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Your search keyword '"Perez-Mancera, Pedro A."' showing total 7 results
Start Over Author "Perez-Mancera, Pedro A." Journal cancer research
7 results on '"Perez-Mancera, Pedro A."'

1. Abstract C084: Oncogenic KRAS signaling drives the activation of tissue-resident fibroblasts and is required to maintain CAF heterogeneity in pancreatic cancer

Author

Caligiuri, Giuseppina, primary, Thalappillil, Jennifer S., additional, Shakiba, Mojdeh, additional, Nadella, Sandeep, additional, Hinds, Juliene, additional, Courtois, Elise, additional, Flynn, William F., additional, Alagesan, Brinda, additional, Yordanov, Georgi N., additional, Kaminow, Benjamin, additional, Robson, Paul, additional, Perez-Mancera, Pedro A., additional, Preall, Jonathan, additional, Dobin, Alexander, additional, Park, Youngku, additional, and Tuveson, David A., additional

Published
2022
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2. Abstract 3647: Oncogenic Kras drives cancer-associated fibroblast heterogeneity and substate changes in pancreatic cancer

Author

Thalappillil, Jennifer S., primary, Caligiuri, Giuseppina, additional, Nadella, Sandeep, additional, Alagesan, Brinda, additional, Yordanov, Georgi N., additional, Shakiba, Mojdeh, additional, Kaminow, Benjamin, additional, Hinds, Juliene, additional, Perez-Mancera, Pedro A., additional, Preall, Jonathan, additional, Dobin, Alexander, additional, Park, Youngkyu, additional, and Tuveson, David A., additional

Published
2022
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3. Fibroblasts from Distinct Pancreatic Pathologies Exhibit Disease-Specific Properties

Author

Barrera, Lawrence N., primary, Evans, Anthony, additional, Lane, Brian, additional, Brumskill, Sarah, additional, Oldfield, Frances E., additional, Campbell, Fiona, additional, Andrews, Timothy, additional, Lu, Zipeng, additional, Perez-Mancera, Pedro A., additional, Liloglou, Triantafillos, additional, Ashworth, Milton, additional, Jalali, Mehdi, additional, Dawson, Rebecca, additional, Nunes, Quentin, additional, Phillips, Phoebe A., additional, Timms, John F., additional, Halloran, Christopher, additional, Greenhalf, William, additional, Neoptolemos, John P., additional, and Costello, Eithne, additional

Published
2020
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4. Chemoresistance in Pancreatic Cancer Is Driven by Stroma-Derived Insulin-Like Growth Factors

Author

Ireland, Lucy, primary, Santos, Almudena, additional, Ahmed, Muhammad S., additional, Rainer, Carolyn, additional, Nielsen, Sebastian R., additional, Quaranta, Valeria, additional, Weyer-Czernilofsky, Ulrike, additional, Engle, Danielle D., additional, Perez-Mancera, Pedro A., additional, Coupland, Sarah E., additional, Taktak, Azzam, additional, Bogenrieder, Thomas, additional, Tuveson, David A., additional, Campbell, Fiona, additional, Schmid, Michael C., additional, and Mielgo, Ainhoa, additional

Published
2016
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5. Abstract 798: Clonal analysis and clinical translation of pancreatic adenocarcinoma genomes.

Author

Barrett, Michael T., primary, Lenkiewicz, Elizabeth, additional, Lisa, Evers, additional, Perez-Mancera, Pedro, additional, Tuveson, David, additional, Aust, Daniela, additional, Pilarsky, Christian, additional, Aziz, Meraj, additional, Posner, Richard, additional, Ramanathan, Ramesh, additional, Velculescu, Victor, additional, Kramer, Amy, additional, Drebin, Jeffrey, additional, and Von Hoff, Daniel D., additional

Published
2013
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7. Scribble Deficiency Promotes Pancreatic Ductal Adenocarcinoma Development and Metastasis.

Author

Bermejo-Rodriguez C, Araos Henríquez J, Caligiuri G, Pinto Teles S, Park Y, Evans A, Barrera LN, Neesse A, Grutzmann R, Aust D, Rümmele P, Knösel T, Narita M, Narita M, Campbell F, Öhlund D, Pilarsky C, Dow LE, Humbert PO, Biffi G, Tuveson DA, and Perez-Mancera PA

Abstract

Perturbation of cell polarity is a hallmark of pancreatic ductal adenocarcinoma (PDAC) progression. Scribble (SCRIB) is a well characterized polarity regulator that has diverse roles in the pathogenesis of human neoplasms. To investigate the impact of SCRIB deficiency on PDAC development and progression, Scrib was genetically ablated in well-established mouse models of PDAC. Scrib loss in combination with KrasG12D did not influence development of pancreatic intraepithelial neoplasms (PanIN) in mice. However, Scrib deletion cooperated with KrasG12D and concomitant Trp53 heterozygous deletion to promote invasive PDAC and metastatic dissemination, leading to reduced overall survival. Immunohistochemical and transcriptome analyses revealed that Scrib-null tumors display a pronounced reduction of collagen content and cancer associated fibroblast (CAF) abundance. Mechanistically, interleukin 1α (IL1α) levels were reduced in Scrib deficient tumors, and Scrib knockdown downregulated IL1α in mouse PDAC organoids (mPDOs), which impaired CAF activation. Furthermore, Scrib loss increased YAP activation in mPDOs and established PDAC cell lines, enhancing cell survival. Clinically, SCRIB expression was decreased in human PDAC, and SCRIB mislocalization was associated with poorer patient outcome. These results indicate that SCRIB deficiency enhances cancer cell survival and remodels the tumor microenvironment to accelerate PDAC development and progression, establishing the tumor suppressor function of SCRIB in advanced pancreatic cancer.

Published
2024
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