Timothy S Pardee, M.D.

Molecular and Cellular Biosciences at Wake Forest University


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Timothy S Pardee, M.D.

Timothy S Pardee, M.D.
  • E-mail:
  • Phone Number: (336) 716-5847
  • Department: Internal Medicine - Hematology/Oncology

Assistant Professor, Hematology & Oncology
Cancer Biology

Clinical Specialties

Acute Leukemias, Chronic Leukemias, Myelodysplastic Syndromes, Hematologic Malignancies

 
Education & Training
  • M.D., University of Buffalo – SUNY , 2003
  • Ph.D., University of Buffalo – SUNY , 1999
  • Residency, Internal Medicine, Massachusetts Gen Hosp, 2005
  • Fellowship, Hematology And Oncology, Stony Brook School of Medicine, 2009

Board Certifications

  • American Board of Internal Medicine

 

Puthiyaveetil AG, Reilly CM, Pardee TS, Caudell DL. Non-homologous end joining mediated DNA repair is impaired in the NUP98-HOXD13 mouse model for myelodysplastic syndrome. Leuk Res. 2013;37(1):112-116.

 

 

Cook GJ, Pardee TS. Animal models of leukemia: any closer to the real thing?. Cancer Metastasis Rev. 2013;32(1-2):63-76.

 

Klepin HD, Geiger AM, Tooze JA, Kritchevsky SB, Williamson JD, Pardee TS, Ellis LR, Powell BL. Geriatric assessment predicts survival for older adults receiving induction chemotherapy for acute myelogenous leukemia. Blood. 2013;121(21):4287-4294.

 

Manny JS, Pardee T, Pettenati M, Pang CS. Near-tetraploid/tetraploid acute myeloid leukemia: morphologic, cytogenetic, and prognostic features [abstract]. Mod Pathol. 2012;25(Suppl 2):354A.

 

Pardee TS, Gomes E, Jennings-Gee J, Caudell D, Gmeiner WH. Unique dual targeting of thymidylate synthase and topoisomerase1 by FdUMP[10] results in high efficacy against AML and low toxicity. Blood. 2012;119(15):3561-3570.

 

 

Cook GJ, Caudell DL, Elford HL, Pardee T. The novel ribonucleotide reductase inhibitor didox is active against AML with limited toxicities [abstract]. Blood. 2012;120(21):Abstr 1513.

 

Pardee TS, Zuber J, Lowe SW. Flt3-ITD alters chemotherapy response in vitro and in vivo in a p53-dependent manner. Exp Hematol. 2011;39(4):473-485.

 

Klepin HD, Geiger AM, Tooze JA, Kritchevsky SB, Williamson JD, Ellis LR, Levitan D, Pardee TS, Isom S, Powell BL. The feasibility of inpatient geriatric assessment for older adults receiving induction chemotherapy for acute myelogenous leukemia. J Am Geriatr Soc. 2011;59(10):1837-1846.

 

Cook GJ, Elford HL, Pardee T. Activity of the novel ribonucleotide reductase inhibitor didox on human and murine models of acute leukemia [abstract]. Blood. 2011;118(21):1553-1554.

 

Pardee T, Gomes E, Jennings-Gee J, Caudell DL, Gmeiner W. Unique dual targeting of thymidylate synthase and topoisomerase1 by FdUMP10 results in high efficacy against AML and low toxicity [abstract]. Blood. 2011;118(21):1109-1110.

 

Pardee T, DeFord-Watts LM, Peronto E, Levitan DA, Hurd DD, Kridel S. Altered lipid and mitochondrial metabolism are viable targets in acute leukemia [abstract]. Blood. 2011;118(21):1546.

 

Pardee T. Over expression of MN1 accelerates leukemia onset and confers resistance to chemotherapy by suppression of p53 and Bim [abstract]. Blood. 2011;118(21):1070.

 

Chiou V, Tiegs J, Isom S, Pettenati MJ, Lyerly S, Ellis LR, Pardee T, Dmitriy B, Powell BL, Levitan DA. A single institution analysis of incidence of recurrent chromosomal abnormalities in adult ALL patients according to race, gender, and age [abstract]. Blood. 2011;118(21):4869.

 

Klepin HD, Tooze JA, Geiger AM, Kritchevsky S, Williamson J, Ellis LR, Levitan D, Pardee T, Isom S, Powell BL. Geriatric assessment predicts overall survival among older adults receiving induction chemotherapy for acute myelogenous leukemia [abstract]. Blood. 2010;116(21):653-654.

 

Pardee T, Mascenik T, Bolemon BH, Cook GJ. Over expression of MN1 confers resistance to chemotherapy in vitro and in vivo [abstract]. Blood. 2010;116(21):427.

 

Pardee T, Gomes E, Jennings-Gee J, Caudell DL, Gmeiner W. The novel fluoropyrimidine FdUMP[10] is highly active against acute myeloid leukemia [abstract]. Blood. 2010;116(21):1353.

 

Pardee T, Zuber J, Lowe S. The FLT3 ITD accelerates an already established myeloid leukemia and alters chemotherapy response in vitro and in vivo in a p53 dependent manner [abstract]. Blood. 2009;114(22):685.

 

My lab is focused on developing a better understanding of Acute Myeloid Leukemia (AML). AML is an aggressive malignancy of the bone marrow where the white blood cells that usually protect us from infections become cancerous, leading to bone marrow failure and death. This cancer is characterized by a high relapse rate and resistance to chemotherapy. It has long been known that different genetic changes present in the leukemia cells can predict how well they will respond to therapy and how likely a patient is to achieve a lasting remission. This information is currently used to provide prognosis and direct therapy however, the mechanisms of how these genetic changes influence the way the cells respond to chemotherapy are not well understood.

To address these questions we utilize several mouse models of AML that incorporate genetic changes found in the human disease. One model uses a fusion protein found in good risk AML (AML-ETO9a) and the other a fusion from poor risk AML (MLL-ENL). These models accurately recapitulate the pathology of the disease and more importantly when mice are treated with the same chemotherapy regimes as patients the outcomes are similar. These models are based on the infection of hematopoetic stem cells with retroviruses that can be engineered to express any gene of interest. In this way different genes implicated in altering prognosis for AML patients can be incorporated into these models and their effects on chemotherapy response can be assessed.

We are currently using these models to assess how common genetic changes seen in AML effect disease onset and response to chemotherapy. The ultimate goal of this work is to better understand the mechanisms of resistance in AML and to design strategies to reverse it. Any promising findings can then be used to inform clinical trials and improve care for patients who suffer from this devastating disease.