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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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4. Methylation Analyses Reveal Promoter Hypermethylation as a Rare Cause of “Second Hit” in Germline BRCA1-Associated Pancreatic Ductal Adenocarcinoma

Author

Zheng-Lin, Binbin, Rainone, Michael, Varghese, Anna M, Yu, Kenneth H, Park, Wungki, Berger, Michael, Mehine, Miika, Chou, Joanne, Capanu, Marinela, Mandelker, Diana, Stadler, Zsofia K, Birsoy, Ozge, Jairam, Sowmya, Yang, Ciyu, Li, Yirong, Wong, Donna, Benhamida, Jamal K, Ladanyi, Marc, Zhang, Liying, and O’Reilly, Eileen M

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Oncology and Carcinogenesis, Digestive Diseases, Rare Diseases, Cancer, Genetics, Pancreatic Cancer, Humans, BRCA1 Protein, Carcinoma, Pancreatic Ductal, Pancreatic Neoplasms, Poly(ADP-ribose) Polymerase Inhibitors, Germ-Line Mutation, DNA Methylation, Promoter Regions, Genetic, Pharmacology and Pharmaceutical Sciences, Oncology & Carcinogenesis, Pharmacology & Pharmacy, Pharmacology and pharmaceutical sciences
Abstract

Background and objectivePancreatic ductal adenocarcinoma (PDAC) is characterized by the occurrence of pathogenic variants in BRCA1/2 in 5-6% of patients. Biallelic loss of BRCA1/2 enriches for response to platinum agents and poly (ADP-ribose) polymerase 1 inhibitors. There is a dearth of evidence on the mechanism of inactivation of the wild-type BRCA1 allele in PDAC tumors with a germline BRCA1 (gBRCA1) pathogenic or likely pathogenic variant (P/LPV). Herein, we examine promotor hypermethylation as a "second hit" mechanism in patients with gBRCA1-PDAC.MethodsWe evaluated patients with PDAC who underwent Memorial Sloan Kettering-Integrated Mutation Profiling of Actionable Cancer Targets (MSK-IMPACT) somatic and germline testing from an institutional database. DNA isolated from tumor tissue and matched normal peripheral blood were sequenced by MSK-IMPACT. In patients with gBRCA1-PDAC, we examined the somatic BRCA1 mutation status and promotor methylation status of the tumor BRCA1 allele via a methylation array analysis. In patients with sufficient remaining DNA, a second methylation analysis by pyrosequencing was performed.ResultsOf 1012 patients with PDAC, 19 (1.9%) were identified to harbor a gBRCA1 P/LPV. Fifteen patients underwent a methylation array and the mean percentage of BRCA1 promotor methylation was 3.62%. In seven patients in whom sufficient DNA was available, subsequent pyrosequencing confirmed an unmethylated BRCA1 promotor. Loss of heterozygosity was detected in 12 of 19 (63%, 95% confidence interval 38-84) patients, demonstrating loss of heterozygosity is the major molecular mechanism of BRCA1 inactivation in PDAC. Two (10.5%) cases had a somatic BRCA1 mutation.ConclusionsIn patients with gBRCA1-P/LPV-PDAC, loss of heterozygosity is the main inactivating mechanism of the wild-type BRCA1 allele in the tumor, and methylation of the BRCA1 promoter is a distinctly uncommon occurrence.

Published
2022

8. Clinical Outcomes Among Patients With Metastatic Pancreatic Ductal Adenocarcinoma Treated With Liposomal Irinotecan

Author

Yu, Kenneth H, Hendifar, Andrew E, Alese, Olatunji B, Draper, Amber, Abdelrahim, Maen, Burns, Ethan, Khan, Gazala, Cockrum, Paul, Bhak, Rachel H, Nguyen, Catherine, DerSarkissian, Maral, Duh, Mei Sheng, and Bahary, Nathan

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Oncology and Carcinogenesis, Pancreatic Cancer, Cancer, Clinical Research, Digestive Diseases, Clinical Trials and Supportive Activities, Rare Diseases, 6.1 Pharmaceuticals, Evaluation of treatments and therapeutic interventions, cancer management, liposomal irinotecan, metastasis, pancreatic cancer, pancreatic ductal adenocarcinoma, Clinical sciences, Oncology and carcinogenesis
Abstract

BackgroundThe NAPOLI-1 trial demonstrated that liposomal irinotecan in combination with fluorouracil (5-FU) and leucovorin (LV) prolonged survival with a manageable safety profile in patients with metastatic pancreatic ductal adenocarcinoma (mPDAC) previously treated with gemcitabine-based therapy. Real-world data on clinical outcomes associated with liposomal irinotecan in NAPOLI-1-based regimens is needed to further substantiate this.MethodsThis real-world, retrospective chart review study included patients with mPDAC who received NAPOLI-1-based regimens from six academic centers in the United States. Liposomal irinotecan initiation defined the index date. Overall survival (OS) and progression-free survival (PFS) were assessed with Kaplan-Meier methodology.ResultsThere were 374 patients evaluated; median age was 68 years, and 51% were female. Among 326 patients with baseline ECOG information, approximately 74% had ECOG score

Published
2021

9. Identification of Resistance Pathways Specific to Malignancy Using Organoid Models of Pancreatic Cancer

Author

Ponz-Sarvise, Mariano, Corbo, Vincenzo, Tiriac, Hervé, Engle, Dannielle D, Frese, Kristopher K, Oni, Tobiloba E, Hwang, Chang-Il, Öhlund, Daniel, Chio, Iok In Christine, Baker, Lindsey A, Filippini, Dea, Wright, Kevin, Bapiro, Tashinga E, Huang, Pearl, Smith, Paul, Yu, Kenneth H, Jodrell, Duncan I, Park, Youngkyu, and Tuveson, David A

Subjects
Cancer, Pancreatic Cancer, Rare Diseases, Digestive Diseases, Clinical Research, Development of treatments and therapeutic interventions, 5.1 Pharmaceuticals, Animals, Antineoplastic Agents, Cell Line, Tumor, Disease Models, Animal, Dose-Response Relationship, Drug, Drug Resistance, Neoplasm, Humans, Mice, Mice, Transgenic, Organoids, Pancreatic Neoplasms, Phosphorylation, Protein Kinase Inhibitors, Proto-Oncogene Proteins c-akt, Signal Transduction, Tissue Culture Techniques, Oncology and Carcinogenesis, Oncology & Carcinogenesis
Abstract

