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Paul M. Campbell, PhD
About
Assistant Professor
The Marvin and Concetta Greenberg Pancreatic Cancer Institute
Research Program
Lab Overview
As a member of the Marvin & Concetta Greenberg Pancreatic Cancer Institute, our lab focuses on the K-Ras oncogene and its signaling in pancreatic ductal adenocarcinoma (PDAC). While K-Ras is commonly hyperactivated (by mutation or extrinsic upstream signaling) in many cancer subtypes, and activating mutations occur in approximately 95% of PDAC cases, it remains a largely intractable target pharmacologically-speaking. Although novel mutation-specific K-Ras inhibitors are currently in clinical trials, their K-Ras G12C target is infrequent (~2%) in PDAC. As such, we are investigating the signaling cascades driven by K-Ras function to illuminate potential therapeutic targets.
Education and Training
Educational Background
- Postdoctoral Fellow, University of North Carolina at Chapel Hill, Lineberger Comprehensive Cancer Center
- PhD, McGill University, Pharmacology & Therapeutics
- MSc, University of Toronto, Physiology
- BSc, University of Toronto, Pharmacology & Toxicology
Memberships
- American Association for Cancer Research
- American Society for Cell Biology
- American Society for Pharmacology and Experimental Therapeutics
Honors & Awards
- AACR Minority Scholar in Cancer Research Award
- Susan G. Komen Breast Cancer Foundation Postdoctoral Fellowship
- University of North Carolina Lineberger Comprehensive Cancer Center Clinical Translational Research Award
- McGill University Centre for Translational Research in Cancer Fellowship
- McGill University Faculty of Medicine Fellowship – Alex Dworkin Scholarship in Oncology
Research Profile
Research Program
Research Facility
Research Interests
Our research revolves around understanding how the Ras family of small GTPases impinges upon tumor invasion and metastasis, specifically in pancreatic ductal cancer. Ras is a nodal point of signaling, with input and activation from a wide range of stimuli including receptor tyrosine kinases, G protein-coupled receptors, integrins and extracellular matrix interactions, and chemokines. Once activated, Ras in turn triggers several signaling cascades that lead to a variety of transformed phenotypes including loss of cell cycle control, decreased cell death, and metastatic spread. Of particular interest to my lab is delineating how Ras activation in epithelial tumor cells drives signaling crosstalk to other compartments of the tumor microenvironment including stromal fibroblasts, macrophages, and vascular components. Paracrine signaling among these disparate cell populations likely contributes to protection of epithelial cells from cell cycle arrest, apoptosis, and senescence, as well as facilitating dedifferentiation and EMT.
At the same time that crosstalk affects the epithelial cells, there is evidence that aberrant activation of Ras leads to changes in extracellular matrix (ECM). Reorganization and dissolution of ECM by proteases and other enzymes accelerates cell migration for locoregional invasion and distal metastasis. In addition to Ras effects on the ECM architecture, we have recently shown that activation of this family of GTPases in pancreatic cancer leads to expression and secretion of CXC chemokines that is in part MAP kinase dependent. Vascular endothelial cells are sensitive to these chemokines via CXCR2 receptors, and respond by showing increased migration, invasion, and organization into vessel precursors. This angiogenesis may provide not only a means to nourish nascent tumors, but also serve as a conduit for malignant spread. As a result, we are interested in testing the hypothesis that small molecule inhibitors of the CXC-CXCR signaling axis may reduce the invasion and metastasis of pancreatic cancer and/or the expansion of already disseminated micrometastases.
Pancreatic cancer is also characterized by having an extensive stromal component. It is hypothesized that this bulk of fibroid tissue may be one of the reasons pancreatic cancer remains particularly insensitive to chemotherapeutic agents. Another arm of our research attempts to investigate whether tumor fibroblasts, like vascular endothelial cells, are responsive to CXC-CXCR crosstalk signaling triggered initially by epithelial K-Ras activation.
It is well established that mutational activation of K-Ras occurs very early in pancreatic ductal dysplasia and remains an important signaling impetus through the development of malignancy. We are investigating whether the signaling crosstalk between Ras and CXC chemokines is similarly triggered early in cancer progression by screening patient samples of initial dysplasia (pancreatic intraepithelial neoplasia, PanIN) to frank adenocarcinoma. By understanding the progression this signaling, we hope to uncover biomarkers to be used for screening and earlier detection.
