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13 results on '"Johns, Amber L"'

1. The Impact of Molecular Subtyping on Pathological Staging of Pancreatic Cancer.

Author

Dreyer, Stephan B., Rae, Sarah, Bisset, Kirsty, Upstill-Goddard, Rosie, Gemenetzis, Georgios, Johns, Amber L., Dickson, Euan J., Mittal, Anubhav, Gill, Anthony J., Duthie, Fraser, Pea, Antonio, Lawlor, Rita T., Scarpa, Aldo, Salvia, Roberto, Pulvirenti, Alessandra, Zerbi, Alessandro, Marchesi, Federica, McKay, Colin J., Biankin, Andrew V., and Samra, Jaswinder S.

Abstract

Background: The long-term outcomes following surgical resection for pancreatic ductal adenocarcinoma (PDAC) remains poor, with only 20% of patients surviving 5 years after pancreatectomy. Patient selection for surgery remains suboptimal largely due to the absence of consideration of aggressive tumor biology. Objective: The aim of this study was to evaluate traditional staging criteria for PDAC in the setting of molecular subtypes. Methods: Clinicopathological data were obtained for 5 independent cohorts of consecutive unselected patients, totaling n = 1298, including n = 442 that underwent molecular subtyping. The main outcome measure was disease-specific survival following surgical resection for PDAC stratified according to the American Joint Commission for Cancer (TNM) staging criteria, margin status, and molecular subtype. Results: TNM staging criteria and margin status confers prognostic value only in tumors with classical pancreatic subtype. Patients with tumors that are of squamous subtype, have a poor outcome irrespective of favorable traditional pathological staging [hazard ratio (HR) 1.54, 95% confidence interval (CI) 1.04–2.28, P = 0.032]. Margin status has no impact on survival in the squamous subtype (16.0 vs 12.1 months, P = 0.374). There were no differences in molecular subtype or gene expression of tumors with positive resection margin status. Conclusions: Aggressive tumor biology as measured by molecular subtype predicts poor outcome following pancreatectomy for PDAC and should be utilized to inform patient selection for surgery. [ABSTRACT FROM AUTHOR]

Published
2023
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2. The Impact of Molecular Subtyping on Pathological Staging of Pancreatic Cancer

Author

Dreyer, Stephan B., Rae, Sarah, Bisset, Kirsty, Upstill-Goddard, Rosie, Gemenetzis, Georgios, Johns, Amber L., Dickson, Euan J., Mittal, Anubhav, Gill, Anthony J., Duthie, Fraser, Pea, Antonio, Lawlor, Rita T., Scarpa, Aldo, Salvia, Roberto, Pulvirenti, Alessandra, Zerbi, Alessandro, Marchesi, Federica, McKay, Colin J., Biankin, Andrew V., Samra, Jaswinder S., Chang, David K., and Jamieson, Nigel B.

Published
2023
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3. Whole-genome landscape of pancreatic neuroendocrine tumours

Author

Scarpa, Aldo, Chang, David K., Nones, Katia, Corbo, Vincenzo, Patch, Ann-Marie, Bailey, Peter, Lawlor, Rita T., Johns, Amber L., Miller, David K., Mafficini, Andrea, Rusev, Borislav, Scardoni, Maria, Antonello, Davide, Barbi, Stefano, Sikora, Katarzyna O., Cingarlini, Sara, Vicentini, Caterina, McKay, Skye, Quinn, Michael C. J., Bruxner, Timothy J. C., Christ, Angelika N., Harliwong, Ivon, Idrisoglu, Senel, McLean, Suzanne, Nourse, Craig, Nourbakhsh, Ehsan, Wilson, Peter J., Anderson, Matthew J., Fink, J. Lynn, Newell, Felicity, Waddell, Nick, Holmes, Oliver, Kazakoff, Stephen H., Leonard, Conrad, Wood, Scott, Xu, Qinying, Nagaraj, Shivashankar Hiriyur, Amato, Eliana, Dalai, Irene, Bersani, Samantha, Cataldo, Ivana, Dei Tos, Angelo P., Capelli, Paola, Davì, Maria Vittoria, Landoni, Luca, Malpaga, Anna, Miotto, Marco, Whitehall, Vicki L. J., Leggett, Barbara A., Harris, Janelle L., Harris, Jonathan, Jones, Marc D., Humphris, Jeremy, Chantrill, Lorraine A., Chin, Venessa, Nagrial, Adnan M., Pajic, Marina, Scarlett, Christopher J., Pinho, Andreia, Rooman, Ilse, Toon, Christopher, Wu, Jianmin, Pinese, Mark, Cowley, Mark, Barbour, Andrew, Mawson, Amanda, Humphrey, Emily S., Colvin, Emily K., Chou, Angela, Lovell, Jessica A., Jamieson, Nigel B., Duthie, Fraser, Gingras, Marie-Claude, Fisher, William E., Dagg, Rebecca A., Lau, Loretta M. S., Lee, Michael, Pickett, Hilda A., Reddel, Roger R., Samra, Jaswinder S., Kench, James G., Merrett, Neil D., Epari, Krishna, Nguyen, Nam Q., Zeps, Nikolajs, Falconi, Massimo, Simbolo, Michele, Butturini, Giovanni, Van Buren, George, Partelli, Stefano, Fassan, Matteo, Khanna, Kum Kum, Gill, Anthony J., Wheeler, David A., Gibbs, Richard A., Musgrove, Elizabeth A., Bassi, Claudio, Tortora, Giampaolo, Pederzoli, Paolo, Pearson, John V., Waddell, Nicola, Biankin, Andrew V., and Grimmond, Sean M.