PURPOSE:KRAS is mutated in the majority of pancreatic ductal adenocarcinoma. MAPK and PI3K-AKT are primary KRAS effector pathways, but combined MAPK and PI3K inhibition has not been demonstrated to be clinically effective to date. We explore the resistance mechanisms uniquely employed by malignant cells. EXPERIMENTAL DESIGN:We evaluated the expression and activation of receptor tyrosine kinases in response to combined MEK and AKT inhibition in KPC mice and pancreatic ductal organoids. In addition, we sought to determine the therapeutic efficacy of targeting resistance pathways induced by MEK and AKT inhibition in order to identify malignant-specific vulnerabilities. RESULTS:Combined MEK and AKT inhibition modestly extended the survival of KPC mice and increased Egfr and ErbB2 phosphorylation levels. Tumor organoids, but not their normal counterparts, exhibited elevated phosphorylation of ERBB2 and ERBB3 after MEK and AKT blockade. A pan-ERBB inhibitor synergized with MEK and AKT blockade in human PDA organoids, whereas this was not observed for the EGFR inhibitor erlotinib. Combined MEK and ERBB inhibitor treatment of human organoid orthotopic xenografts was sufficient to cause tumor regression in short-term intervention studies. CONCLUSIONS:Analyses of normal and tumor pancreatic organoids revealed the importance of ERBB activation during MEK and AKT blockade primarily in the malignant cultures. The lack of ERBB hyperactivation in normal organoids suggests a larger therapeutic index. In our models, pan-ERBB inhibition was synergistic with dual inhibition of MEK and AKT, and the combination of a pan-ERBB inhibitor with MEK antagonists showed the highest activity both in vitro and in vivo.

Published
2019

10. The glycan CA19-9 promotes pancreatitis and pancreatic cancer in mice

Author

Engle, Dannielle D, Tiriac, Hervé, Rivera, Keith D, Pommier, Arnaud, Whalen, Sean, Oni, Tobiloba E, Alagesan, Brinda, Lee, Eun Jung, Yao, Melissa A, Lucito, Matthew S, Spielman, Benjamin, Da Silva, Brandon, Schoepfer, Christina, Wright, Kevin, Creighton, Brianna, Afinowicz, Lauren, Yu, Kenneth H, Grützmann, Robert, Aust, Daniela, Gimotty, Phyllis A, Pollard, Katherine S, Hruban, Ralph H, Goggins, Michael G, Pilarsky, Christian, Park, Youngkyu, Pappin, Darryl J, Hollingsworth, Michael A, and Tuveson, David A

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Prevention, Cancer, Rare Diseases, Pancreatic Cancer, Digestive Diseases, 2.1 Biological and endogenous factors, Aetiology, Acute Disease, Animals, CA-19-9 Antigen, Carcinogenesis, Carcinoma, Pancreatic Ductal, Cell Line, Tumor, Chronic Disease, ErbB Receptors, Extracellular Matrix Proteins, Fucosyltransferases, Galactosyltransferases, Glycosylation, Humans, Mice, Molecular Targeted Therapy, Pancreatic Neoplasms, Pancreatitis, General Science & Technology
Abstract

Glycosylation alterations are indicative of tissue inflammation and neoplasia, but whether these alterations contribute to disease pathogenesis is largely unknown. To study the role of glycan changes in pancreatic disease, we inducibly expressed human fucosyltransferase 3 and β1,3-galactosyltransferase 5 in mice, reconstituting the glycan sialyl-Lewisa, also known as carbohydrate antigen 19-9 (CA19-9). Notably, CA19-9 expression in mice resulted in rapid and severe pancreatitis with hyperactivation of epidermal growth factor receptor (EGFR) signaling. Mechanistically, CA19-9 modification of the matricellular protein fibulin-3 increased its interaction with EGFR, and blockade of fibulin-3, EGFR ligands, or CA19-9 prevented EGFR hyperactivation in organoids. CA19-9-mediated pancreatitis was reversible and could be suppressed with CA19-9 antibodies. CA19-9 also cooperated with the KrasG12D oncogene to produce aggressive pancreatic cancer. These findings implicate CA19-9 in the etiology of pancreatitis and pancreatic cancer and nominate CA19-9 as a therapeutic target.

Published
2019

11. Organoid Profiling Identifies Common Responders to Chemotherapy in Pancreatic Cancer.

Author

Tiriac, Hervé, Belleau, Pascal, Engle, Dannielle D, Plenker, Dennis, Deschênes, Astrid, Somerville, Tim DD, Froeling, Fieke EM, Burkhart, Richard A, Denroche, Robert E, Jang, Gun-Ho, Miyabayashi, Koji, Young, C Megan, Patel, Hardik, Ma, Michelle, LaComb, Joseph F, Palmaira, Randze Lerie D, Javed, Ammar A, Huynh, Jasmine C, Johnson, Molly, Arora, Kanika, Robine, Nicolas, Shah, Minita, Sanghvi, Rashesh, Goetz, Austin B, Lowder, Cinthya Y, Martello, Laura, Driehuis, Else, LeComte, Nicolas, Askan, Gokce, Iacobuzio-Donahue, Christine A, Clevers, Hans, Wood, Laura D, Hruban, Ralph H, Thompson, Elizabeth, Aguirre, Andrew J, Wolpin, Brian M, Sasson, Aaron, Kim, Joseph, Wu, Maoxin, Bucobo, Juan Carlos, Allen, Peter, Sejpal, Divyesh V, Nealon, William, Sullivan, James D, Winter, Jordan M, Gimotty, Phyllis A, Grem, Jean L, DiMaio, Dominick J, Buscaglia, Jonathan M, Grandgenett, Paul M, Brody, Jonathan R, Hollingsworth, Michael A, O'Kane, Grainne M, Notta, Faiyaz, Kim, Edward, Crawford, James M, Devoe, Craig, Ocean, Allyson, Wolfgang, Christopher L, Yu, Kenneth H, Li, Ellen, Vakoc, Christopher R, Hubert, Benjamin, Fischer, Sandra E, Wilson, Julie M, Moffitt, Richard, Knox, Jennifer, Krasnitz, Alexander, Gallinger, Steven, and Tuveson, David A

Subjects
Organoids, Tumor Cells, Cultured, Humans, Pancreatic Neoplasms, Antineoplastic Agents, Drug Screening Assays, Antitumor, Prospective Studies, Gene Expression Profiling, Sequence Analysis, RNA, Gene Expression Regulation, Neoplastic, Drug Resistance, Neoplasm, Gene Regulatory Networks, Molecular Targeted Therapy, Standard of Care, Precision Medicine, Genetics, Pancreatic Cancer, Rare Diseases, Digestive Diseases, Orphan Drug, Cancer, Detection, screening and diagnosis, Development of treatments and therapeutic interventions, 4.1 Discovery and preclinical testing of markers and technologies, 5.1 Pharmaceuticals, Good Health and Well Being, Oncology and Carcinogenesis
Abstract