Lab Description
Our research revolves around understanding how the Ras family of small GTPases impinges upon tumor invasion and metastasis, specifically in pancreatic ductal cancer. Ras is a nodal point of signaling, with input and activation from a wide range of stimuli including receptor tyrosine kinases, G protein-coupled receptors, integrins and extracellular matrix interactions, and chemokines. Once activated, Ras in turn triggers several signaling cascades that lead to a variety of transformed phenotypes including loss of cell cycle control, decreased cell death, and metastatic spread. Of particular interest to my lab is delineating how Ras activation in epithelial tumor cells drives signaling crosstalk to other compartments of the tumor microenvironment including stromal fibroblasts, macrophages, and vascular components. Paracrine signaling among these disparate cell populations likely contributes to protection of epithelial cells from cell cycle arrest, apoptosis, and senescence, as well as facilitating dedifferentiation and a hallmark of tumor progression and metastasis, epithelial-mesenchymal transition (EMT).
At the same time that crosstalk affects the epithelial cells, there is evidence that aberrant activation of Ras leads to changes in extracellular matrix (ECM). Reorganization and dissolution of ECM by proteases and other enzymes accelerates cell migration for locoregional invasion and distal metastasis. In addition to Ras effects on the ECM architecture, we have recently shown that activation of this family of GTPases in pancreatic cancer leads to expression and secretion of CXC chemokines that is in part MAP kinase-dependent. Vascular endothelial cells are sensitive to these chemokines via CXCR2 receptors, and respond by showing increased migration, invasion, and organization into vessel precursors. This angiogenesis may provide not only a means to nourish nascent tumors, but also serve as a conduit for malignant spread. As a result, we are interested in testing the hypothesis that small molecule inhibitors of the CXC-CXCR signaling axis may reduce the invasion and metastasis of pancreatic cancer and/or the expansion of already disseminated micrometastases.
Pancreatic cancer is also characterized by having an extensive stromal component. It is hypothesized that this bulk of fibroid tissue may be one of the reasons pancreatic cancer remains particularly insensitive to chemotherapeutic agents. Another arm of our research attempts to investigate whether tumor fibroblasts, like vascular endothelial cells, are responsive to CXC-CXCR crosstalk signaling triggered initially by epithelial K-Ras activation. It is well established that mutational activation of K-Ras occurs very early in pancreatic ductal dysplasia and remains an important signaling impetus through the development of malignancy. We are investigating whether the signaling crosstalk between Ras and CXC chemokines is similarly triggered early in cancer progression by screening patient samples of initial dysplasia (pancreatic intraepithelial neoplasia, PanIN) to frank adenocarcinoma. By understanding the progression this signaling, we hope to uncover biomarkers to be used for screening and earlier detection.
Finally, some of our recent work has demonstrated an interaction between K-Ras and the RNA-binding protein, HuR. Current investigations are looking at how K-Ras activation via genetic mutation influences HuR function and regulation of the cancer progression transcriptome, and in turn, how HuR governs K-Ras-dependent signaling in tumor epithelial cells.
Lab Staff
Ryan O'Rourke
Undergraduate Student, Franklin & Marshall College, 2021 Jeanne E. and Robert F. Ozols Undergraduate Summer Research Fellow
Room: W463
215-728-2219
Additional Staff
Postdoctoral Fellow
Contact Paul Campbell, PhD, to apply
There is an opening for a motivated Postdoctoral Fellow in the research laboratory of Paul Campbell, PhD, in the Cancer Signaling & Epigenetics Program at Fox Chase Cancer Center (FCCC) in Philadelphia. The lab focuses on gastrointestinal cancers, particularly pancreatic cancer, and the microenvironment signaling that drives cancer progression. We are interested in basic and translational science approaches that ultimately lead to improved therapeutics. The lab is part of the highly collaborative Marvin and Concetta Greenberg Pancreatic Cancer Institute and the associated Pancreatic Cancer Translational Group within FCCC.
