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18 results on '"Zucker, Amanda"'

1. Clinicogenomic landscape of pancreatic adenocarcinoma identifies KRAS mutant dosage as prognostic of overall survival

Author

Varghese, Anna M., Perry, Maria A., Chou, Joanne F., Nandakumar, Subhiksha, Muldoon, Daniel, Erakky, Amanda, Zucker, Amanda, Fong, Christopher, Mehine, Miika, Nguyen, Bastien, Basturk, Olca, Balogun, Fiyinfolu, Kelsen, David P., Brannon, A. Rose, Mandelker, Diana, Vakiani, Efsevia, Park, Wungki, Yu, Kenneth H., Stadler, Zsofia K., Schattner, Mark A., Jarnagin, William R., Wei, Alice C., Chakravarty, Debyani, Capanu, Marinela, Schultz, Nikolaus, Berger, Michael F., Iacobuzio-Donahue, Christine A., Bandlamudi, Chaitanya, and O’Reilly, Eileen M.

Published
2025
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3. Abstract C074: Clinico-genomic characterization of N=2,460 pancreatic adenocarcinoma identifies KRASMUT dosage as prognostic of overall survival across disease stages

Author

Varghese, Anna M., primary, Perry, Maria A., additional, Muldoon, Daniel, additional, Nandakumar, Subhiksha, additional, Erakky, Amanda, additional, Nguyen, Bastien, additional, Zucker, Amanda, additional, Ozkan, Hulya Sahin, additional, Basturk, Olca, additional, Chakravarty, Debyani, additional, Kelsen, David P., additional, Park, Wungki, additional, Yu, Kenneth H., additional, Wei, Alice C., additional, Schultz, Nikolaus, additional, Berger, Michael F., additional, Iacobuzio-Donahue, Christine, additional, Bandlamudi, Chaitanya, additional, and O'Reilly, Eileen M., additional

Published
2024
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4. Minimal functional driver gene heterogeneity among untreated metastases

Author

Reiter, Johannes G., Makohon-Moore, Alvin P., Gerold, Jeffrey M., Heyde, Alexander, Attiyeh, Marc A., Kohutek, Zachary A., Tokheim, Collin J., Brown, Alexia, DeBlasio, Rayne M., Niyazov, Juliana, Zucker, Amanda, Karchin, Rachel, Kinzler, Kenneth W., Iacobuzio-Donahue, Christine A., Vogelstein, Bert, and Nowak, Martin A.

Published
2018

5. Data from The Genetic Evolution of Treatment-Resistant Cutaneous, Acral, and Uveal Melanomas

Author

Makohon-Moore, Alvin P., primary, Lipson, Evan J., primary, Hooper, Jody E., primary, Zucker, Amanda, primary, Hong, Jungeui, primary, Bielski, Craig M., primary, Hayashi, Akimasa, primary, Tokheim, Collin, primary, Baez, Priscilla, primary, Kappagantula, Rajya, primary, Kohutek, Zachary, primary, Makarov, Vladimir, primary, Riaz, Nadeem, primary, Postow, Michael A., primary, Chapman, Paul B., primary, Karchin, Rachel, primary, Socci, Nicholas D., primary, Solit, David B., primary, Chan, Timothy A., primary, Taylor, Barry S., primary, Topalian, Suzanne L., primary, and Iacobuzio-Donahue, Christine A., primary

Published
2023
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6. Tables S1-S8 from The Genetic Evolution of Treatment-Resistant Cutaneous, Acral, and Uveal Melanomas

Author

Makohon-Moore, Alvin P., primary, Lipson, Evan J., primary, Hooper, Jody E., primary, Zucker, Amanda, primary, Hong, Jungeui, primary, Bielski, Craig M., primary, Hayashi, Akimasa, primary, Tokheim, Collin, primary, Baez, Priscilla, primary, Kappagantula, Rajya, primary, Kohutek, Zachary, primary, Makarov, Vladimir, primary, Riaz, Nadeem, primary, Postow, Michael A., primary, Chapman, Paul B., primary, Karchin, Rachel, primary, Socci, Nicholas D., primary, Solit, David B., primary, Chan, Timothy A., primary, Taylor, Barry S., primary, Topalian, Suzanne L., primary, and Iacobuzio-Donahue, Christine A., primary

Published
2023
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7. Figure S4 from The Genetic Evolution of Treatment-Resistant Cutaneous, Acral, and Uveal Melanomas

Author

Makohon-Moore, Alvin P., primary, Lipson, Evan J., primary, Hooper, Jody E., primary, Zucker, Amanda, primary, Hong, Jungeui, primary, Bielski, Craig M., primary, Hayashi, Akimasa, primary, Tokheim, Collin, primary, Baez, Priscilla, primary, Kappagantula, Rajya, primary, Kohutek, Zachary, primary, Makarov, Vladimir, primary, Riaz, Nadeem, primary, Postow, Michael A., primary, Chapman, Paul B., primary, Karchin, Rachel, primary, Socci, Nicholas D., primary, Solit, David B., primary, Chan, Timothy A., primary, Taylor, Barry S., primary, Topalian, Suzanne L., primary, and Iacobuzio-Donahue, Christine A., primary

