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Barbara A. Miller, M.D.

Barbara A. Miller, M.D.

Christopher Millard Endowed Chair; Assoc. Dir. for Pediatrics, Penn State Cancer Institute


Barbara A. Miller, M.D.

Christopher Millard Endowed Chair; Assoc. Dir. for Pediatrics, Penn State Cancer Institute

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
  • 2004-Present Christopher Millard Endowed Chair in Pediatric Oncology
  • 2017-2019 Hope Scholar, Hyundai Hope on Wheels
  • 2018 Elected to the American Pediatric Society (APS)
  • 2018 Kayla Nakonechni Award from Philadelphia Chapter of the Penn State Alumni Association
  • 2017 Top 99th Percentile Award in Patient Satisfaction Nationally
  • 1996-2016 Best Doctors in America
  • 2014-2015 Top 99th Percentile Award in Patient Satisfaction Nationally
  • 2014-2015 Executive Leadership in Academic Medicine Fellow (ELAM)
  • 2013-2015 Hope Scholar, Hyundai Hope on Wheels
  • 2013-2015 Castle Connolly Best Doctors in Pediatric Oncology
  • 2013-2014 Top 90th Percentile Award in Patient Satisfaction
  • 2012 Elected as fellow of the College of Physicians of Philadelphia
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)

2018 Hyundai Hope on Wheels Impact Grant                                         
$100,000 (TDC)
B.A. Miller, Co-PI, 3% Effort       

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. 


Selected Publications

The following are publications of Dr. Miller’s lab since 2012:

Miller BA. TRPM2 in Cancer. Special Issue, Ca2+ Channels in Cancer. Cell Calcium (in press), 2019.

Xu J, Song F, Schleicher E, Pool C, Bann D, Hennessy M, Sheldon K, Batchelder E, Annageldiyev C, Sharma A, Chang Y, Hastie A, Miller B, Goldenberg D, Mineishi S, Claxton D, Moldovan G-L, Yue F, Broach JR. An Integrated Framework for Genome Analysis Reveals Numerous Previously Unrecognizable Structural Variants in Leukemia Patients’ Samples. (Manuscript submitted 2019).

Rao P, Segel JE, McGregor L, Lengerich EJ, Drabick J, Miller BA. Access to NCI and COG Facilities for Children, Adolescents, and Young Adults with Cancer in Pennsylvania: A Statewide Study. (Manuscript Submitted 2019).

Bao L, Freet C, Lee J, Hirschler-Laszkiewicz I, Chen SJ, Keefer K, Liu Z, Wang HG, Cheung JY,  Miller BA. The Human Transient Receptor Potential Melastatin 2 Ion Channel Modulates ROS, GSH, and NADPH through Regulation of Nrf2. (Manuscript Submitted 2019)

Gebru MT, Atkinson JM, Tang Z, Lu P, Young MM, Dower CM, Chen L, Annageldiyev C, Sharma A, Zhao Z, Miller BA, Claxton DF, Wang HG. Anti-inflammatory drugs sensitize drug-tolerant persister FLY3-ITD AML cells to FLT3 inhibitors. (Manuscript submitted)

Chen SJ, Bao L, Keefer K, Shanmughapriya S, Chen L, Lee J, Wang J, Zhang X-Q, Hirschler-Laszkiewicz I, Merali S, Barrero C, Merali C, Kawasawa YI, Dovat S,  Muniswamy M, Cheung JY, Wang HG, Miller BA. Human Ion Channel TRPM2 Modulates AML Proliferation and Survival Through Regulation of Mitochondrial Function and Autophagy. (Manuscript submitted 3-2019).

Miller BA, Wang J, Song J, Zhang X-Q, Hirschler-Laszkiewicz I, Shanmughapriya S, Tomar D, Rajan S, Feldman AM, Madesh M, Sheu S-S, Cheung JY. Trpm2 enhances physiological bioenergetics and protects against pathological oxidative cardiac injury: Role of Pyk2 phosphorylation. Journal of Cellular Physiology: 1-13, 2019.

Dower CM, Bhat N, Gebru MT, Chen L, Miller BA, Wang HG. Targeted Inhibition of ULK1 promotes apoptosis and suppresses tumor growth and metastasis in neuroblastoma. Molecular Cancer Therapeutics 17 (11): 2365-2376, 2018.

Hirschler-Laszkiewicz I, Chen SJ, Bao L, Wang J, Zhang X-Q, Shanmughapriya S, Keefer K, Muniswamy M, Cheung JY, Miller BA. The Human Ion Channel TRPM2 Modulates  Neuroblastoma Survival and Mitochondrial Function through Pyk2, CREB, and MCU Activation. Am J Physiol Cell Physiol 315:C571-C586, 2018.

Bao L, Chen SJ, Conrad K, Keefer K, Abraham T, Lee J, Wang J, Zhang X-Q, Hirschler-Laszkiewicz I, Wang HG, Dovat S, Gans B, 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. Selected by JBC as one of the top ion channel papers of the year for republication in special issue, Ion Channels, Ed Roger Colbran, “Biological Roles of Ion Channels”, JBC, 2017.

Cheung JYC, Miller BA.  Transient Receptor Potential-Melastatin Channel Family Member 2: Friend or Foe.  Transactions of the American Clinical and Climatological Association 128:308-329, 2017.

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.

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).

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.

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. 

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).

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.

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.

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.

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.

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.

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.

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

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. 

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.

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. 

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