The ideal candidate will be engaged in identifying novel mechanisms that promote the development of pancreatic cancer from early lesions through to metastatic disease, using fundamental mechanisms discovered in model organisms as a starting point for discovery. Familiarity with methods for manipulating gene expression and signaling in mammalian cultured cells and mouse models, as well as experience in molecular biology are desired. Please provide a brief summary of future career plans in your application.
Requirements
Applicant should have PhD in biomedical sciences or related field. This position requires considerable experience in cell and molecular biology techniques, with a strong bias towards candidates with signification cancer research experience. Excellent written and oral communication skills in English are required. Recent or soon-to-be graduates are preferred.
Education
Doctorate Degree - PhD in a Biomedical Sciences field (MD acceptable in lieu of PhD) (Required)
Experience
General experience and graduate level knowledge of key scientific concepts and cancer biology lab techniques (Required)
Download print version [PDF]
Publications
Selected Publications
A. Thadi, W.F. Morano, M. Khalili, B.B. Babcock, M.F. Shaikh, D.S. Foster, Y. Piazza, E.M. Gleeson, E. Goldstein, L. Steele, P.M. Campbell, B. Lin, M.R. Pincus, W.B. Bowne. 2021. Molecular targeting of H/MDM-2 oncoprotein in human colon cancer cells and stem-like colonic epithelial derived progenitor cells. Anticancer Res, 41:27-42. Pubmed.
Sliker B.H. and Campbell P.M. 2020. Ras and Ras Signaling as a therapeutic target in cancer. In Comprehensive Pharmacology, Terry Kenakin, Ph.D., editor, in press.
A. Thadi, E.M. Gleeson, M. Khalili, M.F. Shaikh, E. Goldstein, W.F. Morano, L.M. Daniels, N. Grandhi, H. Glatthorn, S.D. Richard, P.M. Campbell, M.R. Pincus, W.B. Bowne. 2020. Anti-cancer tumor cell necrosis of multidrug resistant ovarian cancer cell lines depends on high expression of HDM-2 protein in their membranes. Ann Clin Lab Sci, 50:611-624. Pubmed
A. Thadi, L. Lewis, E. Goldstein, A. Aggarwal, M. Khalili, L. Steele, B. Polyak, S. Seydafkan, M.H. Bluth, K.A. Ward, M. Styler, P.M. Campbell, M.R. Pincus, W.B. Bowne. 2020. Targeting Membrane HDM-2 by PNC-27 Induces Necrosis in Leukemia Cells but Not Normal Hematopoietic Cells. Anticancer Res, 40:4857-4867. Pubmed
M.C. Stout and P.M. Campbell. 2018. RASpecting the oncogene: New pathways to therapeutic advances. Biochem Pharm, 158: 217-228. Pubmed
M.C. Stout, S. Narayan, E.S. Pillet, J.S. Salvino, P.M. Campbell. 2018. Inhibition of CX3CR1 Reduces Cell Motility and Viability in Pancreatic Adenocarcinoma Epithelial Cells. Biochem Biophys Res Commun, 495:2264– 2269. PubMed
S. Lal*, E. Cheung*, M. Zarei*, R. Preet, S.N. Chand, N.C. Mambelli-Lisboa, C. Romeo, M.C. Stout, E. Londin, A. Goetz, C. Yabar, A. Nevler, C.J. Yeo, P.M. Campbell, J.M. Winter, D.A. Dixon, J.R. Brody. 2017. CRISPR knockout of the HuR gene in pancreatic and colorectal cancer cells causes a xenograft lethal phenotype. * Contributed equally. Mol Cancer Res, 15:696-707. PubMed
M.C. Stout, E. Asiimwe, J.R. Birkenstamm, S.Y. Kim, P.M. Campbell. 2014. Analyzing Ras-associated Cell Proliferation Signaling. Methods Mol Biol, 1170:393-409. PubMed
P.M. Campbell. 2014. Oncogenic Ras pushes (and pulls) cell cycle progression through ERK activation. Methods Mol Biol, 1170:155-163. PubMed
H.R. Siddique, D.J. Liao, S.K. Mishra, T. Schuster, L. Wang, B. Matter, P.M. Campbell, P. Villalta, S. Nanda, Y. Deng, M. Saleem. 2012. Epicatechin-rich cocoa polyphenol inhibits Kras-activated pancreatic ductal carcinoma cell growth in vitro and in a mouse model. Int J Cancer, 131:1720–1731. PubMed
J.J. Yeh, J.P. Madigan, P.M. Campbell, P.J. Roberts, L.M. DeGraffrenreid, C.J. Der. 2011. Targeting Ras for anti-cancer drug discovery. In Intercellular Signaling in Development and Disease, E.A. Dennis and R.A. Bradshaw, eds. Elsevier Press, pp. 335-355.
