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3. Engrailed‐1 Promotes Pancreatic Cancer Metastasis

Author

Xu, Jihao, Roe, Jae‐Seok, Lee, EunJung, Tonelli, Claudia, Ji, Keely Y, Younis, Omar W, Somervile, Tim DD, Yao, Melissa, Milazzo, Joseph P, Tiriac, Herve, Kolarzyk, Anna M, Lee, Esak, Grem, Jean L, Lazenby, Audrey J, Grunkemeyer, James A, Hollingsworth, Michael A, Grandgenett, Paul M, Borowsky, Alexander D, Park, Youngkyu, Vakoc, Christopher R, Tuveson, David A, and Hwang, Chang‐Il

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Cancer, Pancreatic Cancer, Biotechnology, Genetics, Digestive Diseases, Rare Diseases, 2.1 Biological and endogenous factors, Humans, Carcinoma, Pancreatic Ductal, Gene Expression Regulation, Pancreatic Neoplasms, Transcription Factors, Homeodomain Proteins, apoptosis, cancer progression, cancer therapeutics, developmental transcription factor, Engrailed-1, epigenetic reprogramming, ERK signaling, metastasis, pancreatic ductal adenocarcinoma
Abstract

Engrailed-1 (EN1) is a critical homeodomain transcription factor (TF) required for neuronal survival, and EN1 expression has been shown to promote aggressive forms of triple negative breast cancer. Here, it is reported that EN1 is aberrantly expressed in a subset of pancreatic ductal adenocarcinoma (PDA) patients with poor outcomes. EN1 predominantly repressed its target genes through direct binding to gene enhancers and promoters, implicating roles in the activation of MAPK pathways and the acquisition of mesenchymal cell properties. Gain- and loss-of-function experiments demonstrated that EN1 promoted PDA transformation and metastasis in vitro and in vivo. The findings nominate the targeting of EN1 and downstream pathways in aggressive PDA.

Published
2024

4. Multi-parametric atlas of the pre-metastatic liver for prediction of metastatic outcome in early-stage pancreatic cancer

Author

Bojmar, Linda, Zambirinis, Constantinos P., Hernandez, Jonathan M., Chakraborty, Jayasree, Shaashua, Lee, Kim, Junbum, Johnson, Kofi Ennu, Hanna, Samer, Askan, Gokce, Burman, Jonas, Ravichandran, Hiranmayi, Zheng, Jian, Jolissaint, Joshua S., Srouji, Rami, Song, Yi, Choubey, Ankur, Kim, Han Sang, Cioffi, Michele, van Beek, Elke, Sigel, Carlie, Jessurun, Jose, Velasco Riestra, Paulina, Blomstrand, Hakon, Jönsson, Carolin, Jönsson, Anette, Lauritzen, Pernille, Buehring, Weston, Ararso, Yonathan, Hernandez, Dylanne, Vinagolu-Baur, Jessica P., Friedman, Madison, Glidden, Caroline, Firmenich, Laetitia, Lieberman, Grace, Mejia, Dianna L., Nasar, Naaz, Mutvei, Anders P., Paul, Doru M., Bram, Yaron, Costa-Silva, Bruno, Basturk, Olca, Boudreau, Nancy, Zhang, Haiying, Matei, Irina R., Hoshino, Ayuko, Kelsen, David, Sagi, Irit, Scherz, Avigdor, Scherz-Shouval, Ruth, Yarden, Yosef, Oren, Moshe, Egeblad, Mikala, Lewis, Jason S., Keshari, Kayvan, Grandgenett, Paul M., Hollingsworth, Michael A., Rajasekhar, Vinagolu K., Healey, John H., Björnsson, Bergthor, Simeone, Diane M., Tuveson, David A., Iacobuzio-Donahue, Christine A., Bromberg, Jaqueline, Vincent, C. Theresa, O’Reilly, Eileen M., DeMatteo, Ronald P., Balachandran, Vinod P., D’Angelica, Michael I., Kingham, T. Peter, Allen, Peter J., Simpson, Amber L., Elemento, Olivier, Sandström, Per, Schwartz, Robert E., Jarnagin, William R., and Lyden, David

Published
2024
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5. Cancer-associated fibroblast-derived acetate promotes pancreatic cancer development by altering polyamine metabolism via the ACSS2–SP1–SAT1 axis

Author

Murthy, Divya, Attri, Kuldeep S., Shukla, Surendra K., Thakur, Ravi, Chaika, Nina V., He, Chunbo, Wang, Dezhen, Jha, Kanupriya, Dasgupta, Aneesha, King, Ryan J., Mulder, Scott E., Souchek, Joshua, Gebregiworgis, Teklab, Rai, Vikant, Patel, Rohit, Hu, Tuo, Rana, Sandeep, Kollala, Sai Sundeep, Pacheco, Camila, Grandgenett, Paul M., Yu, Fang, Kumar, Vikas, Lazenby, Audrey J., Black, Adrian R., Ulhannan, Susanna, Jain, Ajay, Edil, Barish H., Klinkebiel, David L., Powers, Robert, Natarajan, Amarnath, Hollingsworth, Michael A., Mehla, Kamiya, Ly, Quan, Chaudhary, Sarika, Hwang, Rosa F., Wellen, Kathryn E., and Singh, Pankaj K.

Published
2024
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7. Methionine oxidation activates pyruvate kinase M2 to promote pancreatic cancer metastasis

Author

He, Dan, Feng, Huijin, Sundberg, Belen, Yang, Jiaxing, Powers, Justin, Christian, Alec H, Wilkinson, John E, Monnin, Cian, Avizonis, Daina, Thomas, Craig J, Friedman, Richard A, Kluger, Michael D, Hollingsworth, Michael A, Grandgenett, Paul M, Klute, Kelsey A, Toste, F Dean, Chang, Christopher J, and Chio, Iok In Christine

Subjects
Biochemistry and Cell Biology, Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Biological Sciences, Cancer, Digestive Diseases, Pancreatic Cancer, Rare Diseases, 2.1 Biological and endogenous factors, Carcinoma, Pancreatic Ductal, Carrier Proteins, Humans, Membrane Proteins, Methionine, Methionine Sulfoxide Reductases, Oxidation-Reduction, Pancreatic Neoplasms, Pyruvate Kinase, Thyroid Hormones, Thyroid Hormone-Binding Proteins, PKM2, cancer metabolism, glucose oxidation, metastasis, methionine oxidation, pancreatic cancer, redox signaling, Medical and Health Sciences, Developmental Biology, Biological sciences, Biomedical and clinical sciences, Health sciences
Abstract

Cancer mortality is primarily a consequence of its metastatic spread. Here, we report that methionine sulfoxide reductase A (MSRA), which can reduce oxidized methionine residues, acts as a suppressor of pancreatic ductal adenocarcinoma (PDA) metastasis. MSRA expression is decreased in the metastatic tumors of PDA patients, whereas MSRA loss in primary PDA cells promotes migration and invasion. Chemoproteomic profiling of pancreatic organoids revealed that MSRA loss results in the selective oxidation of a methionine residue (M239) in pyruvate kinase M2 (PKM2). Moreover, M239 oxidation sustains PKM2 in an active tetrameric state to promote respiration, migration, and metastasis, whereas pharmacological activation of PKM2 increases cell migration and metastasis in vivo. These results demonstrate that methionine residues can act as reversible redox switches governing distinct signaling outcomes and that the MSRA-PKM2 axis serves as a regulatory nexus between redox biology and cancer metabolism to control tumor metastasis.

