Faculty
Martin Peter Carroll, MD
Associate Professor of Medicine (Hematology-Oncology)
Department: Medicine
Graduate Group Affiliations
Contact information
Room 715, BRB II/III
421 Curie Blvd.
Philadelphia, PA 19104
421 Curie Blvd.
Philadelphia, PA 19104
Office: (215) 573-5217
Fax: (215) 573-7049
Fax: (215) 573-7049
Email:
carroll2@mail.med.upenn.edu
carroll2@mail.med.upenn.edu
Publications
Education
A.B. (English and American Literature)
Harvard College, Cambridge, MA, 1982.
M.D. (Medicine)
Dartmouth Medical School, Hanover, NH, 1988.
Permanent linkA.B. (English and American Literature)
Harvard College, Cambridge, MA, 1982.
M.D. (Medicine)
Dartmouth Medical School, Hanover, NH, 1988.
Description of Research Expertise
Research InterestsMolecular biology of leukemia
Key words: Leukemia, BCR/ABL, signal transduction, PI3 kinase.
Description of Research
My laboratory is broadly interested in the molecular biology of leukemia. There are two active areas of research in the laboratory. The first project focused on acute myeloid leukemia (AML). AML has been hypothesized to arise from a combination of oncogenic translocations that disrupt cellular disruption and dysregulation of cellular growth regulatory mechanisms. Although a number of translocations are identified which block differentiation in AML cells, the mechanism of increased cell growth is poorly understood. We are working to understand the signal transduction pathways activated in primary cells from patients with acute myeloid leukemia (AML). We have recently found that over 80% of AML patient samples have activation of the PI3 kinase signaling pathway and that these cells require activation of the PI3 kinase pathway for survival. We are continuing to work on the PI3 kinase pathway in these primary patient cells in order to determine the exact role of the pathway in AML. Experiments are in progress to test the use of PI3 kinase pathway inhibitors in the therapy of AML using a NOD/SCID xenograft model of the disease. We are also working to develop improved culture conditions for primary AML cells in order to define the growth regulatory pathways that maintain the survival of these cells in patients.
A second project involves the role of genomic instability in progression of chronic myeloid leukemia (CML) from the chronic phase to the terminal blast crisis phase of disease. CML arises because of the t(9;22) translocation which gives rise to the BCR/ABL oncogene. Extensive work has shown that BCR/ABL is a constitutively activated tyrosine kinase that leads to constitutive activation of signal transduction pathways in leukemic cells causing their aberrant growth. However, the role of BCR/ABL in progression to blast crisis is unknown. We have recently demonstrated that BCR/ABL alters the cellular response to DNA damage. After DNA damage, BCR/ABL translocates from the cytoplasm to the nucleus. In the nucleus, the oncogene associates with and disrupts the function of the ataxia-telangiectasia and rad 3 related (ATR) protein which regulates cell cycle checkpoints and DNA repair. We are actively working on trying to define the mechanism of translocation and association with ATR in order to better understand the role of BCR/ABL in progression of this disease.
Rotation Projects
1. Understanding the effects of hypoxia on growth of MDS cells.
2. Defining targets of mTOR signaling in AML.
3. Effects of BCR/ABL on genomic instability.
Lab personnel:
Jamil Dierov PhD, DS. - Staff Scientist
James Thompson, M.D. - Research Associate
Patty Sanchez, Ph.D. - Postdoctoral Fellow
Xiiowei Yang, Ph.D. - Postdoctoral Fellow
Beth Burke - Graduate Student
Kristin Brennan - Research Specialist
Description of Clinical Expertise
Leukemia and myelodysplastic syndromesSelected Publications
Vick B, Jurinovic V, Kuhbandner K, Lagally L, Latzko L, Arnreich C, Hänel G, Muth A, Schönung M, Kloos A, Rothenberg-Thurley M, Dufour AM, Schneider S, Holdt LM, Mura L, Klein F, Frank A, Mehra D, Fröhlich A, Bagnoli JW, André MC, Baldus CD, Carroll M, Dierks C, Ebinger M, Götze KS, Menéndez P, Récher C, Sahal A, Sarry JE, Thiede C, Velasco-Hernández T, Wei X, Klusmann JH, Enard W, von Bergwelt-Baildon M, Hiddemann W, Metzeler KH, Greif PA, Heuser M, Lipka DB, Subklewe M, Vosberg S, Herold T, Spiekermann K, Jeremias I.: A platform of serially transplantable AML PDX models covering subgroups for which no cell lines exist. Hemasphere 10: e70497, Oct 2026.Pursley AJ, Kirmani U, Chen AL, Yu Z, Hanada K, Ade CM, Chien CD, Cha N, Flegel WA, Aplan PD, Carroll M, Taylor NN, Yang JC, Pavletic SZ, Pai SY, Leko V.: HLA-A*11:01-Restricted T Cell Receptors Targeting Mutant NPM1 for Adoptive Cell Therapy in Acute Myeloid Leukemia. bioRxiv Oct 2026.
