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315 results on '"White, Rebekah R."'

1. Tumor FAK orchestrates immunosuppression in ovarian cancer via the CD155/TIGIT axis

Author

Ozmadenci, Duygu, Narayanan, Jayanth S Shankara, Andrew, Jacob, Ojalill, Marjaana, Barrie, Allison M, Jiang, Shulin, Iyer, Samhita, Chen, Xiao Lei, Rose, Michael, Estrada, Valeria, Molinolo, Alfredo, Bertotto, Thomas, Mikulski, Zbigniew, McHale, Michael C, White, Rebekah R, Connolly, Denise C, Pachter, Jonathan A, Kuchroo, Vijay K, Stupack, Dwayne G, and Schlaepfer, David D

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Immunology, Rare Diseases, Cancer, Ovarian Cancer, Development of treatments and therapeutic interventions, 5.1 Pharmaceuticals, Good Health and Well Being, Animals, Carcinoma, Ovarian Epithelial, Female, Focal Adhesion Kinase 1, Focal Adhesion Protein-Tyrosine Kinases, Humans, Immunosuppression Therapy, Ligands, Mice, Ovarian Neoplasms, Receptors, Immunologic, high-grade serous ovarian cancer, immunotherapy, FAK, CD155, tertiary lymphoid structures
Abstract

High-grade serous ovarian cancer (HGSOC) is a lethal malignancy characterized by an immunosuppressive tumor microenvironment containing few tumor infiltrating lymphocytes (TILs) and an insensitivity to checkpoint inhibitor immunotherapies. Gains in the PTK2 gene encoding focal adhesion kinase (FAK) at Chr8 q24.3 occur in ∼70% of HGSOC tumors, and elevated FAK messenger RNA (mRNA) levels are associated with poor patient survival. Herein, we show that active FAK, phosphorylated at tyrosine-576 within catalytic domain, is significantly increased in late-stage HGSOC tumors. Active FAK costained with CD155, a checkpoint receptor ligand for TIGIT (T cell immunoreceptor with immunoglobulin and immunoreceptor tyrosine-based inhibitory motif domains), in HGSOC tumors and a selective association between FAK and TIGIT checkpoint ligands were supported by patient transcriptomic database analysis. HGSOC tumors with high FAK expression were associated with low CD3 mRNA levels. Accordingly, late-stage tumors showed elevated active FAK staining and significantly lower levels of CD3+ TILs. Using the KMF (Kras, Myc, FAK) syngeneic ovarian tumor model containing spontaneous PTK2 (FAK) gene gains, the effects of tumor intrinsic genetic or oral small molecule FAK inhibitior (FAKi; VS-4718) were evaluated in vivo. Blocking FAK activity decreased tumor burden, suppressed ascites KMF-associated CD155 levels, and increased peritoneal TILs. The combination of FAKi with blocking TIGIT antibody (1B4) maintained elevated TIL levels and reduced TIGIT+ T regulatory cell levels, prolonged host survival, increased CXCL13 levels, and led to the formation of omental tertiary lymphoid structures. Collectively, our studies support FAK and TIGIT targeting as a rationale immunotherapy combination for HGSOC.

Published
2022

4. Anti-KIT DNA Aptamer for Targeted Labeling of Gastrointestinal Stromal Tumor

Author

Banerjee, Sudeep, Yoon, Hyunho, Yebra, Mayra, Tang, Chih-Min, Gilardi, Mara, Shankara Narayanan, Jayanth S, White, Rebekah R, Sicklick, Jason K, and Ray, Partha

Subjects
Biological Sciences, Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Rare Diseases, Biotechnology, Digestive Diseases, Cancer, Animals, Antibodies, Monoclonal, Apoptosis, Aptamers, Nucleotide, Cell Proliferation, Female, Gastrointestinal Neoplasms, Gastrointestinal Stromal Tumors, Humans, Mice, Mice, Nude, Proto-Oncogene Proteins c-kit, Tumor Cells, Cultured, Xenograft Model Antitumor Assays, Pharmacology and Pharmaceutical Sciences, Oncology & Carcinogenesis, Biochemistry and cell biology, Oncology and carcinogenesis
Abstract