Pancreatic cancer is the most lethal common solid malignancy. Systemic therapies are often ineffective, and predictive biomarkers to guide treatment are urgently needed. We generated a pancreatic cancer patient-derived organoid (PDO) library that recapitulates the mutational spectrum and transcriptional subtypes of primary pancreatic cancer. New driver oncogenes were nominated and transcriptomic analyses revealed unique clusters. PDOs exhibited heterogeneous responses to standard-of-care chemotherapeutics and investigational agents. In a case study manner, we found that PDO therapeutic profiles paralleled patient outcomes and that PDOs enabled longitudinal assessment of chemosensitivity and evaluation of synchronous metastases. We derived organoid-based gene expression signatures of chemosensitivity that predicted improved responses for many patients to chemotherapy in both the adjuvant and advanced disease settings. Finally, we nominated alternative treatment strategies for chemorefractory PDOs using targeted agent therapeutic profiling. We propose that combined molecular and therapeutic profiling of PDOs may predict clinical response and enable prospective therapeutic selection.Significance: New approaches to prioritize treatment strategies are urgently needed to improve survival and quality of life for patients with pancreatic cancer. Combined genomic, transcriptomic, and therapeutic profiling of PDOs can identify molecular and functional subtypes of pancreatic cancer, predict therapeutic responses, and facilitate precision medicine for patients with pancreatic cancer. Cancer Discov; 8(9); 1112-29. ©2018 AACR.See related commentary by Collisson, p. 1062This article is highlighted in the In This Issue feature, p. 1047.

Published
2018

12. Early results of the PASS-01 trial: Pancreatic adenocarcinoma signature stratification for treatment-01.

Author

Knox, Jennifer J., primary, Jaffee, Elizabeth M., additional, O'Kane, Grainne M., additional, King, Daniel, additional, Laheru, Dan, additional, Yu, Kenneth H., additional, Perez, Kimberly, additional, Habowski, Amber N, additional, Grant, Robert C, additional, Fischer, Sandra, additional, Aguirre, Andrew, additional, Jang, Raymond Woo-Jun, additional, Devoe, Craig E., additional, O'Reilly, Eileen M., additional, Dodd, Anna, additional, Wolpin, Brian M., additional, Ye, Xiang Y, additional, Notta, Faiyaz, additional, Gallinger, Steven, additional, and Tuveson, David A., additional

Published
2024
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14. Precision medicine for pancreatic cancer: characterizing the clinicogenomic landscape and outcomes of KRAS G12C-mutated disease.

Author

Keane, Fergus, Chou, Joanne F, Walch, Henry, Schoenfeld, Joshua, Singhal, Anupriya, Cowzer, Darren, Harrold, Emily, O'Connor, Catherine A, Park, Wungki, Varghese, Anna, Dika, Imane El, Balogun, Fiyinfolu, Yu, Kenneth H, Capanu, Marinela, Schultz, Nikolaus, Yaeger, Rona, and O'Reilly, Eileen M

Subjects
PANCREATIC duct, PANCREATIC cancer, RAS oncogenes, BODY mass index, OVERALL survival
Abstract

Background Mutated Kirsten rat sarcoma viral oncogene homolog (KRAS) is the most common oncogene alteration in pancreatic ductal adenocarcinoma, and KRAS glycine to cystine substitution at codon 12 (G12C) mutations (KRAS G12Cmut) are observed in 1%-2%. Several inhibitors of KRAS G12C have recently demonstrated promise in solid tumors, including pancreatic cancer. Little is known regarding clinical, genomics, and outcome data of this population. Methods Patients with pancreatic cancer and KRAS G12Cmut were identified at Memorial Sloan Kettering Cancer Center and via the American Association of Cancer Research Project Genomics, Evidence, Neoplasia, Information, Exchange database. Clinical, treatment, genomic, and outcomes data were analyzed. A cohort of patients at Memorial Sloan Kettering Cancer Center with non-G12C KRAS pancreatic cancer was included for comparison. Results Among 3571 patients with pancreatic ductal adenocarcinoma, 39 (1.1%) with KRAS G12Cmut were identified. Median age was 67 years, and 56% were female. Median body mass index was 29.2 kg/m2, and 67% had a smoking history. Median overall survival was 13 months (95% CI: 9.4 months, not reached) for stage IV and 26 months (95% CI: 23 months, not reached) for stage I-III. Complete genomic data (via American Association of Cancer Research Project Genomics, Evidence, Neoplasia, Information, Exchange database) was available for 74 patients. Most common co-alterations included TP53 (73%), CDKN2A (33%), SMAD4 (28%), and ARID1A (21%). Compared with a large cohort (n = 2931) of non-G12C KRAS- mutated pancreatic ductal adenocarcinoma, ARID1A co-mutations were more frequent in KRAS G12Cmut (P  < .05). Overall survival did not differ between KRAS G12Cmut and non-G12C KRAS pancreatic ductal adenocarcinoma. Germline pathogenic variants were identified in 17% of patients; 2 patients received KRAS G12C-directed therapy. Conclusion Pancreatic cancer and KRAS G12Cmut may be associated with a distinct clinical phenotype. Genomic features are similar to non-G12C KRAS- mutated pancreatic cancer, although enrichment of ARID1A co-mutations was observed. Targeting of KRAS G12C in pancreatic cancer provides a precedent for broader KRAS targeting in pancreatic cancer. [ABSTRACT FROM AUTHOR]

Published
2024
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16. Concurrent Germline BRCA1/2 and Mismatch Repair Mutations in Young-Onset Pancreatic and Colorectal Cancer: The Importance of Comprehensive Germline and Somatic Characterization to Inform Therapeutic Options

Author

Ozer, Muhammet, Ranganathan, Megha, Lecomte, Nicolas, Schvartzman, Juan M., Walch, Henry S., Chatila, Walid K., Hong, Jungeui, Carlo, Maria I., Walsh, Michael F., Sheehan, Margaret, Mandelker, Diana, Ceyhan-Birsoy, Ozge, Maio, Anna, Kemel, Yelena, Iacobuzio-Donahue, Christine A., OʼReilly, Eileen M., and Yu, Kenneth H.

Published
2022
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17. Pharmacologically controlling protein-protein interactions through epichaperomes for therapeutic vulnerability in cancer

Author

Joshi, Suhasini, Gomes, Erica DaGama, Wang, Tai, Corben, Adriana, Taldone, Tony, Gandu, Srinivasa, Xu, Chao, Sharma, Sahil, Buddaseth, Salma, Yan, Pengrong, Chan, Lon Yin L., Gokce, Askan, Rajasekhar, Vinagolu K., Shrestha, Lisa, Panchal, Palak, Almodovar, Justina, Digwal, Chander S., Rodina, Anna, Merugu, Swathi, Pillarsetty, NagaVaraKishore, Miclea, Vlad, Peter, Radu I., Wang, Wanyan, Ginsberg, Stephen D., Tang, Laura, Mattar, Marissa, de Stanchina, Elisa, Yu, Kenneth H., Lowery, Maeve, Grbovic-Huezo, Olivera, O’Reilly, Eileen M., Janjigian, Yelena, Healey, John H., Jarnagin, William R., Allen, Peter J., Sander, Chris, Erdjument-Bromage, Hediye, Neubert, Thomas A., Leach, Steven D., and Chiosis, Gabriela

Published
2021
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19. Organoid models of human and mouse ductal pancreatic cancer.