P.M. Campbell*, N. Boufaied*, J.J. Fiordalisi, A.D. Cox, P. Falardeau, C.J. Der, H. Gourdeau. 2010. TLN-4601 suppresses growth and induces apoptosis of pancreatic carcinoma cells through inhibition of Ras-MAPK signaling. J Mol Signal, 5:18. * Contributed equally PubMed
Y. Matsuo*, P.M. Campbell*, R.A. Brekken, B. Sung, M.M. Ouellette, J.B. Fleming, B.B. Aggarwal, C.J. Der, S. Guha. 2009. K-Ras promotes angiogenesis mediated by immortalized human pancreatic epithelial cells through MAP kinase signaling pathways. Mol Cancer Res, 7:799-808. * Contributed equally. PubMed
P.M. Campbell, K.M. Lee, M.M. Ouellette, H.J. Kim, A.L. Groehler, V. Khazak, C.J. Der. 2008. Ras-driven transformation of human nestin-positive pancreatic epithelial cells. Methods Enzymol 439:451-65. PubMed
P.M. Campbell, A.L. Groehler, K.M. Lee, M.M. Ouellette, V. Khazak, C.J. Der. 2007. K-Ras promotes growth transformation and invasion of immortalized human pancreatic cells by Raf and phosphatidylinositol 3-kinase signaling. Cancer Res 67:2098-2106. PubMed
Contact Information
Paul.Campbell@fccc.edu
Office Phone: 215-728-2211
Office: W463
Contact Information
Paul.Campbell@fccc.edu
Office Phone: 215-728-2211
Office: W463
Assistant Professor
The Marvin and Concetta Greenberg Pancreatic Cancer Institute
Research Program
Lab Overview
As a member of the Marvin & Concetta Greenberg Pancreatic Cancer Institute, our lab focuses on the K-Ras oncogene and its signaling in pancreatic ductal adenocarcinoma (PDAC). While K-Ras is commonly hyperactivated (by mutation or extrinsic upstream signaling) in many cancer subtypes, and activating mutations occur in approximately 95% of PDAC cases, it remains a largely intractable target pharmacologically-speaking. Although novel mutation-specific K-Ras inhibitors are currently in clinical trials, their K-Ras G12C target is infrequent (~2%) in PDAC. As such, we are investigating the signaling cascades driven by K-Ras function to illuminate potential therapeutic targets.
Education
Educational Background
- Postdoctoral Fellow, University of North Carolina at Chapel Hill, Lineberger Comprehensive Cancer Center
- PhD, McGill University, Pharmacology & Therapeutics
- MSc, University of Toronto, Physiology
- BSc, University of Toronto, Pharmacology & Toxicology
Memberships
- American Association for Cancer Research
- American Society for Cell Biology
- American Society for Pharmacology and Experimental Therapeutics
Honors & Awards
- AACR Minority Scholar in Cancer Research Award
- Susan G. Komen Breast Cancer Foundation Postdoctoral Fellowship
- University of North Carolina Lineberger Comprehensive Cancer Center Clinical Translational Research Award
- McGill University Centre for Translational Research in Cancer Fellowship
- McGill University Faculty of Medicine Fellowship – Alex Dworkin Scholarship in Oncology
Research Profile
Research Facility
Research Interests
Our research revolves around understanding how the Ras family of small GTPases impinges upon tumor invasion and metastasis, specifically in pancreatic ductal cancer. Ras is a nodal point of signaling, with input and activation from a wide range of stimuli including receptor tyrosine kinases, G protein-coupled receptors, integrins and extracellular matrix interactions, and chemokines. Once activated, Ras in turn triggers several signaling cascades that lead to a variety of transformed phenotypes including loss of cell cycle control, decreased cell death, and metastatic spread. Of particular interest to my lab is delineating how Ras activation in epithelial tumor cells drives signaling crosstalk to other compartments of the tumor microenvironment including stromal fibroblasts, macrophages, and vascular components. Paracrine signaling among these disparate cell populations likely contributes to protection of epithelial cells from cell cycle arrest, apoptosis, and senescence, as well as facilitating dedifferentiation and EMT.