Gastrointestinal stromal tumor (GIST), the most common sarcoma, is characterized by KIT protein overexpression, and tumors are frequently driven by oncogenic KIT mutations. Targeted inhibition of KIT revolutionized GIST therapy and ushered in the era of precision medicine for the treatment of solid malignancies. Here, we present the first use of a KIT-specific DNA aptamer for targeted labeling of GIST. We found that an anti-KIT DNA aptamer bound cells in a KIT-dependent manner and was highly specific for GIST cell labeling in vitro Functionally, the KIT aptamer bound extracellular KIT in a manner similar to KIT mAb staining, and was trafficked intracellularly in vitro The KIT aptamer bound dissociated primary human GIST cells in a mutation agnostic manner such that tumors with KIT and PDGFRA mutations were labeled. In addition, the KIT aptamer specifically labeled intact human GIST tissue ex vivo, as well as peritoneal xenografts in mice with high sensitivity. These results represent the first use of an aptamer-based method for targeted detection of GIST in vitro and in vivo.

Published
2020

6. Irreversible Electroporation Combined with Checkpoint Blockade and TLR7 Stimulation Induces Antitumor Immunity in a Murine Pancreatic Cancer Model

Author

Narayanan, Jayanth S Shankara, Ray, Partha, Hayashi, Tomoko, Whisenant, Thomas C, Vicente, Diego, Carson, Dennis A, Miller, Aaron M, Schoenberger, Stephen P, and White, Rebekah R

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Immunology, Cancer, Immunization, Pancreatic Cancer, Rare Diseases, Digestive Diseases, Inflammatory and immune system, Animals, CD8-Positive T-Lymphocytes, Cell Line, Tumor, Disease Models, Animal, Electroporation, Immunity, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Pancreatic Neoplasms, Programmed Cell Death 1 Receptor, Toll-Like Receptor 7, Tumor Microenvironment, Pharmacology and Pharmaceutical Sciences, Oncology and carcinogenesis
Abstract

Irreversible electroporation (IRE) is a nonthermal ablation technique that is used clinically in selected patients with locally advanced pancreatic cancer, but most patients develop recurrent distant metastatic disease. We hypothesize that IRE can induce an in situ vaccination effect by releasing tumor neoantigens in an inflammatory context. Using an immunocompetent mouse model, we demonstrated that IRE alone produced complete regression of subcutaneous tumors in approximately 20% to 30% of mice. IRE was not effective in immunodeficient mice. Mice with complete response to IRE demonstrated prophylactic immunity and remained tumor free when rechallenged with secondary tumors on the contralateral flank. CD8+ T cells from IRE-responsive mice were reactive against peptides representing model-inherent alloantigens and conferred protection against tumor challenge when adoptively transferred into immunocompromised, tumor-naïve mice. Combining IRE with intratumoral Toll-like receptor-7 (TLR7) agonist (1V270) and systemic anti-programmed death-1 receptor (PD)-1 checkpoint blockade resulted in improved treatment responses. This combination also resulted in elimination of untreated concomitant distant tumors (abscopal effects), an effect not seen with IRE alone. These results suggest that the systemic antitumor immune response triggered by IRE can be enhanced by stimulating the innate immune system with a TLR7 agonist and the adaptive immune system with anti-PD-1 checkpoint blockade simultaneously. Combinatorial approaches such as this may help overcome the immunosuppressive pancreatic cancer microenvironment.

Published
2019

8. Polymer-Mediated Inhibition of Pro-invasive Nucleic Acid DAMPs and Microvesicles Limits Pancreatic Cancer Metastasis

Author

Naqvi, Ibtehaj, Gunaratne, Ruwan, McDade, Jessica E, Moreno, Angelo, Rempel, Rachel E, Rouse, Douglas C, Herrera, Silvia Gabriela, Pisetsky, David S, Lee, Jaewoo, White, Rebekah R, and Sullenger, Bruce A