Published
2022

8. Author Correction: Targeting LIF-mediated paracrine interaction for pancreatic cancer therapy and monitoring

Author

Shi, Yu, Gao, Weina, Lytle, Nikki K, Huang, Peiwu, Yuan, Xiao, Dann, Amanda M, Ridinger-Saison, Maya, DelGiorno, Kathleen E, Antal, Corina E, Liang, Gaoyang, Atkins, Annette R, Erikson, Galina, Sun, Huaiyu, Meisenhelder, Jill, Terenziani, Elena, Woo, Gyunghwi, Fang, Linjing, Santisakultarm, Thom P, Manor, Uri, Xu, Ruilian, Becerra, Carlos R, Borazanci, Erkut, Von Hoff, Daniel D, Grandgenett, Paul M, Hollingsworth, Michael A, Leblanc, Mathias, Umetsu, Sarah E, Collisson, Eric A, Scadeng, Miriam, Lowy, Andrew M, Donahue, Timothy R, Reya, Tannishtha, Downes, Michael, Evans, Ronald M, Wahl, Geoffrey M, Pawson, Tony, Tian, Ruijun, and Hunter, Tony

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, General Science & Technology
Abstract

In the version of this Letter initially published, the Acknowledgements section omitted the following note of support from Geoffrey M. Wahl: “Work in the laboratory of G.M.W. was supported, in part, by the Cancer Center Core Grant (CA014195), National Institutes of Health/National Cancer Institute (R35 CA197687), National Institutes of Health Cancer Training Grant (T32 CA009370), the Isacoff Research Foundation Gastrointestinal (ICOF) and the Freeberg Foundation.”.

Published
2021

9. Author Correction: Cancer-associated fibroblast-derived acetate promotes pancreatic cancer development by altering polyamine metabolism via the ACSS2–SP1–SAT1 axis

Author

Murthy, Divya, Attri, Kuldeep S., Shukla, Surendra K., Thakur, Ravi, Chaika, Nina V., He, Chunbo, Wang, Dezhen, Jha, Kanupriya, Dasgupta, Aneesha, King, Ryan J., Mulder, Scott E., Souchek, Joshua, Gebregiworgis, Teklab, Rai, Vikant, Patel, Rohit, Hu, Tuo, Rana, Sandeep, Kollala, Sai Sundeep, Pacheco, Camila, Grandgenett, Paul M., Yu, Fang, Kumar, Vikas, Lazenby, Audrey J., Black, Adrian R., Ulhannan, Susanna, Jain, Ajay, Edil, Barish H., Klinkebiel, David L., Powers, Robert, Natarajan, Amarnath, Hollingsworth, Michael A., Mehla, Kamiya, Ly, Quan, Chaudhary, Sarika, Hwang, Rosa F., Wellen, Kathryn E., and Singh, Pankaj K.

Published
2024
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10. Genomic and Epigenomic Landscaping Defines New Therapeutic Targets for Adenosquamous Carcinoma of the Pancreas

Author

Lenkiewicz, Elizabeth, Malasi, Smriti, Hogenson, Tara L, Flores, Luis F, Barham, Whitney, Phillips, William J, Roesler, Alexander S, Chambers, Kendall R, Rajbhandari, Nirakar, Hayashi, Akimasa, Antal, Corina E, Downes, Michael, Grandgenett, Paul M, Hollingsworth, Michael A, Cridebring, Derek, Xiong, Yuning, Lee, Jeong-Heon, Ye, Zhenqing, Yan, Huihuang, Hernandez, Matthew C, Leiting, Jennifer L, Evans, Ronald M, Ordog, Tamas, Truty, Mark J, Borad, Mitesh J, Reya, Tannishtha, Von Hoff, Daniel D, Fernandez-Zapico, Martin E, and Barrett, Michael T

Subjects
Biological Sciences, Biomedical and Clinical Sciences, Bioinformatics and Computational Biology, Genetics, Oncology and Carcinogenesis, Pancreatic Cancer, Cancer, Orphan Drug, Clinical Research, Stem Cell Research, Rare Diseases, Digestive Diseases, Biotechnology, Human Genome, Cancer Genomics, 2.1 Biological and endogenous factors, Carcinoma, Adenosquamous, Carcinoma, Pancreatic Ductal, Chromatin, Epigenome, Humans, Mutation, Organoids, Pancreatic Neoplasms, Proto-Oncogene Proteins p21(ras), Receptor, Fibroblast Growth Factor, Type 1, Single-Cell Analysis, Smad4 Protein, Exome Sequencing, Oncology & Carcinogenesis, Biochemistry and cell biology, Oncology and carcinogenesis
Abstract

Adenosquamous cancer of the pancreas (ASCP) is a subtype of pancreatic cancer that has a worse prognosis and greater metastatic potential than the more common pancreatic ductal adenocarcinoma (PDAC) subtype. To distinguish the genomic landscape of ASCP and identify actionable targets for this lethal cancer, we applied DNA content flow cytometry to a series of 15 tumor samples including five patient-derived xenografts (PDX). We interrogated purified sorted tumor fractions from these samples with whole-genome copy-number variant (CNV), whole-exome sequencing, and Assay for Transposase-Accessible Chromatin using sequencing (ATAC-seq) analyses. These identified a variety of somatic genomic lesions targeting chromatin regulators in ASCP genomes that were superimposed on well-characterized genomic lesions including mutations in TP53 (87%) and KRAS (73%), amplification of MYC (47%), and homozygous deletion of CDKN2A (40%) that are common in PDACs. Furthermore, a comparison of ATAC-seq profiles of three ASCP and three PDAC genomes using flow-sorted PDX models identified genes with accessible chromatin unique to the ASCP genomes, including the lysine methyltransferase SMYD2 and the pancreatic cancer stem cell regulator RORC in all three ASCPs, and a FGFR1-ERLIN2 fusion associated with focal CNVs in both genes in a single ASCP. Finally, we demonstrate significant activity of a pan FGFR inhibitor against organoids derived from the FGFR1-ERLIN2 fusion-positive ASCP PDX model. Our results suggest that the genomic and epigenomic landscape of ASCP provide new strategies for targeting this aggressive subtype of pancreatic cancer. SIGNIFICANCE: These data provide a unique description of the ASCP genomic and epigenomic landscape and identify candidate therapeutic targets for this dismal cancer.