At the same time that crosstalk affects the epithelial cells, there is evidence that aberrant activation of Ras leads to changes in extracellular matrix (ECM). Reorganization and dissolution of ECM by proteases and other enzymes accelerates cell migration for locoregional invasion and distal metastasis. In addition to Ras effects on the ECM architecture, we have recently shown that activation of this family of GTPases in pancreatic cancer leads to expression and secretion of CXC chemokines that is in part MAP kinase dependent. Vascular endothelial cells are sensitive to these chemokines via CXCR2 receptors, and respond by showing increased migration, invasion, and organization into vessel precursors. This angiogenesis may provide not only a means to nourish nascent tumors, but also serve as a conduit for malignant spread. As a result, we are interested in testing the hypothesis that small molecule inhibitors of the CXC-CXCR signaling axis may reduce the invasion and metastasis of pancreatic cancer and/or the expansion of already disseminated micrometastases.
Pancreatic cancer is also characterized by having an extensive stromal component. It is hypothesized that this bulk of fibroid tissue may be one of the reasons pancreatic cancer remains particularly insensitive to chemotherapeutic agents. Another arm of our research attempts to investigate whether tumor fibroblasts, like vascular endothelial cells, are responsive to CXC-CXCR crosstalk signaling triggered initially by epithelial K-Ras activation.
It is well established that mutational activation of K-Ras occurs very early in pancreatic ductal dysplasia and remains an important signaling impetus through the development of malignancy. We are investigating whether the signaling crosstalk between Ras and CXC chemokines is similarly triggered early in cancer progression by screening patient samples of initial dysplasia (pancreatic intraepithelial neoplasia, PanIN) to frank adenocarcinoma. By understanding the progression this signaling, we hope to uncover biomarkers to be used for screening and earlier detection.
Lab Description
Our research revolves around understanding how the Ras family of small GTPases impinges upon tumor invasion and metastasis, specifically in pancreatic ductal cancer. Ras is a nodal point of signaling, with input and activation from a wide range of stimuli including receptor tyrosine kinases, G protein-coupled receptors, integrins and extracellular matrix interactions, and chemokines. Once activated, Ras in turn triggers several signaling cascades that lead to a variety of transformed phenotypes including loss of cell cycle control, decreased cell death, and metastatic spread. Of particular interest to my lab is delineating how Ras activation in epithelial tumor cells drives signaling crosstalk to other compartments of the tumor microenvironment including stromal fibroblasts, macrophages, and vascular components. Paracrine signaling among these disparate cell populations likely contributes to protection of epithelial cells from cell cycle arrest, apoptosis, and senescence, as well as facilitating dedifferentiation and a hallmark of tumor progression and metastasis, epithelial-mesenchymal transition (EMT).
At the same time that crosstalk affects the epithelial cells, there is evidence that aberrant activation of Ras leads to changes in extracellular matrix (ECM). Reorganization and dissolution of ECM by proteases and other enzymes accelerates cell migration for locoregional invasion and distal metastasis. In addition to Ras effects on the ECM architecture, we have recently shown that activation of this family of GTPases in pancreatic cancer leads to expression and secretion of CXC chemokines that is in part MAP kinase-dependent. Vascular endothelial cells are sensitive to these chemokines via CXCR2 receptors, and respond by showing increased migration, invasion, and organization into vessel precursors. This angiogenesis may provide not only a means to nourish nascent tumors, but also serve as a conduit for malignant spread. As a result, we are interested in testing the hypothesis that small molecule inhibitors of the CXC-CXCR signaling axis may reduce the invasion and metastasis of pancreatic cancer and/or the expansion of already disseminated micrometastases.