Published
2023
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8. Application of high-throughput, high-depth, targeted single-nucleus DNA sequencing in pancreatic cancer

Author

Zhang, Haochen, primary, Karnoub, Elias-Ramzey, additional, Umeda, Shigeaki, additional, Chaligné, Ronan, additional, Masilionis, Ignas, additional, McIntyre, Caitlin, additional, Hayashi, Akimasa, additional, Sashittal, Palash, additional, Zucker, Amanda, additional, Mullen, Katelyn, additional, Makohon-Moore, Alvin, additional, and Iacobuzio-Donahue, Christine, additional

Published
2022
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11. The Genetic Evolution of Treatment-Resistant Cutaneous, Acral, and Uveal Melanomas

Author

Makohon-Moore, Alvin P., primary, Lipson, Evan J., additional, Hooper, Jody E., additional, Zucker, Amanda, additional, Hong, Jungeui, additional, Bielski, Craig M., additional, Hayashi, Akimasa, additional, Tokheim, Collin, additional, Baez, Priscilla, additional, Kappagantula, Rajya, additional, Kohutek, Zachary, additional, Makarov, Vladimir, additional, Riaz, Nadeem, additional, Postow, Michael A., additional, Chapman, Paul B., additional, Karchin, Rachel, additional, Socci, Nicholas D., additional, Solit, David B., additional, Chan, Timothy A., additional, Taylor, Barry S., additional, Topalian, Suzanne L., additional, and Iacobuzio-Donahue, Christine A., additional

Published
2021
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12. Evolutionary Dynamics of Non-Coding Regions in Pancreatic Ductal Adenocarcinoma

Author

Hayashi, Akimasa, primary, Ho, Yu-jui, additional, Makohon-Moore, Alvin P., additional, Zucker, Amanda, additional, Hong, Jungeui, additional, Reiter, Johannes G., additional, Huang, Jinlong, additional, Zhang, Lance, additional, Attiyeh, Marc A., additional, Baez, Priscilla, additional, Kappagantula, Rajya, additional, Melchor, Jerry P., additional, O’Reilly, Eileen M., additional, Socci, Nicholas D., additional, Oki, Shinya, additional, Lowe, Scott W., additional, and Iacobuzio-Donahue, Christine A., additional

Published
2020
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17. The Evolutionary Forest of Pancreatic Cancer.

Author

Mullen KM, Hong J, Attiyeh MA, Hayashi A, Sakamoto H, Kohutek ZA, McIntyre CA, Zhang H, Makohon-Moore AP, Zucker A, Wood LD, Myers MA, Arnold BJ, Zaccaria S, Chou JF, Capanu M, Socci ND, Raphael BJ, and Iacobuzio-Donahue CA

Abstract

The genomic features of pancreatic ductal adenocarcinoma (PDAC) have been well described, yet the evolutionary contexts within which those features occur remains unexplored. We studied the genome landscapes, phylogenies and clonal compositions of 91 PDACs in relation to clinicopathologic features. There was no difference in the number of driver mutations or the evolutionary timing that each mutation occurred. High truncal density, a metric of the accumulation of somatic mutations in the lineage that gave rise to each PDAC, was significantly associated with worse overall survival. Polyclonal, monoclonal or mixed polyclonal/monoclonal metastases were identified across the cohort highlighting multiple forms of inter-tumoral heterogeneity. Advanced stage and treated PDACs had higher odds of being polyclonal, whereas oligometastatic PDACs had fewer driver alterations, a lower fractional allelic loss and increased likelihood of being monoclonal. In sum, our findings reveal novel insights into the dynamic nature of the PDAC genome beyond established genetic paradigms.

Published
2024
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18. Cemiplimab-Induced Hyperosmolar Hyperglycemic State With Concurrent Diabetic Ketoacidosis in a Patient Receiving Treatment for Cutaneous Squamous Cell Carcinoma.

Author

Pyronneau A, Noronha K, Zucker A, Kennett R, and Desai P

Abstract

The immune checkpoint inhibitor (ICI) cemiplimab is a human monoclonal antibody used in the treatment of locally advanced and metastatic cutaneous squamous cell carcinoma (CSCC) not amenable to surgery or radiation therapy. Although cemiplimab shows excellent efficacy with a good tolerability profile, it can cause side effects, including potentially life-threatening endocrinopathies. We discuss the case of a 77-year-old Caucasian female with CSCC treated with only three cycles of cemiplimab who presented with altered mental status and was found to have severe hyperglycemia, hyperosmolarity, ketonemia, glucosuria, and ketonuria concerning for hyperosmolar hyperglycemic syndrome (HHS) with concurrent diabetic ketoacidosis (DKA). The patient made a rapid recovery in the hospital while on standard therapies for HHS/DKA and cemiplimab was discontinued upon discharge. While there have been reports of cemiplimab-induced DKA, to our knowledge, this is the first reported case of cemiplimab-induced HHS-DKA. This report aims to shed light on cemiplimab-induced HHS-DKA and to underscore the need to elucidate the molecular mechanisms underlying ICI-induced diabetes mellitus (ICI-DM)., Competing Interests: The authors have declared that no competing interests exist., (Copyright © 2024, Pyronneau et al.)

Published
2024
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