Published
2020

11. SIRT1–NOX4 signaling axis regulates cancer cachexia

Author

Dasgupta, Aneesha, Shukla, Surendra K, Vernucci, Enza, King, Ryan J, Abrego, Jaime, Mulder, Scott E, Mullen, Nicholas J, Graves, Gavin, Buettner, Kyla, Thakur, Ravi, Murthy, Divya, Attri, Kuldeep S, Wang, Dezhen, Chaika, Nina V, Pacheco, Camila G, Rai, Ibha, Engle, Dannielle D, Grandgenett, Paul M, Punsoni, Michael, Reames, Bradley N, Teoh-Fitzgerald, Melissa, Oberley-Deegan, Rebecca, Yu, Fang, Klute, Kelsey A, Hollingsworth, Michael A, Zimmerman, Matthew C, Mehla, Kamiya, Sadoshima, Junichi, Tuveson, David A, and Singh, Pankaj K

Subjects
Medical Physiology, Biomedical and Clinical Sciences, Digestive Diseases, Rare Diseases, Genetics, Pancreatic Cancer, Cancer, Nutrition, 2.1 Biological and endogenous factors, Aetiology, Adipose Tissue, Animals, Cachexia, Cell Line, Cell Line, Tumor, Disease Models, Animal, Disease Progression, Forkhead Transcription Factors, HEK293 Cells, Humans, Metabolome, Mice, Muscle Fibers, Skeletal, Muscle, Skeletal, Muscular Atrophy, NADPH Oxidase 4, NF-kappa B, Neoplasms, Oxidation-Reduction, Pancreatic Neoplasms, Protein Stability, Reactive Oxygen Species, Resveratrol, Signal Transduction, Sirtuin 1, Wasting Syndrome, Medical and Health Sciences, Immunology, Biomedical and clinical sciences, Health sciences
Abstract

Approximately one third of cancer patients die due to complexities related to cachexia. However, the mechanisms of cachexia and the potential therapeutic interventions remain poorly studied. We observed a significant positive correlation between SIRT1 expression and muscle fiber cross-sectional area in pancreatic cancer patients. Rescuing Sirt1 expression by exogenous expression or pharmacological agents reverted cancer cell-induced myotube wasting in culture conditions and mouse models. RNA-seq and follow-up analyses showed cancer cell-mediated SIRT1 loss induced NF-κB signaling in cachectic muscles that enhanced the expression of FOXO transcription factors and NADPH oxidase 4 (Nox4), a key regulator of reactive oxygen species production. Additionally, we observed a negative correlation between NOX4 expression and skeletal muscle fiber cross-sectional area in pancreatic cancer patients. Knocking out Nox4 in skeletal muscles or pharmacological blockade of Nox4 activity abrogated tumor-induced cachexia in mice. Thus, we conclude that targeting the Sirt1-Nox4 axis in muscles is an effective therapeutic intervention for mitigating pancreatic cancer-induced cachexia.

Published
2020

12. Small-molecule IKKβ activation modulator (IKAM) targets MAP3K1 and inhibits pancreatic tumor growth

Author

Napoleon, John Victor, Sagar, Satish, Kubica, Sydney P., Boghean, Lidia, Kour, Smit, King, Hannah M., Sonawane, Yogesh A., Crawford, Ayrianne J., Gautam, Nagsen, Kizhake, Smitha, Bialk, Pawel A., Kmiec, Eric, Mallareddy, Jayapal Reddy, Patil, Prathamesh P., Rana, Sandeep, Singh, Sarbjit, Prahlad, Janani, Grandgenett, Paul M., Borgstahl, Gloria E. O., Ghosal, Gargi, Alnouti, Yazen, Hollingsworth, Michael A., Radhakrishnan, Prakash, and Natarajan, Amarnath

Published
2022

13. Targeting LIF-mediated paracrine interaction for pancreatic cancer therapy and monitoring

Author

Shi, Yu, Gao, Weina, Lytle, Nikki K, Huang, Peiwu, Yuan, Xiao, Dann, Amanda M, Ridinger-Saison, Maya, DelGiorno, Kathleen E, Antal, Corina E, Liang, Gaoyang, Atkins, Annette R, Erikson, Galina, Sun, Huaiyu, Meisenhelder, Jill, Terenziani, Elena, Woo, Gyunghwi, Fang, Linjing, Santisakultarm, Thom P, Manor, Uri, Xu, Ruilian, Becerra, Carlos R, Borazanci, Erkut, Von Hoff, Daniel D, Grandgenett, Paul M, Hollingsworth, Michael A, Leblanc, Mathias, Umetsu, Sarah E, Collisson, Eric A, Scadeng, Miriam, Lowy, Andrew M, Donahue, Timothy R, Reya, Tannishtha, Downes, Michael, Evans, Ronald M, Wahl, Geoffrey M, Pawson, Tony, Tian, Ruijun, and Hunter, Tony

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Cancer, Orphan Drug, Digestive Diseases, Rare Diseases, Pancreatic Cancer, 2.1 Biological and endogenous factors, 5.1 Pharmaceuticals, 5.2 Cellular and gene therapies, Animals, Antibodies, Monoclonal, Carcinogenesis, Carcinoma, Pancreatic Ductal, Cell Differentiation, Cell Line, Tumor, Disease Progression, Drug Resistance, Neoplasm, Epithelial-Mesenchymal Transition, Female, Humans, Leukemia Inhibitory Factor, Male, Mass Spectrometry, Mice, Pancreatic Neoplasms, Paracrine Communication, Receptors, OSM-LIF, Tumor Microenvironment, General Science & Technology
Abstract