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Immunology, Rare Diseases, Genetics, Digestive Diseases, Pancreatic Cancer, Cancer, 5.1 Pharmaceuticals, Development of treatments and therapeutic interventions, 2.1 Biological and endogenous factors, Aetiology, Alarmins, Animals, Cell Line, Tumor, Cell-Derived Microparticles, Dendrimers, Disease Models, Animal, Exosomes, Humans, Mice, Neoplasm Invasiveness, Neoplasm Staging, Nucleic Acids, Pancreatic Neoplasms, Polymers, Protein Binding, Toll-Like Receptor 9, damage-associated molecular patterns, metastasis, nucleic acid binding polymer, Biological Sciences, Technology, Medical and Health Sciences, Biotechnology, Clinical sciences, Medical biotechnology
Abstract

Nucleic acid binding polymers (NABPs) have been extensively used as vehicles for DNA and RNA delivery. More recently, we discovered that a subset of these NABPs can also serve as anti-inflammatory agents by capturing pro-inflammatory extracellular nucleic acids and associated protein complexes that promote activation of toll-like receptors (TLRs) in diseases such as lupus erythematosus. Nucleic-acid-mediated TLR signaling also facilitates tumor progression and metastasis in several cancers, including pancreatic cancer (PC). In addition, extracellular DNA and RNA circulate on or within lipid microvesicles, such as microparticles or exosomes, which also promote metastasis by inducing pro-tumorigenic signaling in cancer cells and pre-conditioning secondary sites for metastatic establishment. Here, we explore the use of an NABP, the 3rd generation polyamidoamine dendrimer (PAMAM-G3), as an anti-metastatic agent. We show that PAMAM-G3 not only inhibits nucleic-acid-mediated activation of TLRs and invasion of PC tumor cells in vitro, but can also directly bind extracellular microvesicles to neutralize their pro-invasive effects as well. Moreover, we demonstrate that PAMAM-G3 dramatically reduces liver metastases in a syngeneic murine model of PC. Our findings identify a promising therapeutic application of NABPs for combating metastatic disease in PC and potentially other malignancies.

Published
2018

10. Benign and Malignant Tumors of the Liver

Author

White, Rebekah R., Menon, Vijay G., Johanning, Jason, Section editor, Lagoo-Deenadayalan, Sandhya, Section editor, Rosenthal, Ronnie A., editor, Zenilman, Michael E., editor, and Katlic, Mark R., editor

Published
2020
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12. Cell-SELEX Identifies a "Sticky" RNA Aptamer Sequence.

Author

Ray, Partha and White, Rebekah R

Subjects
Biochemistry and Cell Biology
Abstract

Cell-SELEX is performed to select for cell binding aptamers. We employed an additional selection pressure by using RNAse to remove surface-binding aptamers and select for cell-internalizing aptamers. A common RNA sequence was identified from independent cell-SELEX procedures against two different pancreatic cancer cell lines, indicating a strong selection pressure towards this sequence from the large pool of other available sequences present in the aptamer library. The aptamer is not specific for the pancreatic cancer cell lines, and a similar sequence motif is present in previously published internalizing aptamers. The identified sequence forms a structural motif that binds to a surface protein, which either is highly abundant or has strong affinity for the selected aptamer sequence. Deselecting (removing) this sequence during cell-SELEX may increase the probability of identifying aptamers against cell type-specific targets on the cell surface.

Published
2017

14. In Vivo Selection Against Human Colorectal Cancer Xenografts Identifies an Aptamer That Targets RNA Helicase Protein DHX9.

Author

Mi, Jing, Ray, Partha, Liu, Jenny, Kuan, Chien-Tsun, Xu, Jennifer, Hsu, David, Sullenger, Bruce A, White, Rebekah R, and Clary, Bryan M

Subjects
aptamer, colorectal cancer, in vivo SELEX, Cancer, Genetics, Colo-Rectal Cancer, Digestive Diseases, Biotechnology, 5.1 Pharmaceuticals, Biochemistry and Cell Biology, Clinical Sciences
Abstract

The ability to selectively target disease-related tissues with molecules is critical to the design of effective therapeutic and diagnostic reagents. Recognizing the differences between the in vivo environment and in vitro conditions, we employed an in vivo selection strategy to identify RNA aptamers (targeting motifs) that could localize to tumor in situ. One of the selected molecules is an aptamer that binds to the protein DHX9, an RNA helicase that is known to be upregulated in colorectal cancer. Upon systemic administration, the aptamer preferentially localized to the nucleus of cancer cells in vivo and thus has the potential to be used for targeted delivery.

