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Barbara A. Miller, M.D.

Barbara A. Miller, M.D.

Chief, Division of Pediatric Hematology/Oncology; Director of the Four Diamonds Pediatric Cancer Research Center


Barbara A. Miller, M.D.

Chief, Division of Pediatric Hematology/Oncology; Director of the Four Diamonds Pediatric Cancer Research Center

Penn State College of Medicine

500 University Drive
Hershey, PA 17033



  • Fellowship, Pediatric Hematology/Oncology, Children's Hospital Boston (Boston) (1983) 
  • Fellowship, Hematology, Duke University Medical Center (1980) 
  • Residency, Pediatrics, Duke University Medical Center (1979) 
  • M.D., Penn State Hershey College of Medicine (1976)


“Penn State’s commitment to childhood cancer research enables us to provide innovative treatment to all of our pediatric cancer patients.”



Awards Received
  • 1996-2016 Best Doctors in America
  • 2004-Present Christopher Millard Endowed Chair in Pediatric Oncology  
  • 2012 Elected as fellow of the College of Physicians of Philadelphia
  • 2013-2014 Top 90th Percentile Award in Patient Satisfaction 
  • 2013-2015 Castle Connolly Best Doctors in Pediatric Oncology
  • 2013-2015 Hope Scholar, Hyundai Hope on Wheels
  • 2014-2015 Executive Leadership in Academic Medicine Fellow (ELAM) 
  • 2014-2015 Top 99th Percentile Award in Patient Satisfaction Nationally
  • 2017 Top 99th Percentile Award in Patient Satisfaction Nationally
  • 2017-2019 Hope Scholar, Hyundai Hope on Wheels
Grants Funded

“TRPM2, Mitochondria, and Cell Survival”   
$1,202,063 (TC)
B.A. Miller, Principal Investigator, 30% Effort

“TRPM2 in Ischemic Acute Kidney Injury” 
$157,948 (TC- PSU)
B.A. Miller, Co-I, 10% Effort (PI-B. Reeves)

2017 Hyundai Hope on Wheels Scholar Grant
“TRPM2, ROS, and Cell Survival in Leukemia”                                           
$250,000 (TDC)
B.A. Miller, P.I., 10% Effort       

Hyundai Hope on Wheels 
“2015 Hyundai Hope on Wheels Impact Grant Award”
09/01/15 – 10/31/2016
Role: PI

Hyundai Hope on Wheels 
“The Ion Channel TRPM2 Regulates Neuroblastoma Response to Chemotherapy Through Modulation of Oxidative Stress”   
09/01/13 – 12/01/2015
Role:  PI

Alex’s Lemonade Stand Summer Student Award 
“The Ion Channel TRPM2 in Neuroblastoma” 
06/01/2013 – 07/30/2014
Role:  PI/Mentor

NIH R01 DKO46778  
“Signal Transduction Mechanisms of Erythropoietin” 
Role:  PI



Dr. Barbara Miller is internationally recognized for her work on the superfamily of “TRP” ion channels.  Her laboratory studies the role of ion channels in cell survival, cancer and in the response to chemotherapy. Ion channels are pores on the surface of the cells through which ions like calcium and sodium enter a cell. This dramatically affects many processes within cells including the energy production in the powerhouse of the cell, mitochondria.

Dr. Miller’s lab is currently studying an ion channel called TRPM2.  This channel is found on many cell types and has an important role in proliferation and survival.  Dr. Miller’s lab recently demonstrated that TRPM2 channels are highly expressed in neuroblastoma, the most common pediatric solid tumor outside the brain, as well as other cancers including melanoma, lung, breast cancer and leukemia.  

Full length TRPM2 channel allows ion (calcium/sodium) entry into a cell. The channel isoform TRPM2-S (S for short), which is missing the pore, inhibits ion entry through the channel. Using mouse models, Dr. Miller’s lab found that neuroblastomas expressing full length TRPM2 channels grow much larger than tumors in which TRPM2 is inhibited, either by depleting it by cutting it out with a new technique called CRISPR or by inhibiting it with the short isoform, TRPM2-S, that has no pore function. 

Leukemia growth is also significantly reduced by TRPM2 inhibition. Inhibition of calcium entry through TRPM2 reduces energy production in both neuroblastoma and leukemia, increases the levels of harmful oxidants (ROS), blocks the growth of tumors and leukemia, and increases sensitivity to chemotherapy.  

Research currently focuses on better understanding the mechanisms through which TRPM2 modulates cell growth and survival through cellular bioenergetics, and new projects are underway to study its role in metastasis and leukemia.  Dr. Miller’s lab is utilizing a drug discovery approach to identify a TRPM2 inhibitor that can be used as a novel anti-cancer agent in clinical trials. 



The following are publications of Dr. Miller’s lab:

Zhang Z, Zhang W, Jung DY, Ko HJ, Lee YJ, Friedline R, Lee E, Jun J, Ma Z, Kim F, Tsitsilianos N, Chapman K, Morrison A, Cooper MP, Miller BA, Kim JK. TRPM2 Ca2+-Channel Regulates Energy Balance and Glucose Metabolism. American Journal of Physiology: Endocrinology and Metabolism, 302:E807-816, 2012. 

Hirschler-Laszkiewicz I, Zhang W, Keefer K, Conrad K, Tong Q, Chen, S-J, Bronson S, Cheung JY, and Miller BA. Trpc2 Depletion Protects Red Blood Cells from Oxidative Stress-Induced Hemolysis. Experimental Hematology, 40:71-83, 2012.