Pancreatic ductal adenocarcinoma (PDAC) has a dismal prognosis largely owing to inefficient diagnosis and tenacious drug resistance. Activation of pancreatic stellate cells (PSCs) and consequent development of dense stroma are prominent features accounting for this aggressive biology1,2. The reciprocal interplay between PSCs and pancreatic cancer cells (PCCs) not only enhances tumour progression and metastasis but also sustains their own activation, facilitating a vicious cycle to exacerbate tumorigenesis and drug resistance3-7. Furthermore, PSC activation occurs very early during PDAC tumorigenesis8-10, and activated PSCs comprise a substantial fraction of the tumour mass, providing a rich source of readily detectable factors. Therefore, we hypothesized that the communication between PSCs and PCCs could be an exploitable target to develop effective strategies for PDAC therapy and diagnosis. Here, starting with a systematic proteomic investigation of secreted disease mediators and underlying molecular mechanisms, we reveal that leukaemia inhibitory factor (LIF) is a key paracrine factor from activated PSCs acting on cancer cells. Both pharmacologic LIF blockade and genetic Lifr deletion markedly slow tumour progression and augment the efficacy of chemotherapy to prolong survival of PDAC mouse models, mainly by modulating cancer cell differentiation and epithelial-mesenchymal transition status. Moreover, in both mouse models and human PDAC, aberrant production of LIF in the pancreas is restricted to pathological conditions and correlates with PDAC pathogenesis, and changes in the levels of circulating LIF correlate well with tumour response to therapy. Collectively, these findings reveal a function of LIF in PDAC tumorigenesis, and suggest its translational potential as an attractive therapeutic target and circulating marker. Our studies underscore how a better understanding of cell-cell communication within the tumour microenvironment can suggest novel strategies for cancer therapy.

Published
2019

15. 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

17. Supplementary Figure S4 from Structural Basis for Multivalent MUC16 Recognition and Robust Anti-Pancreatic Cancer Activity of Humanized Antibody AR9.6

Author

Aguilar, Eric N., primary, Sagar, Satish, primary, Murray, Brandy R., primary, Rajesh, Christabelle, primary, Lei, Eric K., primary, Michaud, Sarah A., primary, Goodlett, David R., primary, Caffrey, Thomas C., primary, Grandgenett, Paul M., primary, Swanson, Benjamin, primary, Brooks, Teresa M., primary, Black, Adrian R., primary, van Faassen, Henk, primary, Hussack, Greg, primary, Henry, Kevin A., primary, Hollingsworth, Michael A., primary, Brooks, Cory L., primary, and Radhakrishnan, Prakash, primary

Published
2024
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18. Data from Structural Basis for Multivalent MUC16 Recognition and Robust Anti-Pancreatic Cancer Activity of Humanized Antibody AR9.6

Author

Aguilar, Eric N., primary, Sagar, Satish, primary, Murray, Brandy R., primary, Rajesh, Christabelle, primary, Lei, Eric K., primary, Michaud, Sarah A., primary, Goodlett, David R., primary, Caffrey, Thomas C., primary, Grandgenett, Paul M., primary, Swanson, Benjamin, primary, Brooks, Teresa M., primary, Black, Adrian R., primary, van Faassen, Henk, primary, Hussack, Greg, primary, Henry, Kevin A., primary, Hollingsworth, Michael A., primary, Brooks, Cory L., primary, and Radhakrishnan, Prakash, primary

Published
2024
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19. Supplementary Data from Structural Basis for Multivalent MUC16 Recognition and Robust Anti-Pancreatic Cancer Activity of Humanized Antibody AR9.6

Author

Aguilar, Eric N., primary, Sagar, Satish, primary, Murray, Brandy R., primary, Rajesh, Christabelle, primary, Lei, Eric K., primary, Michaud, Sarah A., primary, Goodlett, David R., primary, Caffrey, Thomas C., primary, Grandgenett, Paul M., primary, Swanson, Benjamin, primary, Brooks, Teresa M., primary, Black, Adrian R., primary, van Faassen, Henk, primary, Hussack, Greg, primary, Henry, Kevin A., primary, Hollingsworth, Michael A., primary, Brooks, Cory L., primary, and Radhakrishnan, Prakash, primary

Published
2024
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21. Enhancer Reprogramming Promotes Pancreatic Cancer Metastasis

Author

Roe, Jae-Seok, Hwang, Chang-Il, Somerville, Tim DD, Milazzo, Joseph P, Lee, Eun Jung, Da Silva, Brandon, Maiorino, Laura, Tiriac, Hervé, Young, C Megan, Miyabayashi, Koji, Filippini, Dea, Creighton, Brianna, Burkhart, Richard A, Buscaglia, Jonathan M, Kim, Edward J, Grem, Jean L, Lazenby, Audrey J, Grunkemeyer, James A, Hollingsworth, Michael A, Grandgenett, Paul M, Egeblad, Mikala, Park, Youngkyu, Tuveson, David A, and Vakoc, Christopher R

Subjects
Biochemistry and Cell Biology, Biomedical and Clinical Sciences, Biological Sciences, Cancer, Rare Diseases, Pancreatic Cancer, Digestive Diseases, Adenocarcinoma, Animals, Carcinoma, Pancreatic Ductal, Cell Line, Tumor, Disease Models, Animal, Enhancer Elements, Genetic, Epigenomics, Female, Gene Expression Profiling, Gene Expression Regulation, Neoplastic, Hepatocyte Nuclear Factor 3-alpha, Humans, Male, Mice, Mice, Inbred C57BL, Neoplasm Metastasis, Organoids, Pancreas, Pancreatic Neoplasms, FOXA1, enhancer, metastasis, organoid, pancreatic cancer, pancreatic ductal adenocarcinoma, Medical and Health Sciences, Developmental Biology, Biological sciences, Biomedical and clinical sciences
Abstract

Pancreatic ductal adenocarcinoma (PDA) is one of the most lethal human malignancies, owing in part to its propensity for metastasis. Here, we used an organoid culture system to investigate how transcription and the enhancer landscape become altered during discrete stages of disease progression in a PDA mouse model. This approach revealed that the metastatic transition is accompanied by massive and recurrent alterations in enhancer activity. We implicate the pioneer factor FOXA1 as a driver of enhancer activation in this system, a mechanism that renders PDA cells more invasive and less anchorage-dependent for growth in vitro, as well as more metastatic in vivo. In this context, FOXA1-dependent enhancer reprogramming activates a transcriptional program of embryonic foregut endoderm. Collectively, our study implicates enhancer reprogramming, FOXA1 upregulation, and a retrograde developmental transition in PDA metastasis.

