arnold, Andrew

Abstract

Primary hyperparathyroidism is most often caused by a sporadic single-gland parathyroid adenoma (PTA), a tumor type for which cyclin D1 is the only known and experimentally validated oncoprotein. However, the molecular origins of its frequent overexpression have remained mostly elusive. In this study, we explored a potential tumorigenic mechanism that could increase cyclin D1 stability through a defect in molecules responsible for its degradation.We examined two tumor suppressor genes known to modulate cyclin D1 ubiquitination, PRKNand FBXO4(FBX4), for evidence of classic two-hit tumor suppressor inactivation within a cohort of 82 PTA cases. We examined the cohort for intragenic inactivating and splice site mutations by Sanger sequencing and for locus-associated loss of heterozygosity (LOH) by microsatellite analysis.We identified no evidence of bi-allelic tumor suppressor inactivation of PRKNor FBXO4via inactivating mutation or splice site perturbation, neither in combination with nor independent of LOH. Among the 82 cases, we encountered previously documented benign single nucleotide polymorphisms (SNPs) in 35 tumors at frequencies similar to those reported in the germlines of the general population. Eight cases exhibited intragenic LOH at the PRKNlocus, in some cases extending to cover at least an additional 1.7 Mb of chromosome 6q25-26. FBXO4was not affected by LOH.The absence of evidence for specific bi-allelic inactivation in PRKNand FBXO4in this sizeable cohort suggests that these genes only rarely, if ever, serve as classic driver tumor suppressors responsible for the growth of PTAs.

Published
2021
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