Author

Boj, Sylvia F, Hwang, Chang-Il, Baker, Lindsey A, Chio, Iok In Christine, Engle, Dannielle D, Corbo, Vincenzo, Jager, Myrthe, Ponz-Sarvise, Mariano, Tiriac, Hervé, Spector, Mona S, Gracanin, Ana, Oni, Tobiloba, Yu, Kenneth H, van Boxtel, Ruben, Huch, Meritxell, Rivera, Keith D, Wilson, John P, Feigin, Michael E, Öhlund, Daniel, Handly-Santana, Abram, Ardito-Abraham, Christine M, Ludwig, Michael, Elyada, Ela, Alagesan, Brinda, Biffi, Giulia, Yordanov, Georgi N, Delcuze, Bethany, Creighton, Brianna, Wright, Kevin, Park, Youngkyu, Morsink, Folkert HM, Molenaar, I Quintus, Borel Rinkes, Inne H, Cuppen, Edwin, Hao, Yuan, Jin, Ying, Nijman, Isaac J, Iacobuzio-Donahue, Christine, Leach, Steven D, Pappin, Darryl J, Hammell, Molly, Klimstra, David S, Basturk, Olca, Hruban, Ralph H, Offerhaus, George Johan, Vries, Robert GJ, Clevers, Hans, and Tuveson, David A

Subjects
Pancreas, Organoids, Animals, Mice, Inbred C57BL, Humans, Mice, Mice, Nude, Carcinoma, Pancreatic Ductal, Pancreatic Neoplasms, Organ Culture Techniques, Models, Biological, Cancer, Pancreatic Cancer, Rare Diseases, Biotechnology, Digestive Diseases, Aetiology, 2.1 Biological and endogenous factors, Good Health and Well Being, Biological Sciences, Medical and Health Sciences, Developmental Biology
Abstract

Pancreatic cancer is one of the most lethal malignancies due to its late diagnosis and limited response to treatment. Tractable methods to identify and interrogate pathways involved in pancreatic tumorigenesis are urgently needed. We established organoid models from normal and neoplastic murine and human pancreas tissues. Pancreatic organoids can be rapidly generated from resected tumors and biopsies, survive cryopreservation, and exhibit ductal- and disease-stage-specific characteristics. Orthotopically transplanted neoplastic organoids recapitulate the full spectrum of tumor development by forming early-grade neoplasms that progress to locally invasive and metastatic carcinomas. Due to their ability to be genetically manipulated, organoids are a platform to probe genetic cooperation. Comprehensive transcriptional and proteomic analyses of murine pancreatic organoids revealed genes and pathways altered during disease progression. The confirmation of many of these protein changes in human tissues demonstrates that organoids are a facile model system to discover characteristics of this deadly malignancy.

Published
2015

20. Abstract C104: Dual primary pancreas cancers – Related or independent lesions?

Author

Schoenfeld, Joshua D., primary, Sahan-Ozkan, Hulya, additional, Bilani, Nadeem, additional, D'Angelica, Michael I., additional, Jarnagin, William R., additional, Drebin, Jeffrey, additional, Reidy-Lagunes, Diane, additional, Wei, Alice C., additional, Chalasani, Sree B., additional, Varghese, Anna M., additional, Balogun, Fiyinfolu, additional, Park, Wungki, additional, Yu, Kenneth H., additional, Basturk, Olca, additional, and O'Reilly, Eileen M., additional

Published
2024
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21. 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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22. An Experimental Investigation of Low-Frequency Active Excitation in Scramjet Combustor Using a Micro-Pulse Detonation Engine.

Author

Lee, Keon-Hyeong, Kim, Min-Su, Choi, Jeong-Yeol, and Yu, Kenneth H.

Subjects
COMBUSTION efficiency, AIR heaters, MACH number, FLAME, PRESSURE measurement
Abstract

A micro-pulse detonation engine (μPDE) was designed and installed to a direct-connect scramjet combustor of Pusan National University (PNU-DCSC). The active excitation on the scramjet combustor was experimentally studied using the μPDE operating at frequencies of 10–20 Hz. A vitiation air heater (VAH) was used to supply high-enthalpy vitiated air to the isolator and the scramjet combustor at a Mach number of 2.0, with a total temperature of 1600 K and a total pressure of 1.68 MPa. The exit of μPDE was located at the center of the cavity of the scramjet combustor. Active excitation was performed at equivalence ratios of 0.111 and 0.163, and characteristics were analyzed through Schlieren recording and bottom wall pressure measurement. As a result, when the detonation emitted from the μPDE entered the scramjet combustor, it instantly formed a shock train and moved forward within the scramjet combustor. The flame instantaneously changed from the cavity shear layer flame to the cavity flame. Through bottom wall pressure measurement, it was also observed that active excitation resulted in a significant pressure increase near the cavity compared to when active excitation was not performed. This revealed combustion characteristics, indicating improved combustion efficiency from the pressure increase in the scramjet combustor. [ABSTRACT FROM AUTHOR]

Published
2024
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23. Local Control and Survival After Induction Chemotherapy and Ablative Radiation Versus Resection for Pancreatic Ductal Adenocarcinoma With Vascular Involvement

Author

Jolissaint, Joshua S., Reyngold, Marsha, Bassmann, Jared, Seier, Kenneth P., Gönen, Mithat, Varghese, Anna M., Yu, Kenneth H., Park, Wungki, O’Reilly, Eileen M., Balachandran, Vinod P., D’Angelica, Michael I., Drebin, Jeffrey A., Kingham, T. Peter, Soares, Kevin C., Jarnagin, William R., Crane, Christopher H., and Wei, Alice C.

Published
2021
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28. Phase II trial of veliparib in patients with previously treated BRCA-mutated pancreas ductal adenocarcinoma

Author

Lowery, Maeve A., Kelsen, David P., Capanu, Marinela, Smith, Sloane C., Lee, Jonathan W., Stadler, Zsofia K., Moore, Malcolm J., Kindler, Hedy L., Golan, Talia, Segal, Amiel, Maynard, Hannah, Hollywood, Ellen, Moynahan, MaryEllen, Salo-Mullen, Erin E., Do, Richard Kinh Gian, Chen, Alice P., Yu, Kenneth H., Tang, Laura H., and O'Reilly, Eileen M.

Published
2018
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29. Salvage Ablative Radiotherapy for Isolated Local Recurrence of Pancreatic Adenocarcinoma following Definitive Surgery.