Published
2017

22. Isoforms of MUC16 activate oncogenic signaling through EGF receptors to enhance the progression of pancreatic cancer

Author

Thomas, Divya, Sagar, Satish, Liu, Xiang, Lee, Hye-Rim, Grunkemeyer, James A., Grandgenett, Paul M., Caffrey, Thomas, O’Connell, Kelly A., Swanson, Benjamin, Marcos-Silva, Lara, Steentoft, Catharina, Wandall, Hans H., Maurer, Hans Carlo, Peng, Xianlu Laura, Yeh, Jen Jen, Qiu, Fang, Yu, Fang, Madiyalakan, Ragupathy, Olive, Kenneth P., Mandel, Ulla, Clausen, Henrik, Hollingsworth, Michael A., and Radhakrishnan, Prakash

Published
2021
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23. Extracellular Vesicle and Particle Biomarkers Define Multiple Human Cancers

Author

Hoshino, Ayuko, Kim, Han Sang, Bojmar, Linda, Gyan, Kofi Ennu, Cioffi, Michele, Hernandez, Jonathan, Zambirinis, Constantinos P., Rodrigues, Gonçalo, Molina, Henrik, Heissel, Søren, Mark, Milica Tesic, Steiner, Loïc, Benito-Martin, Alberto, Lucotti, Serena, Di Giannatale, Angela, Offer, Katharine, Nakajima, Miho, Williams, Caitlin, Nogués, Laura, Pelissier Vatter, Fanny A., Hashimoto, Ayako, Davies, Alexander E., Freitas, Daniela, Kenific, Candia M., Ararso, Yonathan, Buehring, Weston, Lauritzen, Pernille, Ogitani, Yusuke, Sugiura, Kei, Takahashi, Naoko, Alečković, Maša, Bailey, Kayleen A., Jolissant, Joshua S., Wang, Huajuan, Harris, Ashton, Schaeffer, L. Miles, García-Santos, Guillermo, Posner, Zoe, Balachandran, Vinod P., Khakoo, Yasmin, Raju, G. Praveen, Scherz, Avigdor, Sagi, Irit, Scherz-Shouval, Ruth, Yarden, Yosef, Oren, Moshe, Malladi, Mahathi, Petriccione, Mary, De Braganca, Kevin C., Donzelli, Maria, Fischer, Cheryl, Vitolano, Stephanie, Wright, Geraldine P., Ganshaw, Lee, Marrano, Mariel, Ahmed, Amina, DeStefano, Joe, Danzer, Enrico, Roehrl, Michael H.A., Lacayo, Norman J., Vincent, Theresa C., Weiser, Martin R., Brady, Mary S., Meyers, Paul A., Wexler, Leonard H., Ambati, Srikanth R., Chou, Alexander J., Slotkin, Emily K., Modak, Shakeel, Roberts, Stephen S., Basu, Ellen M., Diolaiti, Daniel, Krantz, Benjamin A., Cardoso, Fatima, Simpson, Amber L., Berger, Michael, Rudin, Charles M., Simeone, Diane M., Jain, Maneesh, Ghajar, Cyrus M., Batra, Surinder K., Stanger, Ben Z., Bui, Jack, Brown, Kristy A., Rajasekhar, Vinagolu K., Healey, John H., de Sousa, Maria, Kramer, Kim, Sheth, Sujit, Baisch, Jeanine, Pascual, Virginia, Heaton, Todd E., La Quaglia, Michael P., Pisapia, David J., Schwartz, Robert, Zhang, Haiying, Liu, Yuan, Shukla, Arti, Blavier, Laurence, DeClerck, Yves A., LaBarge, Mark, Bissell, Mina J., Caffrey, Thomas C., Grandgenett, Paul M., Hollingsworth, Michael A., Bromberg, Jacqueline, Costa-Silva, Bruno, Peinado, Hector, Kang, Yibin, Garcia, Benjamin A., O’Reilly, Eileen M., Kelsen, David, Trippett, Tanya M., Jones, David R., Matei, Irina R., Jarnagin, William R., and Lyden, David

Published
2020
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25. Image-based detection and targeting of therapy resistance in pancreatic adenocarcinoma.

Author

Fox, Raymond G, Lytle, Nikki K, Jaquish, Dawn V, Park, Frederick D, Ito, Takahiro, Bajaj, Jeevisha, Koechlein, Claire S, Zimdahl, Bryan, Yano, Masato, Kopp, Janel, Kritzik, Marcie, Sicklick, Jason, Sander, Maike, Grandgenett, Paul M, Hollingsworth, Michael A, Shibata, Shinsuke, Pizzo, Donald, Valasek, Mark, Sasik, Roman, Scadeng, Miriam, Okano, Hideyuki, Kim, Youngsoo, MacLeod, A Robert, Lowy, Andrew M, and Reya, Tannishtha

Subjects
Animals, Humans, Mice, Carcinoma, Pancreatic Ductal, Carcinoma in Situ, Pancreatic Neoplasms, Cell Transformation, Neoplastic, Disease Models, Animal, Disease Progression, RNA-Binding Proteins, Nerve Tissue Proteins, Oligonucleotides, Antisense, Survival Rate, Xenograft Model Antitumor Assays, Signal Transduction, Gene Deletion, Drug Resistance, Neoplasm, Genes, Reporter, Models, Genetic, Female, Male, Neoplastic Cells, Circulating, Molecular Imaging, General Science & Technology
Abstract

Pancreatic intraepithelial neoplasia is a pre-malignant lesion that can progress to pancreatic ductal adenocarcinoma, a highly lethal malignancy marked by its late stage at clinical presentation and profound drug resistance. The genomic alterations that commonly occur in pancreatic cancer include activation of KRAS2 and inactivation of p53 and SMAD4 (refs 2-4). So far, however, it has been challenging to target these pathways therapeutically; thus the search for other key mediators of pancreatic cancer growth remains an important endeavour. Here we show that the stem cell determinant Musashi (Msi) is a critical element of pancreatic cancer progression both in genetic models and in patient-derived xenografts. Specifically, we developed Msi reporter mice that allowed image-based tracking of stem cell signals within cancers, revealing that Msi expression rises as pancreatic intraepithelial neoplasia progresses to adenocarcinoma, and that Msi-expressing cells are key drivers of pancreatic cancer: they preferentially harbour the capacity to propagate adenocarcinoma, are enriched in circulating tumour cells, and are markedly drug resistant. This population could be effectively targeted by deletion of either Msi1 or Msi2, which led to a striking defect in the progression of pancreatic intraepithelial neoplasia to adenocarcinoma and an improvement in overall survival. Msi inhibition also blocked the growth of primary patient-derived tumours, suggesting that this signal is required for human disease. To define the translational potential of this work we developed antisense oligonucleotides against Msi; these showed reliable tumour penetration, uptake and target inhibition, and effectively blocked pancreatic cancer growth. Collectively, these studies highlight Msi reporters as a unique tool to identify therapy resistance, and define Msi signalling as a central regulator of pancreatic cancer.

