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Department of Medicine

Department of Medicine

  Division of Hematology/Oncology

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photo Timothy F. Burns, MD, PhD

Assistant Professor of Medicine

Department of Medicine

Division of Hematology/Oncology

University of Pittsburgh Cancer Institute

Email: burnstf@upmc.edu

Phone: 412-623-7770

Contact
Office: Hillman Cancer Center Research Pavilion,
5117 Centre Avenue, Office: Suite 2.18e Lab: 2.7
Pittsburgh, PA 15213
 
Phone: 412-623-7770
Fax: 412-623-7798
E-mail: burnstf@upmc.edu
Administrative Assistant:
Carmella Campbell
Address: Hillman Cancer Center Research Pavilion
Room 2.18
Pittsburgh, PA 15213
Email: campbellcm@upmc.edu
Phone: 412-623-7770
Fax: 412-623-7768
Education and Training
Education
BS with Honors, Cornell University, 1996
M.D./Ph.D., University of Pennsylvania, 2005
Training
Osler Medical Residency, Johns Hopkins Hospital, 2008
Fellowship in Medical Oncology, Johns Hopkins Hospital, 2012
Research Interest
My research and clinical interests revolve around the development of targeted therapies for KRAS-mutant NSCLC. My laboratory has two main areas of focus that both center on the eventually development of therapies of KRAS-mutant NSCLC. The first line of research is on the role of the transcription factor TWIST1 in oncogene-driven NSCLC. We have demonstrated the TWIST1 is essential in several for lung tumorigenesis for several key oncogenic drivers including mutant KRAS. We are currently working on defining the mechanisms through which targeting TWIST1 leads to oncogene-induced senescence and apoptosis both in vitro and in vivo. Furthermore, we are interested in studying the prognostic significance of TWIST1 overexpression in mutationally defined patient samples and developing inhibitors of TWIST1 that we can translate to the clinic. The second line of research in my lab focuses on studying the mechanisms of resistance to the Hsp90 inhibitor, ganetespib, in KRAS-mutant NSCLC in the laboratory while in parallel developing a Phase I/II trial of the combination of an MTOR inhibitor and ganetespib in patients with advanced KRAS-mutant lung adenocarcinoma. These preclinical studies will inform the biomarker analysis of patient samples to be collected during our trial.
Clinical Interest
Lung cancer is the leading cause of cancer death in the United States and worldwide. Recent advances in the treatment of NSCLC have come from recognition that NSCLC is not a single disease entity, but rather a collection of distinct molecularly driven neoplasms. This paradigm is typified by the recent progress made in the treatment of patients with EGFR-mutant and EML4-ALK translocation-driven adenocarcinomas of the lung with tyrosine kinase inhibitors targeting these oncogenes. Unfortunately, little progress has been made in the treatment of patients with the most frequently observed driver oncogene, mutant KRAS. KRAS is mutated in approximately 25% of all NSCLC, and patients with this mutation have an increased risk of recurrence in early stage disease and have a worse prognosis with metastatic disease.
Publications
For my complete bibliography, Click Here.
Selected Publications:
Chatterjee S, Bhattacharya S, ocinski MA, Burns TF. HSP90 inhibitors in lung cancer: promise still unfulfilled. H & O Journal Hematology & Oncology. 2016; 14(5): 346-56.
Bhattachary S, Socinski MA, Burns TF. KRAS mutant lung cancer: progress thus far on an elusive therapeutic target. Clinical and translational medicine. 2015; 4(1): 35.
Gajula RP, Chettiar ST, Williams RD, Nugent K, Kato Y, Wang H, Malek R, Taparra K, Cades J, Annadanam A, Yoon AR, Fertig E, Firulli BA, Mazzacurati L, Burns TF, Firulli AB, An SS, Tran PT. Structure-function studies of the bHLH phosphorylation domain of TWIST1 in prostate cancer cells. Neoplasia. 2015; 17(1): 16-31.
Somasundaram A, Socinski MA, Burns TF. Personalized treatment of EGFR mutant and ALK-positive patients in NSCLC. Expert opinion on pharmacotherapy. 2014; 15(18): 2693-708.
Burns TF, Dobromilskaya I, Murphy SC, Gajula RP, Thiyagarajan S, Chatley SN, Aziz K, Cho YJ, Tran PT, Rudin CM. Inhibition of TWIST1 leads to activation of oncogene-induced senescence in oncogene-driven non-small cell lung cancer. Molecular cancer research. 2013; 11(4): 329-38.
Tran PT, Shroff EH, Burns TF, Thiyagarajan S, Das ST, Zabuawala T, Chen J, Cho YJ, Luong R, Tamayo P, Salih T, Aziz K, Adam SJ, Vicent S, Nielsen CH, Withofs N, Sweet-Cordero A, Gambhir SS, Rudin CM, Felsher DW. Twist1 suppresses senescence programs and thereby accelerates and maintains mutant Kras-induced lung tumorigenesis. Plos genetics. 2012; 8(5): 31002650.
Burns TF, Fei P, Scata KA, Dicker DT, El-Deiry WS. Silencing of the novel p53 target gene Snk/Plk2 leads to mitotic catastrophe in paclitaxel (taxol)-exposed cells. Molecular and cellular biology. 2003; 23(16): 5556-71.
Burns TF, El-Deiry WA. Identification of inhibitors of TRAIL-induced death (ITIDs) in the TRAIL-sensitive colon carcinoma cell line SW480 using a genetic approach. The Journal of biological chemistry. 2001; 276 (41): 37879-86.
Burns TF, Bernhard EJ, El-Deiry WS. Tissue specific expression of p53 target genes suggests a key role for KILLER/DR5 in p53-dependent apoptosis in vivo. Oncogene. 2001; 20(34): 4601-12.
Wu GS, Burns TF, McDonald ER 3rd, Jiang W, Meng R, Krantz ID, Kao G, Gan DD, Zhou JY, Muschel R. KILLER/DR5 is a DNA damage-inducible p53-regulated death receptor gene. Nature genetics. 1997; 17(2): 141-3.
Notable Achievements
Young Investigators Award, ASCO, 2010
Merit Award, IASCL 11th annual Targeted Therapies for the Treatment of Lung Cancer Meeting, 2010
Merit Award, ASCO Annual Meeting, 2011
Scholar in Training Award, AACR Annual Meeting, 2012
Scholar Award, V Foundation, 2013
Junior Faculty, University of Pittsburgh School of Medicine Research Day Award, 2014; 2015
Sidney Kimmel Foundation for Cancer Reseach Kimmel Scholar Award, 2015
Doris Duke Clinical Scientist Development Award, 2016
ASCI Young Physician-Scientist Award, 2016