Michael B. Dwinell, PhD

Professor; Founding Director, Center for Immunology; Director, Bobbie Nick Voss Laboratory for Colon Cancer Research; Leader, Molecular Cancer Therapeutics

Locations

Microbiology & Immunology
BSB 208

Contact Information

General Interests

Inflammation and Immunology, Cancer Biology

Education

PhD, GI Pathophysiology, University of Wisconsin, Madison, 1996

Research Experience

Carcinoma
Chemokines
Defensins
Immunity, Mucosal
Neoplasm Metastasis
Receptors, Chemokine
Receptors, CXCR4
Wound Healing

Research Interests

dwinell-lab

Dwinell Laboratory: Bobbie Nick Voss Laboratory for Colon Cancer Research

Research in the Dwinell laboratory seeks to define the role for extracellular mediators in the progression and metastasis of solid and hematological cancers. Additional studies are examining the role for metabolic reprogramming to influence tumor progression and exploring new mitochondria-targeted compounds as inhibitors of cancer progression. Human and murine 2D and 3D cell culture systems and preclinical models are being used to investigate the cellular, biochemical, and metabolic signaling pathways that regulate cellular proliferation, programmed cell death and motility in inflammation and cancer. Pharmacokinetic / pharmacodynamics, toxicity and potency / efficacy studies following treatment with small molecule or biologic compounds are also being completed. These translational research studies are multidisciplinary and include molecular cloning, cell culture, biochemical assays and signal processing, histopathology, flow cytometry, and small animal imaging and handling. Completion of these studies will strengthen our identification of new targets for therapeutic intervention to improve human health.to improve human health. There are currently two major research directions in the laboratory.

Research in the Dwinell laboratory is supported through grants from the National Institutes of Health, the Medical College of Wisconsin Cancer Center and philanthropic donations.

STING agonist inflames the pancreatic cancer immune microenvironment and reduces tumor burden in mouse models.

(Jing W, McAllister D, Vonderhaar EP, Palen K, Riese MJ, Gershan J, Johnson BD, Dwinell MB.) J Immunother Cancer. 2019 Apr 29;7(1):115.
A Serum-Induced Transcriptome and Serum Cytokine Signature Obtained at Diagnosis Correlates with the Development of Early Pancreatic Ductal Adenocarcinoma Metastasis.

(Tsai S, McOlash L, Jia S, Zhang J, Simpson P, Kaldunski ML, Aldakkak M, Grewal J, Palen K, Dwinell MB, Johnson BD, Mackinnon A, Hessner MJ, Gershan JA.) Cancer Epidemiol Biomarkers Prev. 2019 Apr;28(4):680-689.
Mitochondria-targeted drugs stimulate mitophagy and abrogate colon cancer cell proliferation.

(Boyle KA, Van Wickle J, Hill RB, Marchese A, Kalyanaraman B, Dwinell MB.) J Biol Chem. 2018 09 21;293(38):14891-14904.
Corrigendum to 'A review of the basics of mitochondrial bioenergetics, metabolism, and related signaling pathways in cancer cells: Therapeutic targeting of tumor mitochondria with lipophilic cationic compounds' [REDOX 14C (2017) 316-327].

(Kalyanaraman B, Cheng G, Hardy M, Ouari O, Lopez M, Joseph J, Zielonka J, Dwinell MB.) Redox Biol. 2018 06;16:426-427.
Diacylglycerol kinase ζ (DGKζ) and Casitas b-lineage proto-oncogene b-deficient mice have similar functional outcomes in T cells but DGKζ-deficient mice have increased T cell activation and tumor clearance.

(Wesley EM, Xin G, McAllister D, Malarkannan S, Newman DK, Dwinell MB, Cui W, Johnson BD, Riese MJ.) Immunohorizons. 2018 Apr 01;2(4):107-118.
A review of the basics of mitochondrial bioenergetics, metabolism, and related signaling pathways in cancer cells: Therapeutic targeting of tumor mitochondria with lipophilic cationic compounds.

(Kalyanaraman B, Cheng G, Hardy M, Ouari O, Lopez M, Joseph J, Zielonka J, Dwinell MB.) Redox Biol. 2018 04;14:316-327.
Development of primary human pancreatic cancer organoids, matched stromal and immune cells and 3D tumor microenvironment models.

(Tsai S, McOlash L, Palen K, Johnson B, Duris C, Yang Q, Dwinell MB, Hunt B, Evans DB, Gershan J, James MA.) BMC Cancer. 2018 03 27;18(1):335.
GEMMs Are a Gem When it Comes to Defining the Role of HIF2α in Mucinous Cystic Neoplasms.

(Boyle KA, Dwinell MB.) Cell Mol Gastroenterol Hepatol. 2018;5(2):165-166.
Modified Metformin as a More Potent Anticancer Drug: Mitochondrial Inhibition, Redox Signaling, Antiproliferative Effects and Future EPR Studies.

(Kalyanaraman B, Cheng G, Hardy M, Ouari O, Sikora A, Zielonka J, Dwinell MB.) Cell Biochem Biophys. 2017 Dec;75(3-4):311-317.
Differences in Sulfotyrosine Binding amongst CXCR1 and CXCR2 Chemokine Ligands.

(Moussouras NA, Getschman AE, Lackner ER, Veldkamp CT, Dwinell MB, Volkman BF.) Int J Mol Sci. 2017 Sep 03;18(9).
CCR7 Sulfotyrosine Enhances CCL21 Binding.

(Phillips AJ, Taleski D, Koplinski CA, Getschman AE, Moussouras NA, Richard AM, Peterson FC, Dwinell MB, Volkman BF, Payne RJ, Veldkamp CT.) Int J Mol Sci. 2017 Aug 25;18(9).
Mitochondria-targeted metformins: anti-tumour and redox signalling mechanisms.

(Kalyanaraman B, Cheng G, Hardy M, Ouari O, Sikora A, Zielonka J, Dwinell M.) Interface Focus. 2017 Apr 06;7(2):20160109.

Michael B. Dwinell, PhD