Published
2016

26. Metabolic programming of distinct cancer stem cells promotes metastasis of pancreatic ductal adenocarcinoma

Author

Nimmakayala, Rama Krishna, Leon, Frank, Rachagani, Satyanarayana, Rauth, Sanchita, Nallasamy, Palanisamy, Marimuthu, Saravanakumar, Shailendra, Gautam K., Chhonker, Yashpal S., Chugh, Seema, Chirravuri, Ramakanth, Gupta, Rohitesh, Mallya, Kavita, Prajapati, Dipakkumar R., Lele, Subodh M., C. Caffrey, Thomas, L. Grem, Jean, Grandgenett, Paul M., Hollingsworth, Michael A., Murry, Daryl J., Batra, Surinder K., and Ponnusamy, Moorthy P.

Published
2021
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28. Tumour exosome integrins determine organotropic metastasis

Author

Hoshino, Ayuko, Costa-Silva, Bruno, Shen, Tang-Long, Rodrigues, Goncalo, Hashimoto, Ayako, Tesic Mark, Milica, Molina, Henrik, Kohsaka, Shinji, Di Giannatale, Angela, Ceder, Sophia, Singh, Swarnima, Williams, Caitlin, Soplop, Nadine, Uryu, Kunihiro, Pharmer, Lindsay, King, Tari, Bojmar, Linda, Davies, Alexander E, Ararso, Yonathan, Zhang, Tuo, Zhang, Haiying, Hernandez, Jonathan, Weiss, Joshua M, Dumont-Cole, Vanessa D, Kramer, Kimberly, Wexler, Leonard H, Narendran, Aru, Schwartz, Gary K, Healey, John H, Sandstrom, Per, Jørgen Labori, Knut, Kure, Elin H, Grandgenett, Paul M, Hollingsworth, Michael A, de Sousa, Maria, Kaur, Sukhwinder, Jain, Maneesh, Mallya, Kavita, Batra, Surinder K, Jarnagin, William R, Brady, Mary S, Fodstad, Oystein, Muller, Volkmar, Pantel, Klaus, Minn, Andy J, Bissell, Mina J, Garcia, Benjamin A, Kang, Yibin, Rajasekhar, Vinagolu K, Ghajar, Cyrus M, Matei, Irina, Peinado, Hector, Bromberg, Jacqueline, and Lyden, David

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Cancer, Lung, Liver Disease, Digestive Diseases, Rare Diseases, 2.1 Biological and endogenous factors, Animals, Biomarkers, Brain, Cell Line, Tumor, Endothelial Cells, Epithelial Cells, Exosomes, Female, Fibroblasts, Genes, src, Humans, Integrin alpha6beta1, Integrin alpha6beta4, Integrin beta Chains, Integrin beta4, Integrins, Kupffer Cells, Liver, Mice, Mice, Inbred C57BL, Neoplasm Metastasis, Organ Specificity, Phosphorylation, Receptors, Vitronectin, S100 Proteins, Tropism, General Science & Technology
Abstract

Ever since Stephen Paget's 1889 hypothesis, metastatic organotropism has remained one of cancer's greatest mysteries. Here we demonstrate that exosomes from mouse and human lung-, liver- and brain-tropic tumour cells fuse preferentially with resident cells at their predicted destination, namely lung fibroblasts and epithelial cells, liver Kupffer cells and brain endothelial cells. We show that tumour-derived exosomes uptaken by organ-specific cells prepare the pre-metastatic niche. Treatment with exosomes from lung-tropic models redirected the metastasis of bone-tropic tumour cells. Exosome proteomics revealed distinct integrin expression patterns, in which the exosomal integrins α6β4 and α6β1 were associated with lung metastasis, while exosomal integrin αvβ5 was linked to liver metastasis. Targeting the integrins α6β4 and αvβ5 decreased exosome uptake, as well as lung and liver metastasis, respectively. We demonstrate that exosome integrin uptake by resident cells activates Src phosphorylation and pro-inflammatory S100 gene expression. Finally, our clinical data indicate that exosomal integrins could be used to predict organ-specific metastasis.

Published
2015

31. radioGWAS: link radiome to genome to discover driver genes with somatic mutations for heterogeneous tumor image phenotype in pancreatic cancer

Author

Zheng, Dandan, primary, Grandgenett, Paul M., additional, Zhang, Qi, additional, Baine, Michael, additional, Shi, Yu, additional, Du, Qian, additional, Liang, Xiaoying, additional, Wong, Jeffrey, additional, Iqbal, Subhan, additional, Preuss, Kiersten, additional, Kamal, Ahsan, additional, Yu, Hongfeng, additional, Du, Huijing, additional, Hollingsworth, Michael A., additional, and Zhang, Chi, additional

Published
2023
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32. MUC1 and HIF-1alpha Signaling Crosstalk Induces Anabolic Glucose Metabolism to Impart Gemcitabine Resistance to Pancreatic Cancer

Author

Shukla, Surendra K., Purohit, Vinee, Mehla, Kamiya, Gunda, Venugopal, Chaika, Nina V., Vernucci, Enza, King, Ryan J., Abrego, Jaime, Goode, Gennifer D., Dasgupta, Aneesha, Illies, Alysha L., Gebregiworgis, Teklab, Dai, Bingbing, Augustine, Jithesh J., Murthy, Divya, Attri, Kuldeep S., Mashadova, Oksana, Grandgenett, Paul M., Powers, Robert, Ly, Quan P., Lazenby, Audrey J., Grem, Jean L., Yu, Fang, Matés, José M., Asara, John M., Kim, Jung-whan, Hankins, Jordan H., Weekes, Colin, Hollingsworth, Michael A., Serkova, Natalie J., Sasson, Aaron R., Fleming, Jason B., Oliveto, Jennifer M., Lyssiotis, Costas A., Cantley, Lewis C., Berim, Lyudmyla, and Singh, Pankaj K.

Published
2017
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35. Tumour extracellular vesicles and particles induce liver metabolic dysfunction