Author

Dee, Edward Christopher, Ng, Victor C., O'Reilly, Eileen M., Wei, Alice C., Lobaugh, Stephanie M., Varghese, Anna M., Zinovoy, Melissa, Romesser, Paul B., Wu, Abraham J., Hajj, Carla, Cuaron, John J., Khalil, Danny N., Park, Wungki, Yu, Kenneth H., Zhang, Zhigang, Drebin, Jeffrey A., Jarnagin, William R., Crane, Christopher H., and Reyngold, Marsha

Subjects
ADENOCARCINOMA, CHEMORADIOTHERAPY, PANCREATIC surgery, RADIOTHERAPY, SURGICAL excision, OVERALL survival, RADIATION doses
Abstract

Introduction: The rate of isolated locoregional recurrence after surgery for pancreatic adenocarcinoma (PDAC) approaches 25%. Ablative radiation therapy (A-RT) has improved outcomes for locally advanced disease in the primary setting. We sought to evaluate the outcomes of salvage A-RT for isolated locoregional recurrence and examine the relationship between subsequent patterns of failure, radiation dose, and treatment volume. Methods: We conducted a retrospective analysis of all consecutive participants who underwent A-RT for an isolated locoregional recurrence of PDAC after prior surgery at our institution between 2016 and 2021. Treatment consisted of ablative dose (BED10 98–100 Gy) to the gross disease with an additional prophylactic low dose (BED10 < 50 Gy), with the elective volume covering a 1.5 cm isotropic expansion around the gross disease and the circumference of the involved vessels. Local and locoregional failure (LF and LRF, respectively) estimated by the cumulative incidence function with competing risks, distant metastasis-free and overall survival (DMFS and OS, respectively) estimated by the Kaplan–Meier method, and toxicities scored by CTCAE v5.0 are reported. Location of recurrence was mapped to the dose region on the initial radiation plan. Results: Among 65 participants (of whom two had two A-RT courses), the median age was 67 (range 37–87) years, 36 (55%) were male, and 53 (82%) had undergone pancreaticoduodenectomy with a median disease-free interval to locoregional recurrence of 16 (range, 6–71) months. Twenty-seven participants (42%) received chemotherapy prior to A-RT. With a median follow-up of 35 months (95%CI, 26–56 months) from diagnosis of recurrence, 24-month OS and DMFS were 57% (95%CI, 46–72%) and 22% (95%CI, 14–37%), respectively, while 24-month cumulative incidence of in-field LF and total LRF were 28% (95%CI, 17–40%) and 36% (95%CI 24–48%), respectively. First failure after A-RT was distant in 35 patients (53.8%), locoregional in 12 patients (18.5%), and synchronous distant and locoregional in 10 patients (15.4%). Most locoregional failures occurred in elective low-dose volumes. Acute and chronic grade 3–4 toxicities were noted in 1 (1.5%) and 5 patients (7.5%), respectively. Conclusions: Salvage A-RT achieves favorable OS and local control outcomes in participants with an isolated locoregional recurrence of PDAC after surgical resection. Consideration should be given to extending high-dose fields to include adjacent segments of at-risk vessels beyond direct contact with the gross disease. [ABSTRACT FROM AUTHOR]

Published
2024
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32. Abstract 6421: Molecular profiles and single cell analysis identify immunogenic pancreatic ductal adenocarcinoma (iPDAC)

Author

Park, Wungki, primary, O'Connor, Catherine, additional, Umeda, Shigeaki, additional, Sharma, Roshan, additional, Zhu, Yingjie, additional, Karnoub, Elias-Ramzey, additional, Varghese, Anna, additional, Soares, Kevin C., additional, Jimemez, Alejandro, additional, Yavas, Asli, additional, Yu, Kenneth H., additional, Vinod, Balachandran P., additional, Chou, Joanne F., additional, Khalil, Danny N., additional, David, Kelsen, additional, Ozkan, Hulya Sahin, additional, Basturk, Olca, additional, Capanu, Marinela, additional, Nawy, Tal, additional, Berger, Michael F., additional, Abou-Alfa, Ghassan K., additional, Reis-Filho, Jorge S., additional, Chaligne, Ronan, additional, Riaz, Nadeem, additional, Pe'er, Dana, additional, Iacobuzio-Donahue, Christine, additional, and O'Reilly, Eileen M., additional

Published
2023
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33. Supplementary Table S13 from Cross-Species Single-Cell Analysis of Pancreatic Ductal Adenocarcinoma Reveals Antigen-Presenting Cancer-Associated Fibroblasts

Author

Elyada, Ela, primary, Bolisetty, Mohan, primary, Laise, Pasquale, primary, Flynn, William F., primary, Courtois, Elise T., primary, Burkhart, Richard A., primary, Teinor, Jonathan A., primary, Belleau, Pascal, primary, Biffi, Giulia, primary, Lucito, Matthew S., primary, Sivajothi, Santhosh, primary, Armstrong, Todd D., primary, Engle, Dannielle D., primary, Yu, Kenneth H., primary, Hao, Yuan, primary, Wolfgang, Christopher L., primary, Park, Youngkyu, primary, Preall, Jonathan, primary, Jaffee, Elizabeth M., primary, Califano, Andrea, primary, Robson, Paul, primary, and Tuveson, David A., primary

Published
2023
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34. Table S3 from Organoid Profiling Identifies Common Responders to Chemotherapy in Pancreatic Cancer

Author

Tiriac, Hervé, primary, Belleau, Pascal, primary, Engle, Dannielle D., primary, Plenker, Dennis, primary, Deschênes, Astrid, primary, Somerville, Tim D. D., primary, Froeling, Fieke E. M., primary, Burkhart, Richard A., primary, Denroche, Robert E., primary, Jang, Gun-Ho, primary, Miyabayashi, Koji, primary, Young, C. Megan, primary, Patel, Hardik, primary, Ma, Michelle, primary, LaComb, Joseph F., primary, Palmaira, Randze Lerie D., primary, Javed, Ammar A., primary, Huynh, Jasmine C., primary, Johnson, Molly, primary, Arora, Kanika, primary, Robine, Nicolas, primary, Shah, Minita, primary, Sanghvi, Rashesh, primary, Goetz, Austin B., primary, Lowder, Cinthya Y., primary, Martello, Laura, primary, Driehuis, Else, primary, LeComte, Nicolas, primary, Askan, Gokce, primary, Iacobuzio-Donahue, Christine A., primary, Clevers, Hans, primary, Wood, Laura D., primary, Hruban, Ralph H., primary, Thompson, Elizabeth, primary, Aguirre, Andrew J., primary, Wolpin, Brian M., primary, Sasson, Aaron, primary, Kim, Joseph, primary, Wu, Maoxin, primary, Bucobo, Juan Carlos, primary, Allen, Peter, primary, Sejpal, Divyesh V., primary, Nealon, William, primary, Sullivan, James D., primary, Winter, Jordan M., primary, Gimotty, Phyllis A., primary, Grem, Jean L., primary, DiMaio, Dominick J., primary, Buscaglia, Jonathan M., primary, Grandgenett, Paul M., primary, Brody, Jonathan R., primary, Hollingsworth, Michael A., primary, O'Kane, Grainne M., primary, Notta, Faiyaz, primary, Kim, Edward, primary, Crawford, James M., primary, Devoe, Craig, primary, Ocean, Allyson, primary, Wolfgang, Christopher L., primary, Yu, Kenneth H., primary, Li, Ellen, primary, Vakoc, Christopher R., primary, Hubert, Benjamin, primary, Fischer, Sandra E., primary, Wilson, Julie M., primary, Moffitt, Richard, primary, Knox, Jennifer, primary, Krasnitz, Alexander, primary, Gallinger, Steven, primary, and Tuveson, David A., primary