Abstract

The diagnosis of pancreatic neuroendocrine tumours (PanNETs) is increasing owing to more sensitive detection methods, and this increase is creating challenges for clinical management. We performed whole-genome sequencing of 102 primary PanNETs and defined the genomic events that characterize their pathogenesis. Here we describe the mutational signatures they harbour, including a deficiency in G:C > T:A base excision repair due to inactivation of MUTYH, which encodes a DNA glycosylase. Clinically sporadic PanNETs contain a larger-than-expected proportion of germline mutations, including previously unreported mutations in the DNA repair genes MUTYH, CHEK2 and BRCA2. Together with mutations in MEN1 and VHL, these mutations occur in 17% of patients. Somatic mutations, including point mutations and gene fusions, were commonly found in genes involved in four main pathways: chromatin remodelling, DNA damage repair, activation of mTOR signalling (including previously undescribed EWSR1 gene fusions), and telomere maintenance. In addition, our gene expression analyses identified a subgroup of tumours associated with hypoxia and HIF signalling.

Published
2017
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4. Genomic analyses identify molecular subtypes of pancreatic cancer

Author

Bailey, Peter, Chang, David K., Nones, Katia, Johns, Amber L., Patch, Ann-Marie, Gingras, Marie-Claude, Miller, David K., Christ, Angelika N., Bruxner, Tim J. C., Quinn, Michael C., Nourse, Craig, Murtaugh, L. Charles, Harliwong, Ivon, Idrisoglu, Senel, Manning, Suzanne, Nourbakhsh, Ehsan, Wani, Shivangi, Fink, Lynn, Holmes, Oliver, Chin, Venessa, Anderson, Matthew J., Kazakoff, Stephen, Leonard, Conrad, Newell, Felicity, Waddell, Nick, Wood, Scott, Xu, Qinying, Wilson, Peter J., Cloonan, Nicole, Kassahn, Karin S., Taylor, Darrin, Quek, Kelly, Robertson, Alan, Pantano, Lorena, Mincarelli, Laura, Sanchez, Luis N., Evers, Lisa, Wu, Jianmin, Pinese, Mark, Cowley, Mark J., Jones, Marc D., Colvin, Emily K., Nagrial, Adnan M., Humphrey, Emily S., Chantrill, Lorraine A., Mawson, Amanda, Humphris, Jeremy, Chou, Angela, Pajic, Marina, Scarlett, Christopher J., Pinho, Andreia V., Giry-Laterriere, Marc, Rooman, Ilse, Samra, Jaswinder S., Kench, James G., Lovell, Jessica A., Merrett, Neil D., Toon, Christopher W., Epari, Krishna, Nguyen, Nam Q., Barbour, Andrew, Zeps, Nikolajs, Moran-Jones, Kim, Jamieson, Nigel B., Graham, Janet S., Duthie, Fraser, Oien, Karin, Hair, Jane, Grützmann, Robert, Maitra, Anirban, Iacobuzio-Donahue, Christine A., Wolfgang, Christopher L., Morgan, Richard A., Lawlor, Rita T., Corbo, Vincenzo, Bassi, Claudio, Rusev, Borislav, Capelli, Paola, Salvia, Roberto, Tortora, Giampaolo, Mukhopadhyay, Debabrata, Petersen, Gloria M., Munzy, Donna M., Fisher, William E., Karim, Saadia A., Eshleman, James R., Hruban, Ralph H., Pilarsky, Christian, Morton, Jennifer P., Sansom, Owen J., Scarpa, Aldo, Musgrove, Elizabeth A., Bailey, Ulla-Maja Hagbo, Hofmann, Oliver, Sutherland, Robert L., Wheeler, David A., Gill, Anthony J., Gibbs, Richard A., Pearson, John V., Waddell, Nicola, Biankin, Andrew V., and Grimmond, Sean M.