Author

Wang, Gang, Li, Jianlong, Bojmar, Linda, Chen, Haiyan, Li, Zhong, Tobias, Gabriel C., Hu, Mengying, Homan, Edwin A., Lucotti, Serena, Zhao, Fengbo, Posada, Valentina, Oxley, Peter R., Cioffi, Michele, Kim, Han Sang, Wang, Huajuan, Lauritzen, Pernille, Boudreau, Nancy, Shi, Zhanjun, Burd, Christin E., Zippin, Jonathan H., Lo, James C., Pitt, Geoffrey S., Hernandez, Jonathan, Zambirinis, Constantinos P., Hollingsworth, Michael A., Grandgenett, Paul M., Jain, Maneesh, Batra, Surinder K., DiMaio, Dominick J., Grem, Jean L., Klute, Kelsey A., Trippett, Tanya M., Egeblad, Mikala, Paul, Doru, Bromberg, Jacqueline, Kelsen, David, Rajasekhar, Vinagolu K., Healey, John H., Matei, Irina R., Jarnagin, William R., Schwartz, Robert E., Zhang, Haiying, Lyden, David, Wang, Gang, Li, Jianlong, Bojmar, Linda, Chen, Haiyan, Li, Zhong, Tobias, Gabriel C., Hu, Mengying, Homan, Edwin A., Lucotti, Serena, Zhao, Fengbo, Posada, Valentina, Oxley, Peter R., Cioffi, Michele, Kim, Han Sang, Wang, Huajuan, Lauritzen, Pernille, Boudreau, Nancy, Shi, Zhanjun, Burd, Christin E., Zippin, Jonathan H., Lo, James C., Pitt, Geoffrey S., Hernandez, Jonathan, Zambirinis, Constantinos P., Hollingsworth, Michael A., Grandgenett, Paul M., Jain, Maneesh, Batra, Surinder K., DiMaio, Dominick J., Grem, Jean L., Klute, Kelsey A., Trippett, Tanya M., Egeblad, Mikala, Paul, Doru, Bromberg, Jacqueline, Kelsen, David, Rajasekhar, Vinagolu K., Healey, John H., Matei, Irina R., Jarnagin, William R., Schwartz, Robert E., Zhang, Haiying, and Lyden, David

Abstract

Cancer alters the function of multiple organs beyond those targeted by metastasis(1,2). Here we show that inflammation, fatty liver and dysregulated metabolism are hallmarks of systemically affected livers in mouse models and in patients with extrahepatic metastasis. We identified tumour-derived extracellular vesicles and particles (EVPs) as crucial mediators of cancer-induced hepatic reprogramming, which could be reversed by reducing tumour EVP secretion via depletion of Rab27a. All EVP subpopulations, exosomes and principally exomeres, could dysregulate hepatic function. The fatty acid cargo of tumour EVPs-particularly palmitic acid-induced secretion of tumour necrosis factor (TNF) by Kupffer cells, generating a pro-inflammatory microenvironment, suppressing fatty acid metabolism and oxidative phosphorylation, and promoting fatty liver formation. Notably, Kupffer cell ablation or TNF blockade markedly decreased tumour-induced fatty liver generation. Tumour implantation or pre-treatment with tumour EVPs diminished cytochrome P450 gene expression and attenuated drug metabolism in a TNF-dependent manner. We also observed fatty liver and decreased cytochrome P450 expression at diagnosis in tumour-free livers of patients with pancreatic cancer who later developed extrahepatic metastasis, highlighting the clinical relevance of our findings. Notably, tumour EVP education enhanced side effects of chemotherapy, including bone marrow suppression and cardiotoxicity, suggesting that metabolic reprogramming of the liver by tumour-derived EVPs may limit chemotherapy tolerance in patients with cancer. Our results reveal how tumour-derived EVPs dysregulate hepatic function and their targetable potential, alongside TNF inhibition, for preventing fatty liver formation and enhancing the efficacy of chemotherapy., Funding Agencies|National Cancer Institute; Thompson Family Foundation; Tortolani Foundation; Pediatric Oncology Experimental Therapeutics Investigators Consortium; Malcolm Hewitt Weiner Foundation; Manning Foundation; Sohn Foundation; AHEPA Vth District Cancer Research Foundation; Childrens Cancer and Blood Foundation; Hartwell Foundation; National Institutes of Health; United States Department of Defense; Paul G. Allen Family Foundation; National Natural Science Foundation of China; Guangdong Foundation of Medical Science and Technology; China Scholarship Council (CSC) [CA232093, CA163117, CA207983, CA218513]; Swedish Cancer Society Pancreatic Cancer Fellowship; Lions International Postdoctoral fellowship; Sweden-America stipend; Alan and Sandra Gerry Metastasis and Tumor Ecosystems Center of Memorial Sloan Kettering Cancer Center; NIH/NCI Cancer Center Support Grant; [R01CA234614]; [2R01AI107301]; [R01DK121072]; [R01CA237213]; [R01CA254036]; [W81XWH-21-1-0978]; [UWSC13448]; [81902730]; [A2019213]; [202008440567]; [P30 CA008748]

Published
2023
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36. Tumour extracellular vesicles and particles induce liver metabolic dysfunction

Author

Wang, Gang, primary, Li, Jianlong, additional, Bojmar, Linda, additional, Chen, Haiyan, additional, Li, Zhong, additional, Tobias, Gabriel C., additional, Hu, Mengying, additional, Homan, Edwin A., additional, Lucotti, Serena, additional, Zhao, Fengbo, additional, Posada, Valentina, additional, Oxley, Peter R., additional, Cioffi, Michele, additional, Kim, Han Sang, additional, Wang, Huajuan, additional, Lauritzen, Pernille, additional, Boudreau, Nancy, additional, Shi, Zhanjun, additional, Burd, Christin E., additional, Zippin, Jonathan H., additional, Lo, James C., additional, Pitt, Geoffrey S., additional, Hernandez, Jonathan, additional, Zambirinis, Constantinos P., additional, Hollingsworth, Michael A., additional, Grandgenett, Paul M., additional, Jain, Maneesh, additional, Batra, Surinder K., additional, DiMaio, Dominick J., additional, Grem, Jean L., additional, Klute, Kelsey A., additional, Trippett, Tanya M., additional, Egeblad, Mikala, additional, Paul, Doru, additional, Bromberg, Jacqueline, additional, Kelsen, David, additional, Rajasekhar, Vinagolu K., additional, Healey, John H., additional, Matei, Irina R., additional, Jarnagin, William R., additional, Schwartz, Robert E., additional, Zhang, Haiying, additional, and Lyden, David, additional

Published
2023
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37. Data from Oncofetal Chondroitin Sulfate Glycosaminoglycans Are Key Players in Integrin Signaling and Tumor Cell Motility

Author

Clausen, Thomas Mandel, primary, Pereira, Marina Ayres, primary, Al Nakouzi, Nader, primary, Oo, Htoo Zarni, primary, Agerbæk, Mette Ø, primary, Lee, Sherry, primary, Ørum-Madsen, Maj Sofie, primary, Kristensen, Anders Riis, primary, El-Naggar, Amal, primary, Grandgenett, Paul M., primary, Grem, Jean L., primary, Hollingsworth, Michael A., primary, Holst, Peter J., primary, Theander, Thor, primary, Sorensen, Poul H., primary, Daugaard, Mads, primary, and Salanti, Ali, primary

Published
2023
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38. Supplementary Fig S2 from IgE-Based Therapeutic Combination Enhances Antitumor Response in Preclinical Models of Pancreatic Cancer