Published
2023
Full Text
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35. Data from Organoid Profiling Identifies Common Responders to Chemotherapy in Pancreatic Cancer

Author

Tiriac, Hervé, primary, Belleau, Pascal, primary, Engle, Dannielle D., primary, Plenker, Dennis, primary, Deschênes, Astrid, primary, Somerville, Tim D. D., primary, Froeling, Fieke E. M., primary, Burkhart, Richard A., primary, Denroche, Robert E., primary, Jang, Gun-Ho, primary, Miyabayashi, Koji, primary, Young, C. Megan, primary, Patel, Hardik, primary, Ma, Michelle, primary, LaComb, Joseph F., primary, Palmaira, Randze Lerie D., primary, Javed, Ammar A., primary, Huynh, Jasmine C., primary, Johnson, Molly, primary, Arora, Kanika, primary, Robine, Nicolas, primary, Shah, Minita, primary, Sanghvi, Rashesh, primary, Goetz, Austin B., primary, Lowder, Cinthya Y., primary, Martello, Laura, primary, Driehuis, Else, primary, LeComte, Nicolas, primary, Askan, Gokce, primary, Iacobuzio-Donahue, Christine A., primary, Clevers, Hans, primary, Wood, Laura D., primary, Hruban, Ralph H., primary, Thompson, Elizabeth, primary, Aguirre, Andrew J., primary, Wolpin, Brian M., primary, Sasson, Aaron, primary, Kim, Joseph, primary, Wu, Maoxin, primary, Bucobo, Juan Carlos, primary, Allen, Peter, primary, Sejpal, Divyesh V., primary, Nealon, William, primary, Sullivan, James D., primary, Winter, Jordan M., primary, Gimotty, Phyllis A., primary, Grem, Jean L., primary, DiMaio, Dominick J., primary, Buscaglia, Jonathan M., primary, Grandgenett, Paul M., primary, Brody, Jonathan R., primary, Hollingsworth, Michael A., primary, O'Kane, Grainne M., primary, Notta, Faiyaz, primary, Kim, Edward, primary, Crawford, James M., primary, Devoe, Craig, primary, Ocean, Allyson, primary, Wolfgang, Christopher L., primary, Yu, Kenneth H., primary, Li, Ellen, primary, Vakoc, Christopher R., primary, Hubert, Benjamin, primary, Fischer, Sandra E., primary, Wilson, Julie M., primary, Moffitt, Richard, primary, Knox, Jennifer, primary, Krasnitz, Alexander, primary, Gallinger, Steven, primary, and Tuveson, David A., primary

Published
2023
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36. Supplementary Tables S1, S2, S3, S5, S7, S9, S11, S12, S17, S19, S21 from Cross-Species Single-Cell Analysis of Pancreatic Ductal Adenocarcinoma Reveals Antigen-Presenting Cancer-Associated Fibroblasts

Author

Elyada, Ela, primary, Bolisetty, Mohan, primary, Laise, Pasquale, primary, Flynn, William F., primary, Courtois, Elise T., primary, Burkhart, Richard A., primary, Teinor, Jonathan A., primary, Belleau, Pascal, primary, Biffi, Giulia, primary, Lucito, Matthew S., primary, Sivajothi, Santhosh, primary, Armstrong, Todd D., primary, Engle, Dannielle D., primary, Yu, Kenneth H., primary, Hao, Yuan, primary, Wolfgang, Christopher L., primary, Park, Youngkyu, primary, Preall, Jonathan, primary, Jaffee, Elizabeth M., primary, Califano, Andrea, primary, Robson, Paul, primary, and Tuveson, David A., primary

Published
2023
Full Text
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37. Supplemental Figures from Organoid Profiling Identifies Common Responders to Chemotherapy in Pancreatic Cancer

Author

Tiriac, Hervé, primary, Belleau, Pascal, primary, Engle, Dannielle D., primary, Plenker, Dennis, primary, Deschênes, Astrid, primary, Somerville, Tim D. D., primary, Froeling, Fieke E. M., primary, Burkhart, Richard A., primary, Denroche, Robert E., primary, Jang, Gun-Ho, primary, Miyabayashi, Koji, primary, Young, C. Megan, primary, Patel, Hardik, primary, Ma, Michelle, primary, LaComb, Joseph F., primary, Palmaira, Randze Lerie D., primary, Javed, Ammar A., primary, Huynh, Jasmine C., primary, Johnson, Molly, primary, Arora, Kanika, primary, Robine, Nicolas, primary, Shah, Minita, primary, Sanghvi, Rashesh, primary, Goetz, Austin B., primary, Lowder, Cinthya Y., primary, Martello, Laura, primary, Driehuis, Else, primary, LeComte, Nicolas, primary, Askan, Gokce, primary, Iacobuzio-Donahue, Christine A., primary, Clevers, Hans, primary, Wood, Laura D., primary, Hruban, Ralph H., primary, Thompson, Elizabeth, primary, Aguirre, Andrew J., primary, Wolpin, Brian M., primary, Sasson, Aaron, primary, Kim, Joseph, primary, Wu, Maoxin, primary, Bucobo, Juan Carlos, primary, Allen, Peter, primary, Sejpal, Divyesh V., primary, Nealon, William, primary, Sullivan, James D., primary, Winter, Jordan M., primary, Gimotty, Phyllis A., primary, Grem, Jean L., primary, DiMaio, Dominick J., primary, Buscaglia, Jonathan M., primary, Grandgenett, Paul M., primary, Brody, Jonathan R., primary, Hollingsworth, Michael A., primary, O'Kane, Grainne M., primary, Notta, Faiyaz, primary, Kim, Edward, primary, Crawford, James M., primary, Devoe, Craig, primary, Ocean, Allyson, primary, Wolfgang, Christopher L., primary, Yu, Kenneth H., primary, Li, Ellen, primary, Vakoc, Christopher R., primary, Hubert, Benjamin, primary, Fischer, Sandra E., primary, Wilson, Julie M., primary, Moffitt, Richard, primary, Knox, Jennifer, primary, Krasnitz, Alexander, primary, Gallinger, Steven, primary, and Tuveson, David A., primary