Published
2016

22. Supplementary Figures and Tables from Irreversible Electroporation Combined with Checkpoint Blockade and TLR7 Stimulation Induces Antitumor Immunity in a Murine Pancreatic Cancer Model

Author

Narayanan, Jayanth S. Shankara, primary, Ray, Partha, primary, Hayashi, Tomoko, primary, Whisenant, Thomas C., primary, Vicente, Diego, primary, Carson, Dennis A., primary, Miller, Aaron M., primary, Schoenberger, Stephen P., primary, and White, Rebekah R., primary

Published
2023
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28. Contributors

Author

Abbas, Abbas E., primary, Adams, David B., additional, Aggarwal, Piyush, additional, Ahmed, Bestoun H., additional, Albanese, Craig, additional, Albert, Matthew R., additional, Ali, Abubaker, additional, Alicuben, Evan, additional, Allaix, Marco E., additional, Altman, Ashley, additional, Ando, Hisami, additional, Andolfi, Ciro, additional, Annamalai, Alagappan, additional, Asare, Elliot A., additional, Asti, Emanuele, additional, Auchincloss, Hugh G., additional, Babic, Benjamin, additional, Baker, Talia B., additional, Ball, Chad G., additional, Barbetta, Arianna, additional, Barlow, John M., additional, Barr, Justin, additional, Barreto, Juan Camilo, additional, Barry, Linda, additional, Beal, Eliza W., additional, Beard, Kristin Wilson, additional, Beck, David E., additional, Behrns, Kevin E., additional, Bellevue, Oliver C., additional, Bellorin-Marin, Omar E., additional, Bergman, Jacques, additional, Berry, James, additional, Besselink, Marc G.H., additional, Bharucha, Adil E., additional, Bilchik, Anton J., additional, Bildzukewicz, Nikolai A., additional, Bingham, Jason, additional, Birnbaum, Elisa, additional, Black, Sylvester M., additional, Blackmon, Shanda H., additional, Bleier, Joshua I.S., additional, Bodzin, Adam S., additional, Boland, C. Richard, additional, Bolton, John, additional, Bolton, Nathan, additional, Bonavina, Luigi, additional, Bonds, Morgan, additional, Bouwense, Stefan A.W., additional, Boys, Joshua A., additional, Bravo-Infante, Raquel, additional, Bremner, Ross M., additional, Brenner, Bruce M., additional, Brown, Shaun R., additional, Callery, Mark P., additional, Cameron, John L., additional, Camilleri, Michael, additional, Campbell, Jacob, additional, Cassim, Riaz, additional, Castillo-Angeles, Manuel, additional, Cauley, Christy, additional, Cavaness, Keith M., additional, Cerfolio, Robert J., additional, Champagne, Bradley J., additional, Chandrasoma, Parakrama, additional, Chang, Alex L., additional, Chapman, Christopher G., additional, Chapman, William C., additional, Cheek, Susannah, additional, Chen, Harvey S., additional, Cho, Clifford S., additional, Choi, Eric T., additional, Choi, Eugene A., additional, Chojnacki, Karen A., additional, Choti, Michael A., additional, Christie, Ian, additional, Chua, Heidi, additional, Church, James M., additional, Cioffi, Jessica L., additional, Clark, Susannah, additional, Clavien, Pierre-Alain, additional, Cloud, Adam, additional, Colavita, Paul D., additional, Colquhoun, Steven D., additional, Conway, William, additional, Cools-Lartigue, Jonathan, additional, Coosemans, Willy, additional, Cornwell, Edward E., additional, Costantini, Mario, additional, Coyle, Yvonne, additional, Craig, Daniel A., additional, Croome, Kristopher P., additional, Cullen, Joseph J., additional, D'Andrea, Anthony P., additional, Dassopoulos, Themistocles, additional, Davila, Marta L., additional, Davila, Raquel E., additional, DeMeester, Steven R., additional, DeMeester, Tom R., additional, Dempsey, Daniel T., additional, dePrisco, Gregory, additional, Depypere, Lieven, additional, Dietz, David W., additional, Dillhoff, Mary E., additional, DiNorcia, Joseph, additional, Doane, Stephen M., additional, Dogeas, Epameinondas, additional, Dozois, Eric J., additional, Dumon, Kristoffel, additional, Dunn, Stephen P., additional, Dunst, Christy M., additional, Dussel, John N., additional, Dyer, Matthew, additional, Efron, Jonathan, additional, El-Gohary, Yousef, additional, Lakis, Mustapha El, additional, Ellison, E. Christopher, additional, Ellsmere, James, additional, Essani, Rahila, additional, Evans, Douglas B., additional, Fang, Sandy H., additional, Fasen, Geoffrey, additional, Fernando, Hiran C., additional, Ferri, Lorenzo, additional, Fichera, Alessandro, additional, Finck, Christine, additional, Fisher, Oliver M., additional, Fleshman, James W., additional, Fong, Yuman, additional, Foreman, Michael