Miller, BA. TRPM2 Function and Potential as a Drug Target. (Chapter 5) In: Methods in Pharmacology and Toxicology: TRP Channels in Drug Discovery, Szallasi A, Ed., pp 89-102, 2012. 

Miller, BA. Hematopoietin Receptors.  In: Lennarz WJ, Lane, MD (Eds). The Encyclopedia of Biological Chemistry, Vol.2, 526-531, 2013. Waltham, MA: Academic Press. 

Chen SJ,   Zhang W, Tong Q, Conrad K, Hirschler-Laszkiewicz I, Bayerl M, Kim J,  Cheung JY, Miller BA. Role of TRPM2-S in Cell Proliferation and Susceptibility to Oxidative Stress. American Journal of Physiology: Cell Physiology, 304:C548-560, 2013.

Miller BA, Wang J, Hirschler-Laszkiewicz I, Gao E, Song J, Zhang X-Q, Koch WJ, Muniswany M, Mallilankaraman K, Gu T, Chen S-J, Keefer K, Conrad K, Feldman AM, Cheung JY. The Second Member of the Transient Receptor Potential-Melastatin (TRPM2) Channel Family Protects Hearts from Ischemia-Reperfusion Injury. American Journal of Physiology: Heart and Circulatory Physiology, 304:H1010-H1022, 2013.

Miller BA, Hoffman NE, Merali S. Zhang X-Q, Wang J, Rajan S, Gao E, Barrero CA, Mallilankaraman K, Song J, Gu T, Hirschler-Laszkiewicz I, Koch WJ, Feldman AM, Muniswamy M, Cheung JU.  TRPM2 Channels Protect Against Cardiac Ischemia-Reperfusion Injury:  Role of Mitochondria. J. Biol. Chem.289:7615-7629, 2014.

Bogardus H, Schulz VP, Maksimova Y, Miller BA, Li P, Forget B, Gallagher PG. Severe Hereditary Spherocytosis due to Maternal Uniparity Disomy at the SPTA1 Locus. Haematologica 99(9):e168-e170, 2014.

Chen SJ, Hoffman NE, Shanmughapriya S, Bao L, Keefer K, Conrad K, Merali S, Takahashi Y, Abraham T, Hirschler-Laszkiewicz I, Wang J, Zhang X-Q, Song J, Barrero C, Shi Y, Kawasawa YI, Bayerl M, Sun T, Barbour M, Wang HG, Muniswamy M, Cheung JY, Miller BA.  A  Splice Variant of the Human Ion Channel TRPM2-L Modulates Neuroblastoma Tumor Growth Through HIF-1/2α.  J. Biol. Chem. 289(52):36284-36302, 2014.

Gao G, Wang W, Tadagavadi R, Briley N, Love M, Miller BA, Reeves WB. TRPM2 mediates ischemic kidney injury and oxidant stress through Rac1.  J Clin Invest 124 (11):4989-5001, 2014.

Miller, BA. TRPC2. In:  Handbook of Experimental Pharmacology: Mammalian Transient Receptor Potential (TRP) Cation Channels, Nilus, B. and Flockerzi, V, Ed., pp 53-65, 2014.  

Hoffman NE, Miller BA,  Wang J, Elrod JW, Rajan S, Gao E,  Song J, Zhang X-Q,  Hirschler-Laszkiewicz I Shanmughapriya S, Koch WJ, Feldman A, Muniswamy M, Cheung JY.  Ca2+ entry via TRPM2 is essential for cardiac myocyte bioenergetics maintenance. American Journal of Physiology: Heart and Circulatory Physiology 308:H637-H650, 2015. (APSselect April 2015 for distinction in scholarship).

Shakerley NL, Chandrasekaran A, Trebak M, Miller BA, Melendez JA. Francisella tularensis Catalase Restricts Immune Function by Impairing TRPM2 Channel Activity. J. Biol. Chem. 291(8):3871-3881, 2016. 

Miller BA, Cheung JYC. TRPM2 protects against tissue damage following oxidative stress and ischaemia-reperfusion. (Symposium Review). Journal of Physiology 594.15: 4181-4191, 2016.

Katsnelson MA, Lozada-Soto KM, Russo HM, Miller BA, Dubyak GR. NLRP3 Inflammasome Signaling is Activated by Low-Level Lysosome Disruption but Inhibited by Extensive Lysosome Disruption: Roles for K+ Efflux and Ca2+ Influx. American Journal of Physiology-Cell Physiology 311:C83-C100, 2016. (APSselect July 2016 for distinction in scholarship).

Bao L, Chen SJ, Conrad K, Keefer K, Abraham T, Lee J, Wang J, Zhang X-Q, Hirschler-Laszkiewicz I, Wang HG, Dovat S, Muniswamy M, Cheung JY, Miller BA. Depletion of the Human Ion Channel TRPM2 in Neuroblastoma Demonstrates its Key Role in Cell Survival through Modulation of Mitochondrial ROS and Bioenergetics. J. Biol. CHem 291:24449-24464, 2016.

Cheung JYC, Miller BA.  Transient Receptor Potential-Melastatin Channel Family Member 2: Friend or Foe.  Transactions of the American Clinical and Climatological Association Review, in press, 2017.

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