Published
2023
Full Text
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38. Data from Cross-Species Single-Cell Analysis of Pancreatic Ductal Adenocarcinoma Reveals Antigen-Presenting Cancer-Associated Fibroblasts

Author

Elyada, Ela, primary, Bolisetty, Mohan, primary, Laise, Pasquale, primary, Flynn, William F., primary, Courtois, Elise T., primary, Burkhart, Richard A., primary, Teinor, Jonathan A., primary, Belleau, Pascal, primary, Biffi, Giulia, primary, Lucito, Matthew S., primary, Sivajothi, Santhosh, primary, Armstrong, Todd D., primary, Engle, Dannielle D., primary, Yu, Kenneth H., primary, Hao, Yuan, primary, Wolfgang, Christopher L., primary, Park, Youngkyu, primary, Preall, Jonathan, primary, Jaffee, Elizabeth M., primary, Califano, Andrea, primary, Robson, Paul, primary, and Tuveson, David A., primary

Published
2023
Full Text
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39. Supplemental Table Legends from Organoid Profiling Identifies Common Responders to Chemotherapy in Pancreatic Cancer

Author

Tiriac, Hervé, primary, Belleau, Pascal, primary, Engle, Dannielle D., primary, Plenker, Dennis, primary, Deschênes, Astrid, primary, Somerville, Tim D. D., primary, Froeling, Fieke E. M., primary, Burkhart, Richard A., primary, Denroche, Robert E., primary, Jang, Gun-Ho, primary, Miyabayashi, Koji, primary, Young, C. Megan, primary, Patel, Hardik, primary, Ma, Michelle, primary, LaComb, Joseph F., primary, Palmaira, Randze Lerie D., primary, Javed, Ammar A., primary, Huynh, Jasmine C., primary, Johnson, Molly, primary, Arora, Kanika, primary, Robine, Nicolas, primary, Shah, Minita, primary, Sanghvi, Rashesh, primary, Goetz, Austin B., primary, Lowder, Cinthya Y., primary, Martello, Laura, primary, Driehuis, Else, primary, LeComte, Nicolas, primary, Askan, Gokce, primary, Iacobuzio-Donahue, Christine A., primary, Clevers, Hans, primary, Wood, Laura D., primary, Hruban, Ralph H., primary, Thompson, Elizabeth, primary, Aguirre, Andrew J., primary, Wolpin, Brian M., primary, Sasson, Aaron, primary, Kim, Joseph, primary, Wu, Maoxin, primary, Bucobo, Juan Carlos, primary, Allen, Peter, primary, Sejpal, Divyesh V., primary, Nealon, William, primary, Sullivan, James D., primary, Winter, Jordan M., primary, Gimotty, Phyllis A., primary, Grem, Jean L., primary, DiMaio, Dominick J., primary, Buscaglia, Jonathan M., primary, Grandgenett, Paul M., primary, Brody, Jonathan R., primary, Hollingsworth, Michael A., primary, O'Kane, Grainne M., primary, Notta, Faiyaz, primary, Kim, Edward, primary, Crawford, James M., primary, Devoe, Craig, primary, Ocean, Allyson, primary, Wolfgang, Christopher L., primary, Yu, Kenneth H., primary, Li, Ellen, primary, Vakoc, Christopher R., primary, Hubert, Benjamin, primary, Fischer, Sandra E., primary, Wilson, Julie M., primary, Moffitt, Richard, primary, Knox, Jennifer, primary, Krasnitz, Alexander, primary, Gallinger, Steven, primary, and Tuveson, David A., primary

Published
2023
Full Text
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40. Supplementary Figures S1-S8 from Cross-Species Single-Cell Analysis of Pancreatic Ductal Adenocarcinoma Reveals Antigen-Presenting Cancer-Associated Fibroblasts

Author

Elyada, Ela, primary, Bolisetty, Mohan, primary, Laise, Pasquale, primary, Flynn, William F., primary, Courtois, Elise T., primary, Burkhart, Richard A., primary, Teinor, Jonathan A., primary, Belleau, Pascal, primary, Biffi, Giulia, primary, Lucito, Matthew S., primary, Sivajothi, Santhosh, primary, Armstrong, Todd D., primary, Engle, Dannielle D., primary, Yu, Kenneth H., primary, Hao, Yuan, primary, Wolfgang, Christopher L., primary, Park, Youngkyu, primary, Preall, Jonathan, primary, Jaffee, Elizabeth M., primary, Califano, Andrea, primary, Robson, Paul, primary, and Tuveson, David A., primary

Published
2023
Full Text
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41. Supplemental Figure Legends from Organoid Profiling Identifies Common Responders to Chemotherapy in Pancreatic Cancer

Author

Tiriac, Hervé, primary, Belleau, Pascal, primary, Engle, Dannielle D., primary, Plenker, Dennis, primary, Deschênes, Astrid, primary, Somerville, Tim D. D., primary, Froeling, Fieke E. M., primary, Burkhart, Richard A., primary, Denroche, Robert E., primary, Jang, Gun-Ho, primary, Miyabayashi, Koji, primary, Young, C. Megan, primary, Patel, Hardik, primary, Ma, Michelle, primary, LaComb, Joseph F., primary, Palmaira, Randze Lerie D., primary, Javed, Ammar A., primary, Huynh, Jasmine C., primary, Johnson, Molly, primary, Arora, Kanika, primary, Robine, Nicolas, primary, Shah, Minita, primary, Sanghvi, Rashesh, primary, Goetz, Austin B., primary, Lowder, Cinthya Y., primary, Martello, Laura, primary, Driehuis, Else, primary, LeComte, Nicolas, primary, Askan, Gokce, primary, Iacobuzio-Donahue, Christine A., primary, Clevers, Hans, primary, Wood, Laura D., primary, Hruban, Ralph H., primary, Thompson, Elizabeth, primary, Aguirre, Andrew J., primary, Wolpin, Brian M., primary, Sasson, Aaron, primary, Kim, Joseph, primary, Wu, Maoxin, primary, Bucobo, Juan Carlos, primary, Allen, Peter, primary, Sejpal, Divyesh V., primary, Nealon, William, primary, Sullivan, James D., primary, Winter, Jordan M., primary, Gimotty, Phyllis A., primary, Grem, Jean L., primary, DiMaio, Dominick J., primary, Buscaglia, Jonathan M., primary, Grandgenett, Paul M., primary, Brody, Jonathan R., primary, Hollingsworth, Michael A., primary, O'Kane, Grainne M., primary, Notta, Faiyaz, primary, Kim, Edward, primary, Crawford, James M., primary, Devoe, Craig, primary, Ocean, Allyson, primary, Wolfgang, Christopher L., primary, Yu, Kenneth H., primary, Li, Ellen, primary, Vakoc, Christopher R., primary, Hubert, Benjamin, primary, Fischer, Sandra E., primary, Wilson, Julie M., primary, Moffitt, Richard, primary, Knox, Jennifer, primary, Krasnitz, Alexander, primary, Gallinger, Steven, primary, and Tuveson, David A., primary

