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Paul M. Campbell, PhD

Paul Campbell, PhD
About

Research Program


Research Technician, Full-Time
Contact Paul Campbell, PhD, to apply

A full time research technician position is available in a cancer biology laboratory in the Cancer Biology Program at Fox Chase Cancer Center. The research focus for the lab is to understand the molecular mechanisms of cancer with a particular emphasis on invasion, metastasis, and the tumor microenvironment.

Qualifications

Bachelor’s degree in a basic medical science discipline (physiology, biochemistry, molecular biology etc.) or biology and at least 1 year of experience working in a research laboratory is required.

Experience in basic mammalian cell culture (maintenance of cell lines, transfection, generation of stable cell lines), basic molecular biology techniques (transformation, gene subcloning, DNA mini- and maxi-preps, PCR), and basic biochemistry techniques (SDS-PAGE, western blots, immunoprecipitation, immunohistochemistry) is strongly preferred.
Excellent communication skills (verbal and written) and interpersonal skills are required.
Excellent organizational skills required: ability to multitask will be essential in this position.

Responsibilities

The successful candidate will conduct, under supervision of the principal investigator, experiments in signaling biology, biochemistry, and molecular pharmacology aimed at understanding the molecular mechanisms of action of cancer invasion with a goal of discovering and validating new therapeutic targets and biomarkers.

In addition, the successful candidate will be responsible for ordering and organizing laboratory supplies, maintaining equipment, cataloging reagents, and other organizational tasks.
It is expected that the individual will present his/her research findings internally as well as local and national conferences.
Download print version [PDF]

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.

Ras activates multiple downstream effector pathways

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.

Tumor Microenvironment

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.


Research Technician, Full-Time
Contact Paul Campbell, PhD, to apply

A full time research technician position is available in a cancer biology laboratory in the Cancer Biology Program at Fox Chase Cancer Center. The research focus for the lab is to understand the molecular mechanisms of cancer with a particular emphasis on invasion, metastasis, and the tumor microenvironment.

Qualifications

Bachelor’s degree in a basic medical science discipline (physiology, biochemistry, molecular biology etc.) or biology and at least 1 year of experience working in a research laboratory is required.

Experience in basic mammalian cell culture (maintenance of cell lines, transfection, generation of stable cell lines), basic molecular biology techniques (transformation, gene subcloning, DNA mini- and maxi-preps, PCR), and basic biochemistry techniques (SDS-PAGE, western blots, immunoprecipitation, immunohistochemistry) is strongly preferred.
Excellent communication skills (verbal and written) and interpersonal skills are required.
Excellent organizational skills required: ability to multitask will be essential in this position.

Responsibilities

The successful candidate will conduct, under supervision of the principal investigator, experiments in signaling biology, biochemistry, and molecular pharmacology aimed at understanding the molecular mechanisms of action of cancer invasion with a goal of discovering and validating new therapeutic targets and biomarkers.

In addition, the successful candidate will be responsible for ordering and organizing laboratory supplies, maintaining equipment, cataloging reagents, and other organizational tasks.
It is expected that the individual will present his/her research findings internally as well as local and national conferences.
Download print version [PDF]

Lab Staff

Matthew Stout

PhD candidate

Room: W463
215.728.2219

Bailee Sliker, PhD

Postdoctoral Fellow

Room: W463
215.728.2219

Julia Bacon-Henderson

Undergraduate Student, Chestnut Hill College

Room: W463
215.728.2219

Sofia Neaher

Jeanne E. and Robert F. Ozols Undergraduate Summer Research Fellow, Williams College

Room: W463
215.728.2219

Additional Staff

Research Technician, Full-Time
Contact Paul Campbell, PhD, to apply

A full time research technician position is available in a cancer biology laboratory in the Cancer Biology Program at Fox Chase Cancer Center. The research focus for the lab is to understand the molecular mechanisms of cancer with a particular emphasis on invasion, metastasis, and the tumor microenvironment.

Qualifications

Bachelor’s degree in a basic medical science discipline (physiology, biochemistry, molecular biology etc.) or biology and at least 1 year of experience working in a research laboratory is required.

Experience in basic mammalian cell culture (maintenance of cell lines, transfection, generation of stable cell lines), basic molecular biology techniques (transformation, gene subcloning, DNA mini- and maxi-preps, PCR), and basic biochemistry techniques (SDS-PAGE, western blots, immunoprecipitation, immunohistochemistry) is strongly preferred.
Excellent communication skills (verbal and written) and interpersonal skills are required.
Excellent organizational skills required: ability to multitask will be essential in this position.

Responsibilities

The successful candidate will conduct, under supervision of the principal investigator, experiments in signaling biology, biochemistry, and molecular pharmacology aimed at understanding the molecular mechanisms of action of cancer invasion with a goal of discovering and validating new therapeutic targets and biomarkers.

In addition, the successful candidate will be responsible for ordering and organizing laboratory supplies, maintaining equipment, cataloging reagents, and other organizational tasks.
It is expected that the individual will present his/her research findings internally as well as local and national conferences.
Download print version [PDF]

Publications

Selected Publications

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

This Fox Chase professor participates in the Undergraduate Summer Research Fellowship
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