L., additional, Francone, Todd D., additional, Franko, Edward R., additional, French, Daniel, additional, Fuchs, Hans Friedrich, additional, Fuchs, Karl Hermann, additional, Funaki, Brian, additional, Funk, Geoffrey A., additional, Fusco, Joseph, additional, Gaitonde, Shrawan G., additional, Gajjar, Aakash H., additional, Garcia-Aguilar, Julio, additional, Gearhart, Susan, additional, Geller, David A., additional, Ghobadi, Comeron, additional, Gilbert, Sebastien, additional, Giles, David, additional, Gillaspie, Erin, additional, Girotti, Micah, additional, Gittes, George K., additional, Goodman, Michael D., additional, Gooszen, Hein G., additional, Gores, Gregory J., additional, Griffin, James F., additional, Griffin, S. Michael, additional, Grimm, Leander, additional, Grochola, L.F., additional, Habib, Fahim, additional, Hanks, John B., additional, Harris, James E., additional, Hartwig, Matthew G., additional, Hassan, Imran, additional, Hedrick, Traci L., additional, Hicks, Terry C., additional, Hodin, Richard, additional, Hofstetter, Wayne L., additional, Hogg, Melissa, additional, Hu, Yue-Yung, additional, Hungness, Eric S., additional, Hunt, Steven R., additional, Huseynova, Khumara, additional, Hyman, Neil H., additional, Iannitti, David A., additional, Indes, Jeffrey, additional, Jenkins, Megan, additional, Jensen, Todd, additional, Jeziorczak, Paul M., additional, Jilani, Danial, additional, Jiménez-Toscano, Marta, additional, Jobe, Blair A., additional, Johnston, Lily E., additional, Kahrilas, Peter J., additional, Kalady, Matthew F., additional, Kassira, Noor, additional, Katkhouda, Namir, additional, Katz, Philip O., additional, Keller, Deborah S., additional, Kelley, Matthew P., additional, Kennedy, Gregory D., additional, Kent, Tara Sotsky, additional, Kia, Leila, additional, Kibbe, Melina R., additional, Kim, John, additional, King, Alice, additional, Kiran, Ravi P., additional, Kirton, Orlando C., additional, Klein, Andrew, additional, Klein, Eric N., additional, Kohn, Geoffrey P., additional, Kovell, Robert Caleb, additional, Kozol, Robert, additional, Lacy, Antonio M., additional, Ladner, Daniela P., additional, Lagarde, S.M., additional, Laituri, Carrie A., additional, Landmann, Alessandra, additional, Lee, Janet T., additional, Lee, Lawrence L., additional, Leinicke, Jennifer A., additional, Lerut, Toni, additional, Levi, David M., additional, Li, Chao, additional, Liang, Yu, additional, Lichliter, Andrew H., additional, Lichliter, Warren E., additional, Lightner, Amy L., additional, Lile, Deacon J., additional, Lillemoe, Keith D., additional, Lin, Jules, additional, Lin, Shu S., additional, Lipham, John C., additional, Litle, Virginia R., additional, Lodhia, Nayna A., additional, Longo, Walter E., additional, Lord, Reginald V.N., additional, Louie, Brian E., additional, Low, Donald E., additional, Lowe, Val J., additional, Luc, Jessica G.Y., additional, Luketich, James D., additional, Ma, Yanling, additional, MacCarty, Robert L., additional, MacDonald, Blair, additional, Madoff, Robert D., additional, Magge, Deepa, additional, Maheshwari, Anurag, additional, Mahmoud, Najjia N., additional, Mahvi, David A., additional, Mahvi, David M., additional, Mak, Grace Z., additional, Mansfield, Sara A., additional, Manzano, Maricarmen, additional, Maron, David J., additional, Mathew, Melvy S., additional, Mathis, Kellie L., additional, Matthews, Jeffrey B., additional, McFadden, David W., additional, Merchea, Amit, additional, Messaris, Evangelos, additional, Miller, Daniel L., additional, Miller, Heidi J., additional, Millis, J. Michael, additional, Mittal, Sumeet K., additional, Molena, Daniela, additional, Montgomery, Stephanie C., additional, Moore, Ryan, additional, Morgan, Katherine A., additional, Mortenson, Melinda M., additional, Mulholland, Michael W., additional, Mulvihill, Michael S., additional, Mutch, Matthew, additional, Nafteux, Philippe Robert, additional, Nagaraju, Arun, additional, Nagorney, David M., additional, Nathan, Hari, additional, Natoli, Karen R., additional, Navuluri, Rakesh, additional, Nissen, Nicholas N., additional, Nobel, Tamar B., additional, Noordman, B.J., additional, Norton, Jeffrey A., additional, Novitsky, Yuri W., additional, Nussbaum, Michael S., additional, Nyberg, Scott L., additional, Oelschlager, Brant K., additional, Oh, Daniel S., additional, Otero-Piñeiro, Ana, additional, Oto, Aytekin, additional, Pachter, H. Leon, additional, Paidas, Charles