Published
2023
Full Text
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42. Data from Clinico-genomic Characterization of ATM and HRD in Pancreas Cancer: Application for Practice

Author

Park, Wungki, primary, O'Connor, Catherine A., primary, Bandlamudi, Chaitanya, primary, Forman, Daniella, primary, Chou, Joanne F., primary, Umeda, Shigeaki, primary, Reyngold, Marsha, primary, Varghese, Anna M., primary, Keane, Fergus, primary, Balogun, Fiyinfolu, primary, Yu, Kenneth H., primary, Kelsen, David P., primary, Crane, Christopher, primary, Capanu, Marinela, primary, Iacobuzio-Donahue, Christine, primary, and O'Reilly, Eileen M., primary

Published
2023
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43. Supplementary Figure from Clinico-genomic Characterization of ATM and HRD in Pancreas Cancer: Application for Practice

Author

Park, Wungki, primary, O'Connor, Catherine A., primary, Bandlamudi, Chaitanya, primary, Forman, Daniella, primary, Chou, Joanne F., primary, Umeda, Shigeaki, primary, Reyngold, Marsha, primary, Varghese, Anna M., primary, Keane, Fergus, primary, Balogun, Fiyinfolu, primary, Yu, Kenneth H., primary, Kelsen, David P., primary, Crane, Christopher, primary, Capanu, Marinela, primary, Iacobuzio-Donahue, Christine, primary, and O'Reilly, Eileen M., primary

Published
2023
Full Text
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44. Supplementary Data from Clinico-genomic Characterization of ATM and HRD in Pancreas Cancer: Application for Practice

Author

Park, Wungki, primary, O'Connor, Catherine A., primary, Bandlamudi, Chaitanya, primary, Forman, Daniella, primary, Chou, Joanne F., primary, Umeda, Shigeaki, primary, Reyngold, Marsha, primary, Varghese, Anna M., primary, Keane, Fergus, primary, Balogun, Fiyinfolu, primary, Yu, Kenneth H., primary, Kelsen, David P., primary, Crane, Christopher, primary, Capanu, Marinela, primary, Iacobuzio-Donahue, Christine, primary, and O'Reilly, Eileen M., primary

Published
2023
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45. Supplemental Tables 1 - 3 and Figures 1 - 2 from Pharmacogenomic Modeling of Circulating Tumor and Invasive Cells for Prediction of Chemotherapy Response and Resistance in Pancreatic Cancer

Author

Yu, Kenneth H., primary, Ricigliano, Mark, primary, Hidalgo, Manuel, primary, Abou-Alfa, Ghassan K., primary, Lowery, Maeve A., primary, Saltz, Leonard B., primary, Crotty, Joseph F., primary, Gary, Kristen, primary, Cooper, Brandon, primary, Lapidus, Rena, primary, Sadowska, Mariola, primary, and O'Reilly, Eileen M., primary

Published
2023
Full Text
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46. Supplementary Figure Legends from Genomic Methods Identify Homologous Recombination Deficiency in Pancreas Adenocarcinoma and Optimize Treatment Selection

Author

Park, Wungki, primary, Chen, Jiapeng, primary, Chou, Joanne F., primary, Varghese, Anna M., primary, Yu, Kenneth H., primary, Wong, Winston, primary, Capanu, Marinela, primary, Balachandran, Vinod, primary, McIntyre, Caitlin A., primary, El Dika, Imane, primary, Khalil, Danny N., primary, Harding, James J., primary, Ghalehsari, Nima, primary, McKinnell, Zoe, primary, Chalasani, Sree B., primary, Makarov, Vladimir, primary, Selenica, Pier, primary, Pei, Xin, primary, Lecomte, Nicolas, primary, Kelsen, David P., primary, Abou-Alfa, Ghassan K., primary, Robson, Mark E., primary, Zhang, Liying, primary, Berger, Michael F., primary, Schultz, Nikolaus, primary, Chan, Timothy A., primary, Powell, Simon N., primary, Reis-Filho, Jorge S., primary, Iacobuzio-Donahue, Christine A., primary, Riaz, Nadeem, primary, and O'Reilly, Eileen M., primary

Published
2023
Full Text
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47. Supplementary Data from Identification of Resistance Pathways Specific to Malignancy Using Organoid Models of Pancreatic Cancer

Author

Ponz-Sarvise, Mariano, primary, Corbo, Vincenzo, primary, Tiriac, Hervé, primary, Engle, Dannielle D., primary, Frese, Kristopher K., primary, Oni, Tobiloba E., primary, Hwang, Chang-Il, primary, Öhlund, Daniel, primary, Chio, Iok In Christine, primary, Baker, Lindsey A., primary, Filippini, Dea, primary, Wright, Kevin, primary, Bapiro, Tashinga E., primary, Huang, Pearl, primary, Smith, Paul, primary, Yu, Kenneth H., primary, Jodrell, Duncan I., primary, Park, Youngkyu, primary, and Tuveson, David A., primary

Published
2023
Full Text
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48. Supplementary from Genomic Methods Identify Homologous Recombination Deficiency in Pancreas Adenocarcinoma and Optimize Treatment Selection

Author

Park, Wungki, primary, Chen, Jiapeng, primary, Chou, Joanne F., primary, Varghese, Anna M., primary, Yu, Kenneth H., primary, Wong, Winston, primary, Capanu, Marinela, primary, Balachandran, Vinod, primary, McIntyre, Caitlin A., primary, El Dika, Imane, primary, Khalil, Danny N., primary, Harding, James J., primary, Ghalehsari, Nima, primary, McKinnell, Zoe, primary, Chalasani, Sree B., primary, Makarov, Vladimir, primary, Selenica, Pier, primary, Pei, Xin, primary, Lecomte, Nicolas, primary, Kelsen, David P., primary, Abou-Alfa, Ghassan K., primary, Robson, Mark E., primary, Zhang, Liying, primary, Berger, Michael F., primary, Schultz, Nikolaus, primary, Chan, Timothy A., primary, Powell, Simon N., primary, Reis-Filho, Jorge S., primary, Iacobuzio-Donahue, Christine A., primary, Riaz, Nadeem, primary, and O'Reilly, Eileen M., primary

Published
2023
Full Text
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