Abstract

Integrated genomic analysis of 456 pancreatic ductal adenocarcinomas identified 32 recurrently mutated genes that aggregate into 10 pathways: KRAS, TGF-β, WNT, NOTCH, ROBO/SLITsignalling, G1/Stransition, SWI-SNF, chromatin modification, DNA repair and RNA processing. Expression analysis defined 4 subtypes: (1) squamous; (2) pancreatic progenitor; (3) immunogenic; and (4) aberrantly differentiated endocrine exocrine (ADEX) that correlate with histopathological characteristics. Squamous tumours are enriched for TP53and KDM6Amutations, upregulation of the TP63∆Ntranscriptional network, hypermethylation of pancreatic endodermal cell-fate determining genes and have a poor prognosis. Pancreatic progenitor tumours preferentially express genes involved in early pancreatic development (FOXA2/3, PDX1and MNX1). ADEX tumours displayed upregulation of genes that regulate networks involved in KRASactivation, exocrine (NR5A2and RBPJL), and endocrine differentiation (NEUROD1and NKX2-2). Immunogenic tumours contained upregulated immune networks including pathways involved in acquired immune suppression. These data infer differences in the molecular evolution of pancreatic cancer subtypes and identify opportunities for therapeutic development.

Published
2016
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5. Ampullary Cancers Harbor ELF3Tumor Suppressor Gene Mutations and Exhibit Frequent WNTDysregulation

Author

Gingras, Marie-Claude, Covington, Kyle R., Chang, David K., Donehower, Lawrence A., Gill, Anthony J., Ittmann, Michael M., Creighton, Chad J., Johns, Amber L., Shinbrot, Eve, Dewal, Ninad, Fisher, William E., Pilarsky, Christian, Grützmann, Robert, Overman, Michael J., Jamieson, Nigel B., Van Buren, George, Drummond, Jennifer, Walker, Kimberly, Hampton, Oliver A., Xi, Liu, Muzny, Donna M., Doddapaneni, Harsha, Lee, Sandra L., Bellair, Michelle, Hu, Jianhong, Han, Yi, Dinh, Huyen H., Dahdouli, Mike, Samra, Jaswinder S., Bailey, Peter, Waddell, Nicola, Pearson, John V., Harliwong, Ivon, Wang, Huamin, Aust, Daniela, Oien, Karin A., Hruban, Ralph H., Hodges, Sally E., McElhany, Amy, Saengboonmee, Charupong, Duthie, Fraser R., Grimmond, Sean M., Biankin, Andrew V., Wheeler, David A., and Gibbs, Richard A.

Abstract

The ampulla of Vater is a complex cellular environment from which adenocarcinomas arise to form a group of histopathologically heterogenous tumors. To evaluate the molecular features of these tumors, 98 ampullary adenocarcinomas were evaluated and compared to 44 distal bile duct and 18 duodenal adenocarcinomas. Genomic analyses revealed mutations in the WNTsignaling pathway among half of the patients and in all three adenocarcinomas irrespective of their origin and histological morphology. These tumors were characterized by a high frequency of inactivating mutations of ELF3,a high rate of microsatellite instability, and common focal deletions and amplifications, suggesting common attributes in the molecular pathogenesis are at play in these tumors. The high frequency of WNTpathway activating mutation, coupled with small-molecule inhibitors of β-catenin in clinical trials, suggests future treatment decisions for these patients may be guided by genomic analysis.

Published
2016
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6. Histomolecular Phenotypes and Outcome in Adenocarcinoma of the Ampulla of Vater.