N., additional, Palazzo, Francesco, additional, Paniccia, Alessandro, additional, Papaconstantinou, Harry T., additional, Pappas, Theodore N., additional, Pappou, Emmanouil P., additional, Parikh, Manish, additional, Paruch, Jennifer L., additional, Patel, Asish D., additional, Patel, Mikin, additional, Patti, Marco G., additional, Paulson, Emily Carter, additional, Pawlik, Timothy M., additional, Payne, Isaac, additional, Pemberton, John H., additional, Pendola, Michael, additional, Perez, Alexander, additional, Pernar, Luise I.M., additional, Peters, Walter R., additional, Petrowsky, Henrik, additional, Peyre, Christian G., additional, Phillips, Alexander W., additional, Pillai, Lashmikumar, additional, Plummer, Joseph M., additional, Pointer, David T., additional, Poruk, Katherine E., additional, Posner, Mitchell C., additional, Postier, Russell, additional, Prachand, Vivek N., additional, Pritts, Timothy A., additional, Quatrino, Gregory, additional, Ranka, Sagar, additional, Rattner, David W., additional, Reavis, Kevin M., additional, Reddy, Vikram B., additional, Remzi, Feza H., additional, Ricciardi, Rocco, additional, Rice, Thomas W., additional, Richman, Aaron, additional, Rider, Paul, additional, Roberts, John Paul, additional, Roberts, Patricia L., additional, Roggin, Kevin K., additional, Roll, Garrett Richard, additional, Rona, Kais, additional, Rosen, Charles B., additional, Ross, Samuel Wade, additional, Roth, J. Scott, additional, Rushing, Amy P., additional, Safar, Bashar, additional, Saldinger, Pierre F., additional, Samakar, Kamran, additional, Sandhu, Kulmeet K., additional, Schaheen, Lara W., additional, Schirmer, Bruce, additional, Schneider, Andrew, additional, Schulick, Richard D., additional, Schwab, Ben, additional, Scurci, Stephanie, additional, Senagore, Anthony, additional, Shah, Adil A., additional, Shah, Shimul A., additional, Shames, Brian, additional, Shanmugan, Skandan, additional, Shapiro, David S., additional, Silviera, Matthew, additional, Slakey, Douglas P., additional, Sloan, Joshua, additional, Smallwood, Nathan, additional, Smith, Shane P., additional, Smithers, B. Mark, additional, Smoot, Rory L., additional, Soares, Kevin C., additional, Soffer, Edy, additional, Solomina, Julia, additional, Soper, Nathaniel J., additional, Spechler, Stuart Jon, additional, Sridhar, Praveen, additional, Steele, Scott R., additional, Sternbach, Joel M., additional, Stevenson, Christina E., additional, Strong, Scott A., additional, Sucandy, Iswanto, additional, Sundaram, Magesh, additional, Sundaresan, Sudhir, additional, Swanstrom, Lee L., additional, Sylla, Patricia, additional, Takada, Tadahiro, additional, Talbot, Ethan, additional, Tam, Vernissia, additional, Tamm, Eric P., additional, Tatarian, Talar, additional, Tavakkoli, Ali, additional, Te, Helen S., additional, Teitelbaum, Ezra N., additional, Ternent, Charles A., additional, Thompson, Jon S., additional, Thomson, Iain, additional, Thorson, Alan G., additional, Thorson, Chad M., additional, Totten, Crystal F., additional, Truty, Mark J., additional, Tsai, Susan, additional, Tseng, Jennifer, additional, Tullius, Tom, additional, Tzakis, Andreas G., additional, van Lanschot, J.J.B., additional, van Santvoort, Hjalmar C., additional, Van Veer, Hans, additional, Vega, Jorge A., additional, Velanovich, Vic, additional, Vogler, Sarah A., additional, Wang, Huamin, additional, Ward, Mark A., additional, Warner, Brad W., additional, Warner, Susanne G., additional, Watson, Thomas J., additional, Waxman, Irving, additional, Webster-Lake, Carissa, additional, Wei, Benjamin, additional, Weiser, Martin R., additional, Wells, Dennis, additional, Wells, Katerina, additional, Welton, Mark Lane, additional, Wen, Yuxiang, additional, Wendling, Mark R., additional, Wesson, Hadley K.H., additional, Wexner, Steven D., additional, White, Rebekah R., additional, Whitlow, Charles B., additional, Wijnhoven, B.P.L., additional, Wilkes, Justin, additional, Wilson, Rickesha L., additional, Witkowski, Piotr, additional, Wolfgang, Christopher L., additional, Worrell, Stephanie G., additional, Yang, Jian, additional, Yeo, Charles J., additional, Yeung, Ching, additional, Yung, Evan E., additional, Zafar, Syed Nabeel, additional, Zaninotto, Giovanni, additional, Zeh, Herbert, additional, Zehetner, Joerg, additional, Zenilman, Michael E., additional, Zimmerman, Pamela, additional, and Zuccaro, Gregory, additional