Author

Markov, Spas Dimitrov, primary, Caffrey, Thomas C., primary, O'Connell, Kelly A., primary, Grunkemeyer, James A., primary, Shin, Simon, primary, Hanson, Ryan, primary, Patil, Prathamesh P., primary, Shukla, Surendra K., primary, Gonzalez, Daisy, primary, Crawford, Ayrianne J., primary, Vance, Krysten E., primary, Huang, Ying, primary, Eberle, Kirsten C., primary, Radhakrishnan, Prakash, primary, Grandgenett, Paul M., primary, Singh, Pankaj K., primary, Madiyalakan, Ragupathy, primary, Daniels-Wells, Tracy R., primary, Penichet, Manuel L., primary, Nicodemus, Christopher F., primary, Poole, Jill A., primary, Jaffee, Elizabeth M., primary, Hollingsworth, Michael A., primary, and Mehla, Kamiya, primary

Published
2023
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39. Supplemental Figure 3 from Oncofetal Chondroitin Sulfate Glycosaminoglycans Are Key Players in Integrin Signaling and Tumor Cell Motility

Author

Clausen, Thomas Mandel, primary, Pereira, Marina Ayres, primary, Al Nakouzi, Nader, primary, Oo, Htoo Zarni, primary, Agerbæk, Mette Ø, primary, Lee, Sherry, primary, Ørum-Madsen, Maj Sofie, primary, Kristensen, Anders Riis, primary, El-Naggar, Amal, primary, Grandgenett, Paul M., primary, Grem, Jean L., primary, Hollingsworth, Michael A., primary, Holst, Peter J., primary, Theander, Thor, primary, Sorensen, Poul H., primary, Daugaard, Mads, primary, and Salanti, Ali, primary

Published
2023
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40. Supplemental Figure 1 from Oncofetal Chondroitin Sulfate Glycosaminoglycans Are Key Players in Integrin Signaling and Tumor Cell Motility

Author

Clausen, Thomas Mandel, primary, Pereira, Marina Ayres, primary, Al Nakouzi, Nader, primary, Oo, Htoo Zarni, primary, Agerbæk, Mette Ø, primary, Lee, Sherry, primary, Ørum-Madsen, Maj Sofie, primary, Kristensen, Anders Riis, primary, El-Naggar, Amal, primary, Grandgenett, Paul M., primary, Grem, Jean L., primary, Hollingsworth, Michael A., primary, Holst, Peter J., primary, Theander, Thor, primary, Sorensen, Poul H., primary, Daugaard, Mads, primary, and Salanti, Ali, primary

Published
2023
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41. Supplemental Figure 2 from Oncofetal Chondroitin Sulfate Glycosaminoglycans Are Key Players in Integrin Signaling and Tumor Cell Motility

Author

Clausen, Thomas Mandel, primary, Pereira, Marina Ayres, primary, Al Nakouzi, Nader, primary, Oo, Htoo Zarni, primary, Agerbæk, Mette Ø, primary, Lee, Sherry, primary, Ørum-Madsen, Maj Sofie, primary, Kristensen, Anders Riis, primary, El-Naggar, Amal, primary, Grandgenett, Paul M., primary, Grem, Jean L., primary, Hollingsworth, Michael A., primary, Holst, Peter J., primary, Theander, Thor, primary, Sorensen, Poul H., primary, Daugaard, Mads, primary, and Salanti, Ali, primary

Published
2023
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42. 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
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43. Data from MUC16 Promotes Liver Metastasis of Pancreatic Ductal Adenocarcinoma by Upregulating NRP2-Associated Cell Adhesion

Author

Marimuthu, Saravanakumar, primary, Lakshmanan, Imayavaramban, primary, Muniyan, Sakthivel, primary, Gautam, Shailendra K., primary, Nimmakayala, Rama Krishna, primary, Rauth, Sanchita, primary, Atri, Pranita, primary, Shah, Ashu, primary, Bhyravbhatla, Namita, primary, Mallya, Kavita, primary, Grandgenett, Paul M., primary, Hollingsworth, Michael A., primary, Datta, Kaustubh, primary, Jain, Maneesh, primary, Ponnusamy, Moorthy P., primary, and Batra, Surinder K., primary

Published
2023
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44. 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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45. 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
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46. Supplemental Data from Oncofetal Chondroitin Sulfate Glycosaminoglycans Are Key Players in Integrin Signaling and Tumor Cell Motility

Author

Clausen, Thomas Mandel, primary, Pereira, Marina Ayres, primary, Al Nakouzi, Nader, primary, Oo, Htoo Zarni, primary, Agerbæk, Mette Ø, primary, Lee, Sherry, primary, Ørum-Madsen, Maj Sofie, primary, Kristensen, Anders Riis, primary, El-Naggar, Amal, primary, Grandgenett, Paul M., primary, Grem, Jean L., primary, Hollingsworth, Michael A., primary, Holst, Peter J., primary, Theander, Thor, primary, Sorensen, Poul H., primary, Daugaard, Mads, primary, and Salanti, Ali, primary

Published
2023
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47. 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
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48. Supplementary Figure from MUC16 Promotes Liver Metastasis of Pancreatic Ductal Adenocarcinoma by Upregulating NRP2-Associated Cell Adhesion

Author

Marimuthu, Saravanakumar, primary, Lakshmanan, Imayavaramban, primary, Muniyan, Sakthivel, primary, Gautam, Shailendra K., primary, Nimmakayala, Rama Krishna, primary, Rauth, Sanchita, primary, Atri, Pranita, primary, Shah, Ashu, primary, Bhyravbhatla, Namita, primary, Mallya, Kavita, primary, Grandgenett, Paul M., primary, Hollingsworth, Michael A., primary, Datta, Kaustubh, primary, Jain, Maneesh, primary, Ponnusamy, Moorthy P., primary, and Batra, Surinder K., primary

Published
2023
Full Text
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49. Supplementary Table from MUC16 Promotes Liver Metastasis of Pancreatic Ductal Adenocarcinoma by Upregulating NRP2-Associated Cell Adhesion

Author

Marimuthu, Saravanakumar, primary, Lakshmanan, Imayavaramban, primary, Muniyan, Sakthivel, primary, Gautam, Shailendra K., primary, Nimmakayala, Rama Krishna, primary, Rauth, Sanchita, primary, Atri, Pranita, primary, Shah, Ashu, primary, Bhyravbhatla, Namita, primary, Mallya, Kavita, primary, Grandgenett, Paul M., primary, Hollingsworth, Michael A., primary, Datta, Kaustubh, primary, Jain, Maneesh, primary, Ponnusamy, Moorthy P., primary, and Batra, Surinder K., primary

Published
2023
Full Text
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50. 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
View/download PDF

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