Pancreatic cancer is also characterized by having an extensive stromal component. It is hypothesized that this bulk of fibroid tissue may be one of the reasons pancreatic cancer remains particularly insensitive to chemotherapeutic agents. Another arm of our research attempts to investigate whether tumor fibroblasts, like vascular endothelial cells, are responsive to CXC-CXCR crosstalk signaling triggered initially by epithelial K-Ras activation. It is well established that mutational activation of K-Ras occurs very early in pancreatic ductal dysplasia and remains an important signaling impetus through the development of malignancy. We are investigating whether the signaling crosstalk between Ras and CXC chemokines is similarly triggered early in cancer progression by screening patient samples of initial dysplasia (pancreatic intraepithelial neoplasia, PanIN) to frank adenocarcinoma. By understanding the progression this signaling, we hope to uncover biomarkers to be used for screening and earlier detection.
Finally, some of our recent work has demonstrated an interaction between K-Ras and the RNA-binding protein, HuR. Current investigations are looking at how K-Ras activation via genetic mutation influences HuR function and regulation of the cancer progression transcriptome, and in turn, how HuR governs K-Ras-dependent signaling in tumor epithelial cells.
Lab Staff
Ryan O'Rourke
Undergraduate Student, Franklin & Marshall College, 2021 Jeanne E. and Robert F. Ozols Undergraduate Summer Research Fellow
Room: W463
215-728-2219
Additional Staff
Postdoctoral Fellow
Contact Paul Campbell, PhD, to apply
There is an opening for a motivated Postdoctoral Fellow in the research laboratory of Paul Campbell, PhD, in the Cancer Signaling & Epigenetics Program at Fox Chase Cancer Center (FCCC) in Philadelphia. The lab focuses on gastrointestinal cancers, particularly pancreatic cancer, and the microenvironment signaling that drives cancer progression. We are interested in basic and translational science approaches that ultimately lead to improved therapeutics. The lab is part of the highly collaborative Marvin and Concetta Greenberg Pancreatic Cancer Institute and the associated Pancreatic Cancer Translational Group within FCCC.
The ideal candidate will be engaged in identifying novel mechanisms that promote the development of pancreatic cancer from early lesions through to metastatic disease, using fundamental mechanisms discovered in model organisms as a starting point for discovery. Familiarity with methods for manipulating gene expression and signaling in mammalian cultured cells and mouse models, as well as experience in molecular biology are desired. Please provide a brief summary of future career plans in your application.
Requirements
Applicant should have PhD in biomedical sciences or related field. This position requires considerable experience in cell and molecular biology techniques, with a strong bias towards candidates with signification cancer research experience. Excellent written and oral communication skills in English are required. Recent or soon-to-be graduates are preferred.
Education
Doctorate Degree - PhD in a Biomedical Sciences field (MD acceptable in lieu of PhD) (Required)
Experience
General experience and graduate level knowledge of key scientific concepts and cancer biology lab techniques (Required)
Download print version [PDF]
Publications
Selected Publications
A. Thadi, W.F. Morano, M. Khalili, B.B. Babcock, M.F. Shaikh, D.S. Foster, Y. Piazza, E.M. Gleeson, E. Goldstein, L. Steele, P.M. Campbell, B. Lin, M.R. Pincus, W.B. Bowne. 2021. Molecular targeting of H/MDM-2 oncoprotein in human colon cancer cells and stem-like colonic epithelial derived progenitor cells. Anticancer Res, 41:27-42. Pubmed.
Sliker B.H. and Campbell P.M. 2020. Ras and Ras Signaling as a therapeutic target in cancer. In Comprehensive Pharmacology, Terry Kenakin, Ph.D., editor, in press.