Published
2019
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29. Data from Targeting eNOS in Pancreatic Cancer

Author

Lampson, Benjamin L., primary, Kendall, S. DiSean, primary, Ancrile, Brooke B., primary, Morrison, Meghan M., primary, Shealy, Michael J., primary, Barrientos, Katharine S., primary, Crowe, Matthew S., primary, Kashatus, David F., primary, White, Rebekah R., primary, Gurley, Susan B., primary, Cardona, Diana M., primary, and Counter, Christopher M., primary

Published
2023
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30. Supplementary Figure Legends 1-3 from Targeting eNOS in Pancreatic Cancer

Author

Lampson, Benjamin L., primary, Kendall, S. DiSean, primary, Ancrile, Brooke B., primary, Morrison, Meghan M., primary, Shealy, Michael J., primary, Barrientos, Katharine S., primary, Crowe, Matthew S., primary, Kashatus, David F., primary, White, Rebekah R., primary, Gurley, Susan B., primary, Cardona, Diana M., primary, and Counter, Christopher M., primary

Published
2023
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31. Supplementary Figure 3 from Targeting eNOS in Pancreatic Cancer

Author

Lampson, Benjamin L., primary, Kendall, S. DiSean, primary, Ancrile, Brooke B., primary, Morrison, Meghan M., primary, Shealy, Michael J., primary, Barrientos, Katharine S., primary, Crowe, Matthew S., primary, Kashatus, David F., primary, White, Rebekah R., primary, Gurley, Susan B., primary, Cardona, Diana M., primary, and Counter, Christopher M., primary