Author

Chang, David K., Jamieson, Nigel B., Johns, Amber L., Scarlett, Christopher J., Pajic, Marina, Chou, Angela, Pinese, Mark, Humphris, Jeremy L., Jones, Marc D., Toon, Christopher, Nagrial, Adnan M., Chantrill, Lorraine A., Chin, Venessa T., Pinho, Andreia V., Rooman, Ilse, Cowley, Mark J., Jianmin Wu, Mead, R. Scott, Colvin, Emily K., and Samra, Jaswinder S.

Published
2013
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7. Synoptic reporting improves histopathological assessment of pancreatic resection specimens

Author

Gill, Anthony J., Johns, Amber L., Eckstein, Robert, Samra, Jaswinder S., Kaufman, Antony, Chang, David K., Merrett, Neil D., Cosman, Peter H., Smith, Ross C., Biankin, Andrew V., and Kench, James G.

Abstract

We examined whether introduction of a standardised pancreatic cancer minimum data set improved the reporting of key pathological features across multiple institutions.

Published
2009
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8. HNF4Aand GATA6Loss Reveals Therapeutically Actionable Subtypes in Pancreatic Cancer

Author

Brunton, Holly, Caligiuri, Giuseppina, Cunningham, Richard, Upstill-Goddard, Rosie, Bailey, Ulla-Maja, Garner, Ian M., Nourse, Craig, Dreyer, Stephan, Jones, Marc, Moran-Jones, Kim, Wright, Derek W., Paulus-Hock, Viola, Nixon, Colin, Thomson, Gemma, Jamieson, Nigel B., McGregor, Grant A., Evers, Lisa, McKay, Colin J., Gulati, Aditi, Brough, Rachel, Bajrami, Ilirjana, Pettitt, Stephen J., Dziubinski, Michele L., Barry, Simon T., Grützmann, Robert, Brown, Robert, Curry, Edward, Allison, Sarah, Biankin, Andrew V., Chang, David K., Cooke, Susanna L., Dreyer, Stephan, Grimwood, Paul, Kelly, Shane, Marshall, John, McDade, Brian, McElroy, Daniel, Ramsay, Donna, Upstill-Goddard, Rosie, Rebus, Selma, Hair, Jane, Jamieson, Nigel B., McKay, Colin J., Westwood, Paul, Williams, Nicola, Duthie, Fraser, Biankin, Andrew V., Johns, Amber L., Mawson, Amanda, Chang, David K., Scarlett, Christopher J., Brancato, Mary-Anne L., Rowe, Sarah J., Simpson, Skye H., Martyn-Smith, Mona, Thomas, Michelle T., Chantrill, Lorraine A., Chin, Venessa T., Chou, Angela, Cowley, Mark J., Humphris, Jeremy L., Mead, R. Scott, Nagrial, Adnan M., Pajic, Marina, Pettit, Jessica, Pinese, Mark, Rooman, Ilse, Wu, Jianmin, Tao, Jiang, DiPietro, Renee, Watson, Clare, Steinmann, Angela, Lee, Hong Ching, Wong, Rachel, Pinho, Andreia V., Giry-Laterriere, Marc, Daly, Roger J., Musgrove, Elizabeth A., Sutherland, Robert L., Grimmond, Sean M., Waddell, Nicola, Kassahn, Karin S., Miller, David K., Wilson, Peter J., Patch, Ann-Marie, Song, Sarah, Harliwong, Ivon, Idrisoglu, Senel, Nourbakhsh, Ehsan, Manning, Suzanne, Wani, Shivangi, Gongora, Milena, Anderson, Matthew, Holmes, Oliver, Leonard, Conrad, Taylor, Darrin, Wood, Scott, Xu, Christina, Nones, Katia, Fink, J. Lynn, Christ, Angelika, Bruxner, Tim, Cloonan, Nicole, Newell, Felicity, Pearson, John V., Quinn, Michael, Nagaraj, Shivashankar, Kazakoff, Stephen, Waddell, Nick, Krisnan, Keerthana, Quek, Kelly, Wood, David, Samra, Jaswinder S., Gill, Anthony J., Pavlakis, Nick, Guminski, Alex, Toon, Christopher, Asghari, Ray, Merrett, Neil D., Pavey, Darren, Das, Amitabha, Cosman, Peter H., Ismail, Kasim, O’Connnor, Chelsie, Lam, Vincent W., McLeod, Duncan, Pleass, Henry C., Richardson, Arthur, James, Virginia, Kench, James G., Cooper, Caroline L., Joseph, David, Sandroussi, Charbel, Crawford, Michael, Gallagher, James, Texler, Michael, Forest, Cindy, Laycock, Andrew, Epari, Krishna P., Ballal, Mo, Fletcher, David R., Mukhedkar, Sanjay, Spry, Nigel A., DeBoer, Bastiaan, Chai, Ming, Zeps, Nikolajs, Beilin, Maria, Feeney, Kynan, Nguyen, Nan Q., Ruszkiewicz, Andrew R., Worthley, Chris, Tan, Chuan P., Debrencini, Tamara, Chen, John, Brooke-Smith, Mark E., Papangelis, Virginia, Tang, Henry, Barbour, Andrew P., Clouston, Andrew D., Martin, Patrick, O’Rourke, Thomas J., Chiang, Amy, Fawcett, Jonathan W., Slater, Kellee, Yeung, Shinn, Hatzifotis, Michael, Hodgkinson, Peter, Christophi, Christopher, Nikfarjam, Mehrdad, Mountain, Angela, Eshleman, James R., Hruban, Ralph H., Maitra, Anirban, Iacobuzio-Donahue, Christine A., Schulick, Richard D., Wolfgang, Christopher L., Morgan, Richard A., Hodgin, Mary, Scarpa, Aldo, Lawlor, Rita T., Beghelli, Stefania, Corbo, Vincenzo, Scardoni, Maria, Bassi, Claudio, Tempero, Margaret A., Nourse, Craig, Jamieson, Nigel B., Graham, Janet S., Pajic, Marina, Musgrove, Elizabeth A., Petersen, Gloria M., Shanks, Emma, Ashworth, Alan, Crawford, Howard C., Simeone, Diane M., Froeling, Fieke E.M., Lord, Christopher J., Mukhopadhyay, Debabrata, Pilarsky, Christian, Grimmond, Sean E., Morton, Jennifer P., Sansom, Owen J., Chang, David K., Bailey, Peter J., and Biankin, Andrew V.