Venkataraman R, Puccio N, Hsueh TY, Bonner EA, Chang FY, Arriaga-Gomez EA, Song A, Miyagawa T, Rahman J, Akinwande O, Sinha S, El Marabti E, Welner RS, Lu R, Ferrell PB, Carroll M, Appelbaum JS, Stirewalt DL, Abdel-Wahab O, Rongvaux A, Chen X, Naresh KN, Fica SM, Lee SC.: Somatic DDX41 mutations confer neomorphic splicing activity in the pathogenesis of myelodysplastic neoplasms. bioRxiv Sep 2026.
Peramangalam PS, Konde M, Karakaslar O, Wolf S, Zheng S, Salimov A, Surapally S, Griffioen M, Gu T, Rao S, Tenen DG, Oellerich T, van den Akker E, Carroll M, Saygin C, Pulikkan JA.: Human CEBPA -N AML exhibits enhanced engraftment and a C/EBP α -p30-driven leukemic stem cell program. bioRxiv Aug 2026.
Joshi SK, Maazi H, Pittsenbarger J, Garana BB, Kaempf A, Huang A, Gritsenko MA, Hutchinson-Bunch C, Weitz KK, Chu RK, Gosline SJC, Piehowski PD, Eisfeld AK, Carroll MP, Perl AE, Rodland KD, Chang BH, Revenko AS, Tyner JW, Druker BJ, Traer E.: NRAS knockdown reverses monocytic cell state and resensitizes resistant FLT3-AML cells to gilteritinib. Blood Aug 2026.
Buono R, Juarez D, Paul M, Skuli SJ, Wong IB, Tarnekar I, Ying Z, Le IMF, Chen WP, Zhang M, Wertheim G, Bakayoko A, Kruidenier M, Nicholas DA, Gupta P, Sebti SM, Konopleva M, Fleischman AG, Jang C, Carroll M, Fruman DA.: Pitavastatin counteracts venetoclax resistance mechanisms including TP53 mutation in acute myeloid leukemia. Blood Neoplasia 3: 100296, Aug 2026.
Kumar A, Hamane K, Duault C, Lima-Junior JR, Jung DH, Qin H, Salcido S, Huang M, Guo X, Taghi Khani A, Sanchez Ortiz A, Ghoda L, Marcucci G, Lacayo NJ, Sakamoto KM, Hurtz C, Carroll M, Tasian SK, Geng H, Ji L, Armenian S, Izraeli S, Wu X, Maecker HT, Swaminathan S.: Tumor-induced dendritic cell deregulation perturbs T cell proliferation and predicts clinical outcome in acute lymphoblastic leukemia. Cell Rep Med 7: 102945, Jul 2026.
Cao Z, Yu S, Peng J, Barrett DR, Liu Y, Sussman JH, Chen C, Thadi A, Liu L, Alikarami F, Xu J, Carroll MP, Tan K, Bernt KM, Shi J.: CRISPR-based functional genomics for dissecting therapeutic dependency in primary acute myeloid leukemia samples. Mol Cell 86: 968-985, Mar 2026.
Neelamraju Y, Rapaport F, Gandara JA, Paudel BB, DeWolf S, Dunham N, Fan H, Lee T, Mayo MW, Othman J, Sheridan C, Sol-Church K, Solga MD, Wang L, Cripe LD, Dillon R, Kleppe M, Carroll M, Mason CE, Roboz GJ, Sun Z, Tallman MS, Zhang Y, Paietta E, Levine R, Melnick AM, Bekiranov S, Garrett-Bakelman FE.: Elevated levels of TNF and its targets characterize better-risk older acute myeloid leukemia patients. Leukemia 2026.
Buono R, Juarez D, Paul M, Skuli SJ, Wong IB, Tarnekar I, Ying Z, Le I, Wertheim G, Bakayoko A, Kruidenier M, Sebti SM, Konopleva M, Fleischman AG, Jang C, Carroll M, Fruman DA.: Pitavastatin counteracts venetoclax resistance mechanisms in acute myeloid leukemia by depleting geranylgeranyl pyrophosphate. bioRxiv Nov 2025.
© The Trustees of the University of Pennsylvania | Site best viewed in a supported browser. | Site Design: PMACS Web Team.