Published
2023
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32. Supplementary Figure 2 from Targeting eNOS in Pancreatic Cancer

Author

Lampson, Benjamin L., primary, Kendall, S. DiSean, primary, Ancrile, Brooke B., primary, Morrison, Meghan M., primary, Shealy, Michael J., primary, Barrientos, Katharine S., primary, Crowe, Matthew S., primary, Kashatus, David F., primary, White, Rebekah R., primary, Gurley, Susan B., primary, Cardona, Diana M., primary, and Counter, Christopher M., primary

Published
2023
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33. Treatment of pancreatic cancer with irreversible electroporation and intratumoral CD40 antibody stimulates systemic immune responses that inhibit liver metastasis in an orthotopic model

Author

Shankara Narayanan, Jayanth S, primary, Hayashi, Tomoko, additional, Erdem, Suna, additional, McArdle, Sara, additional, Tiriac, Herve, additional, Ray, Partha, additional, Pu, Minya, additional, Mikulski, Zbigniew, additional, Miller, Aaron, additional, Messer, Karen, additional, Carson, Dennis, additional, Schoenberger, Stephen, additional, and White, Rebekah R, additional

Published
2023
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34. Treatment of pancreatic cancer with irreversible electroporation and intratumoral CD40 antibody stimulates systemic immune responses that inhibit liver metastasis in an orthotopic model

Author

Narayanan, Jayanth S. Shankara, primary, Hayashi, Tomoko, additional, Erdem, Suna, additional, McArdle, Sara, additional, Tiriac, Herve, additional, Ray, Partha, additional, Pu, Minya, additional, Mikulski, Zbigniew, additional, Miller, Aaron, additional, Messer, Karen, additional, Carson, Dennis, additional, Schoenberger, Stephen P., additional, and White, Rebekah R., additional

Published
2022
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38. Diagnostic Laparoscopy for Malignancy

Author

White, Rebekah R., Tyler, Douglas S., MacFadyen, Bruce V., Jr., editor, Arregui, Maurice E., editor, Eubanks, Steve, editor, Olsen, Douglas O., editor, Peters, Jeffrey H., editor, Soper, Nathaniel J., editor, Swanström, Lee L., editor, and Wexner, Steven D., editor

Published
2004
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49. Comparing human pancreatic cell secretomes by in vitro aptamer selection identifies cyclophilin B as a candidate pancreatic cancer biomarker

Author

Ray, Partha, Rialon-Guevara, Kristy L., Veras, Emanuela, Sullenger, Bruce A., and White, Rebekah R.

Subjects
Cyclophilin -- Identification and classification -- Research, Tumor markers -- Identification and classification -- Research, Peptide aptamers -- Research, Pancreatic cancer -- Diagnosis -- Research, Health care industry
Abstract

Most cases of pancreatic cancer are not diagnosed until they are no longer curable with surgery. Therefore, it is critical to develop a sensitive, preferably noninvasive, method for detecting the disease at an earlier stage. In order to identify biomarkers for pancreatic cancer, we devised an in vitro positive/negative selection strategy to identify RNA ligands (aptamers) that could detect structural differences between the secretomes of pancreatic cancer and non-cancerous cells. Using this molecular recognition approach, we identified an aptamer (M9-5) that differentially bound conditioned media from cancerous and non-cancerous human pancreatic cell lines. This aptamer further discriminated between the sera of pancreatic cancer patients and healthy volunteers with high sensitivity and specificity. We utilized biochemical purification methods and mass-spectrometric analysis to identify the M9-5 target as cyclophilin B (CypB). This molecular recognition-based strategy simultaneously identified CypB as a serum biomarker and generated a new reagent to recognize it in body fluids. Moreover, this approach should be generalizable to other diseases and complementary to traditional approaches that focus on differences in expression level between samples. Finally, we suggest that the aptamer we identified has the potential to serve as a tool for the early detection of pancreatic cancer., Introduction At the time of diagnosis, the vast majority of patients with pancreatic cancer have locally advanced or distant metastatic disease that is not resectable (1). Earlier detection of the [...]

Published
2012
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