Abstract

Pancreatic ductal adenocarcinoma (PDAC) can be divided into transcriptomic subtypes with two broad lineages referred to as classical (pancreatic) and squamous. We find that these two subtypes are driven by distinct metabolic phenotypes. Loss of genes that drive endodermal lineage specification, HNF4Aand GATA6, switch metabolic profiles from classical (pancreatic) to predominantly squamous, with glycogen synthase kinase 3 beta (GSK3β) a key regulator of glycolysis. Pharmacological inhibition of GSK3β results in selective sensitivity in the squamous subtype; however, a subset of these squamous patient-derived cell lines (PDCLs) acquires rapid drug tolerance. Using chromatin accessibility maps, we demonstrate that the squamous subtype can be further classified using chromatin accessibility to predict responsiveness and tolerance to GSK3β inhibitors. Our findings demonstrate that distinct patterns of chromatin accessibility can be used to identify patient subgroups that are indistinguishable by gene expression profiles, highlighting the utility of chromatin-based biomarkers for patient selection in the treatment of PDAC.

Published
2020
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9. Hypermutation In Pancreatic Cancer.

Author

Humphris, Jeremy L., Patch, Ann-Marie, Nones, Katia, Bailey, Peter J., Johns, Amber L., McKay, Skye, Chang, David K., Miller, David K., Pajic, Marina, Kassahn, Karin S., Quinn, Michael C.J., Bruxner, Timothy J.C., Christ, Angelika N., Harliwong, Ivon, Idrisoglu, Senel, Manning, Suzanne, Nourse, Craig, Nourbakhsh, Ehsan, Stone, Andrew, and Wilson, Peter J.

Abstract

Pancreatic cancer is molecularly diverse, with few effective therapies. Increased mutation burden and defective DNA repair are associated with response to immune checkpoint inhibitors in several other cancer types. We interrogated 385 pancreatic cancer genomes to define hypermutation and its causes. Mutational signatures inferring defects in DNA repair were enriched in those with the highest mutation burdens. Mismatch repair deficiency was identified in 1% of tumors harboring different mechanisms of somatic inactivation of MLH1 and MSH2 . Defining mutation load in individual pancreatic cancers and the optimal assay for patient selection may inform clinical trial design for immunotherapy in pancreatic cancer. [ABSTRACT FROM AUTHOR]

Published
2017
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10. Corrigendum: Whole-genome landscape of pancreatic neuroendocrine tumours

