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Pathology

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Faculty

Mark Jackson

Mark Jackson

Associate Professor
Director, Cancer Biology Training Program, Department of Pathology
Associate Director of Cancer Training and Education, Case Comprehensive Cancer Center

mark.w.jackson@case.edu (216) 368-1276 (o) (216) 368-8919 (f)

Mark W. Jackson joined the Department of Pathology and the Case Comprehensive Cancer Center in the fall of 2007. He received a Bachelor’s degree from Kent State University in 1996, and a Ph.D. from Wright State University (Boonshoft School of Medicine) in 2001. After completing his Ph.D., Dr. Jackson joined the lab of Dr. George Stark in the Molecular Genetics Department at the Cleveland Clinic for as a postdoctoral fellow. In addition to the research described below, Dr. Jackson is actively involved in training our next generation of cancer researchers, serving as the Director of the Cancer Biology Training Program, Director of this Cancer Biology Training Grant (T32), and the Associate Director of Training and Education in the Case Comprehensive Cancer Center. Nationally, he serves on the board of the Cancer Biology Training Consortium (CABTRAC).

Research summary

The Jackson laboratory focuses on genetic events that contribute to epithelial cell transformation. We have developed a breast cancer model that starts with normal human mammary epithelial cells (HMECs), and utilizes four genetic alterations associated with breast cancer, including inactivation of two tumor suppressors, p16INK4a and p53, and elevated expression of MYC and oncogenic HER2 or RAS. The resulting cells grow anchorage-independently, and possess hallmarks associated with cancer cells. Using this model we can interrogate the contribution of breast specific tumor-suppressive signaling and define how oncogene activation dismantles these suppressive signals to drive transformation and cancer progression. Two major focus areas include:

  • The identification of novel transforming genetic elements.  We have developed a set of insertional mutagenesis lentiviral vectors (VBIM, validation-based insertional mutagenesis). The VBIM strategy has been extremely successful at identifying novel proteins that regulate cancer cell signaling pathways, including NFĸB, EGFR, MAPK and PI3K/AKT as well as proteins that confer resistance to paclitaxel, quinacrine, or Erlotinib. By merging HMEC transformation models with a VBIM forward genetic screens, we recently identified FAM83B based on its ability to substitute for RAS in the transformation of human mammary epithelial cells (HMECs). Interestingly, FAM83B is one of eight members of a protein family (FAM83). We have studied the oncogenic role of five FAM83 members thus far, in a variety of cancers. Our findings suggest that the FAM83 proteins constitute a novel oncogene family that provides vital new targets for therapeutic intervention that may significantly impact an oncologist's ability to treat cancer. We continue to refine the VBIM strategy, and continue searching for novel effectors important in cancer biology.
  • The influence of tumor microenvironmental factors in cancer progression. We seek to define the contribution of cytokines to both the transformation process, epithelial-mesenchymal plasticity, and the acquisition of cancer stem cell (CSC) properties. We have determined that cross-talk between the IL-6 family cytokine Oncostatin M (OSM), the TGFβ/BMP family, and Interferon signaling cascades can regulate the plasticity of transformed cells that drive metastasis and chemotherapy resistance.

For a complete list, see:

http://www.ncbi.nlm.nih.gov/myncbi/browse/collection/43395421/?sort=date&direction=descending