A. Thadi, E.M. Gleeson, M. Khalili, M.F. Shaikh, E. Goldstein, W.F. Morano, L.M. Daniels, N. Grandhi, H. Glatthorn, S.D. Richard, P.M. Campbell, M.R. Pincus, W.B. Bowne. 2020. Anti-cancer tumor cell necrosis of multidrug resistant ovarian cancer cell lines depends on high expression of HDM-2 protein in their membranes. Ann Clin Lab Sci, 50:611-624. Pubmed
A. Thadi, L. Lewis, E. Goldstein, A. Aggarwal, M. Khalili, L. Steele, B. Polyak, S. Seydafkan, M.H. Bluth, K.A. Ward, M. Styler, P.M. Campbell, M.R. Pincus, W.B. Bowne. 2020. Targeting Membrane HDM-2 by PNC-27 Induces Necrosis in Leukemia Cells but Not Normal Hematopoietic Cells. Anticancer Res, 40:4857-4867. Pubmed
M.C. Stout and P.M. Campbell. 2018. RASpecting the oncogene: New pathways to therapeutic advances. Biochem Pharm, 158: 217-228. Pubmed
M.C. Stout, S. Narayan, E.S. Pillet, J.S. Salvino, P.M. Campbell. 2018. Inhibition of CX3CR1 Reduces Cell Motility and Viability in Pancreatic Adenocarcinoma Epithelial Cells. Biochem Biophys Res Commun, 495:2264– 2269. PubMed
S. Lal*, E. Cheung*, M. Zarei*, R. Preet, S.N. Chand, N.C. Mambelli-Lisboa, C. Romeo, M.C. Stout, E. Londin, A. Goetz, C. Yabar, A. Nevler, C.J. Yeo, P.M. Campbell, J.M. Winter, D.A. Dixon, J.R. Brody. 2017. CRISPR knockout of the HuR gene in pancreatic and colorectal cancer cells causes a xenograft lethal phenotype. * Contributed equally. Mol Cancer Res, 15:696-707. PubMed
M.C. Stout, E. Asiimwe, J.R. Birkenstamm, S.Y. Kim, P.M. Campbell. 2014. Analyzing Ras-associated Cell Proliferation Signaling. Methods Mol Biol, 1170:393-409. PubMed
P.M. Campbell. 2014. Oncogenic Ras pushes (and pulls) cell cycle progression through ERK activation. Methods Mol Biol, 1170:155-163. PubMed
H.R. Siddique, D.J. Liao, S.K. Mishra, T. Schuster, L. Wang, B. Matter, P.M. Campbell, P. Villalta, S. Nanda, Y. Deng, M. Saleem. 2012. Epicatechin-rich cocoa polyphenol inhibits Kras-activated pancreatic ductal carcinoma cell growth in vitro and in a mouse model. Int J Cancer, 131:1720–1731. PubMed
J.J. Yeh, J.P. Madigan, P.M. Campbell, P.J. Roberts, L.M. DeGraffrenreid, C.J. Der. 2011. Targeting Ras for anti-cancer drug discovery. In Intercellular Signaling in Development and Disease, E.A. Dennis and R.A. Bradshaw, eds. Elsevier Press, pp. 335-355.
P.M. Campbell*, N. Boufaied*, J.J. Fiordalisi, A.D. Cox, P. Falardeau, C.J. Der, H. Gourdeau. 2010. TLN-4601 suppresses growth and induces apoptosis of pancreatic carcinoma cells through inhibition of Ras-MAPK signaling. J Mol Signal, 5:18. * Contributed equally PubMed
Y. Matsuo*, P.M. Campbell*, R.A. Brekken, B. Sung, M.M. Ouellette, J.B. Fleming, B.B. Aggarwal, C.J. Der, S. Guha. 2009. K-Ras promotes angiogenesis mediated by immortalized human pancreatic epithelial cells through MAP kinase signaling pathways. Mol Cancer Res, 7:799-808. * Contributed equally. PubMed
P.M. Campbell, K.M. Lee, M.M. Ouellette, H.J. Kim, A.L. Groehler, V. Khazak, C.J. Der. 2008. Ras-driven transformation of human nestin-positive pancreatic epithelial cells. Methods Enzymol 439:451-65. PubMed
P.M. Campbell, A.L. Groehler, K.M. Lee, M.M. Ouellette, V. Khazak, C.J. Der. 2007. K-Ras promotes growth transformation and invasion of immortalized human pancreatic cells by Raf and phosphatidylinositol 3-kinase signaling. Cancer Res 67:2098-2106. PubMed
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