Author

Scarpa, Aldo, Chang, David K., Nones, Katia, Corbo, Vincenzo, Patch, Ann-Marie, Bailey, Peter, Lawlor, Rita T., Johns, Amber L., Miller, David K., Mafficini, Andrea, Rusev, Borislav, Scardoni, Maria, Antonello, Davide, Barbi, Stefano, Sikora, Katarzyna O., Cingarlini, Sara, Vicentini, Caterina, McKay, Skye, Quinn, Michael C. J., Bruxner, Timothy J. C., Christ, Angelika N., Harliwong, Ivon, Idrisoglu, Senel, McLean, Suzanne, Nourse, Craig, Nourbakhsh, Ehsan, Wilson, Peter J., Anderson, Matthew J., Fink, J. Lynn, Newell, Felicity, Waddell, Nick, Holmes, Oliver, Kazakoff, Stephen H., Leonard, Conrad, Wood, Scott, Xu, Qinying, Hiriyur Nagaraj, Shivashankar, Amato, Eliana, Dalai, Irene, Bersani, Samantha, Cataldo, Ivana, Dei Tos, Angelo P., Capelli, Paola, Vittoria Davì, Maria, Landoni, Luca, Malpaga, Anna, Miotto, Marco, Whitehall, Vicki L. J., Leggett, Barbara A., Harris, Janelle L., Harris, Jonathan, Jones, Marc D., Humphris, Jeremy, Chantrill, Lorraine A., Chin, Venessa, Nagrial, Adnan M., Pajic, Marina, Scarlett, Christopher J., Pinho, Andreia, Rooman, Ilse, Toon, Christopher, Wu, Jianmin, Pinese, Mark, Cowley, Mark, Barbour, Andrew, Mawson, Amanda, Humphrey, Emily S., Colvin, Emily K., Chou, Angela, Lovell, Jessica A., Jamieson, Nigel B., Duthie, Fraser, Gingras, Marie-Claude, Fisher, William E., Dagg, Rebecca A., Lau, Loretta M. S., Lee, Michael, Pickett, Hilda A., Reddel, Roger R., Samra, Jaswinder S., Kench, James G., Merrett, Neil D., Epari, Krishna, Nguyen, Nam Q., Zeps, Nikolajs, Falconi, Massimo, Simbolo, Michele, Butturini, Giovanni, Van Buren, George, Partelli, Stefano, Fassan, Matteo, Khanna, Kum Kum, Gill, Anthony J., Wheeler, David A., Gibbs, Richard A., Musgrove, Elizabeth A., Bassi, Claudio, Tortora, Giampaolo, Pederzoli, Paolo, Pearson, John V., Waddell, Nicola, Biankin, Andrew V., and Grimmond, Sean M.

Abstract

This corrects the article DOI: 10.1038/nature21063

Published
2017
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11. Transient tissue priming via ROCK inhibition uncouples pancreatic cancer progression, sensitivity to chemotherapy, and metastasis

Author

Vennin, Claire, Chin, Venessa T., Warren, Sean C., Lucas, Morghan C., Herrmann, David, Magenau, Astrid, Melenec, Pauline, Walters, Stacey N., del Monte-Nieto, Gonzalo, Conway, James R. W., Nobis, Max, Allam, Amr H., McCloy, Rachael A., Currey, Nicola, Pinese, Mark, Boulghourjian, Alice, Zaratzian, Anaiis, Adam, Arne A. S., Heu, Celine, Nagrial, Adnan M., Chou, Angela, Steinmann, Angela, Drury, Alison, Froio, Danielle, Giry-Laterriere, Marc, Harris, Nathanial L. E., Phan, Tri, Jain, Rohit, Weninger, Wolfgang, McGhee, Ewan J., Whan, Renee, Johns, Amber L., Samra, Jaswinder S., Chantrill, Lorraine, Gill, Anthony J., Kohonen-Corish, Maija, Harvey, Richard P., Biankin, Andrew V., Evans, T. R. Jeffry, Anderson, Kurt I., Grey, Shane T., Ormandy, Christopher J., Gallego-Ortega, David, Wang, Yingxiao, Samuel, Michael S., Sansom, Owen J., Burgess, Andrew, Cox, Thomas R., Morton, Jennifer P., Pajic, Marina, and Timpson, Paul

Abstract

Fine-tuned manipulation of tumor tension and vasculature enhances response to chemotherapy and impairs metastatic spread in pancreatic cancer.

Published
2017
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