  • FAM83 proteins: Fostering new interactions to drive oncogenic signaling and therapeutic resistance. Bartel CA, Parameswaran N, Cipriano R, Jackson MW. Oncotarget. 2016. PMID:27221039
  • Cancer Stem Cell Plasticity Drives Therapeutic Resistance. Doherty MR, Smigiel JM, Junk DJ, Jackson MW. Cancers. 2016; 8(1). PMID: 26742077; PMCID: PMC4728455
  • Conserved Oncogenic Behavior of the FAM83 Family Regulates MAPK Signaling in Human Cancer. Cipriano R, Miskimen KL, Bryson BL, Foy CR, Bartel CA, Jackson MW. Mol Cancer Res. 2014 Apr 15. PMID: 24736947; PMCID: PMC4135001.
  • Junk DJ, Bryson BL, Jackson MW. HiJAK'd Signaling; the STAT3 Paradox in Senescence and Cancer Progression. Cancers. 2014 Mar 26;6(2):741-55. PMID: 24675570; PMCID: PMC4074801.
  • Junk DJ, Cipriano R, Bryson BL, Gilmore HL, Jackson MW. Tumor Microenvironmental Signaling Elicits Epithelial-Mesenchymal Plasticity through Cooperation with Transforming Genetic Events. Neoplasia. 2013 Sep;15 (9):1100-9. PMID: 24027434; PMCID: PMC3769888.
    • Featured in Cancer Stem Cell News and Mammary Cell News
  • Cipriano R, Bryson BL, Miskimen KL, Bartel CA, Hernandez-Sanchez W, Bruntz RC, Scott SA, Lindsley CW, Brown HA, Jackson MW. Hyperactivation of EGFR and downstream effector phospholipase D1 by oncogenic FAM83B. Oncogene. 2013 Aug 5. PMID: 23912460;PMCID: PMC3923847 
  • Cipriano R, Miskimen KL, Bryson BL, Foy CR, Bartel CA, Jackson MW. FAM83B-mediated activation of PI3K/AKT and MAPK signaling cooperates to promote epithelial cell transformation and resistance to targeted therapies. Oncotarget. 2013 May;4(5):729-38. PMID: 23676467; PMCID: PMC3742833
  • Cipriano R, Graham J, Miskimen KL, Bryson BL, Bruntz RC, Scott SA, Brown HA, Stark GR, and Jackson MW. FAM83B mediates EGFR- and RAS-driven oncogenic transformation. J Clin Invest. 2012 Sep 4;122(9):3197-210 PMID: 22886302; PMCID: PMC3428078
    • Featured in a Commentary by Steven Grant "FAM83A and FAM83B: candidate oncogenes and TKI resistance mediators". J Clin Invest. 2012, Aug 13
    • Write-up in Cancer Discovery titled "FAM83 Proteins Promote Tumorigenesis and Drug Resistance". Cancer Discov. 2012 Oct; 2(10)
    • Featured as the Top Story, Mammary Cell News 3.39, August 16th, 2012.
  • Kan CE, Cipriano R, and Jackson MW. c-MYC Functions as a Molecular Switch to Alter the Response of Human Mammary Epithelial Cells to Oncostatin M. Cancer Res. 2011 Nov 8. PMID: 21975934; PMCID: PMC4116142.
    • Featured as the Top Story, Mammary Cell News 3.39, October 6, 2011.
  • Cipriano R and Jackson MW. Delineating oncogene/tumor suppressor interactions in human mammary epithelial cells. Cell Cycle. 2011 Aug 15;10(16). PMID: 21785262.
  • Cipriano R, Kan CE, Graham J, Danielpour D, Stampfer M, Jackson MW. TGF-β signaling engages an ATM-CHK2-p53-independent RAS-induced senescence and prevents malignant transformation in human mammary epithelial cells. Proc Natl Acad Sci U S A. 2011 May 24;108(21):8668-73. PMID: 21555587; PMCID: PMC3102347
  • Lu T*, Jackson MW*, Singhi AD* (* equal contributing author), Kandel ES, Yang M, Zhang Y, Gudkov AV, Stark GR. Validation-based insertional mutagenesis identifies lysine demethylase FBXL11 as a negative regulator of NFkappaB. Proc Natl Acad Sci U S A. 2009 Sep 22;106(38):16339-44. PMID: 19805303; PMCID: PMC2736141.
  • De S, Cipriano R, Jackson MW, Stark GR. Overexpression of kinesins mediates docetaxel resistance in breast cancer cells. Cancer Res. 2009 Oct 15;69(20):8035-42. PMID: 19789344.