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Eli E. Bar, PhD

Academic Title:

Associate Professor

Primary Appointment:


Secondary Appointment(s):


Additional Title:

Secondary Appointment, Department of Neurosurgery; Member, Molecular Medicine Program; Member, Marlene and Stewart Greenebaum Comprehensive Cancer Center

Phone (Primary):

410-706-4826 (office)

Phone (Secondary):

410-706-2299 (lab)



Education and Training


Doctor of Philosophy, Molecular Biology, University of Illinois at Chicago

Residencies, Internships and Fellowships

Postdoctoral Fellow, Cancer Cell Biology, The Johns Hopkins University

Highlighted Publications

1. Targeting BCL-xL improves the efficacy of bromodomain and extra-terminal protein inhibitors in triple-negative breast cancer by eliciting the death of senescent cells.

Gayle SS, Sahni JM, Webb BM, Weber-Bonk KL, Shively MS, Spina R, Bar EE, Summers MK, Keri RA.

J Biol Chem. 2019 Jan 18;294(3):875-886. doi: 10.1074/jbc.RA118.004712. Epub 2018 Nov 27.

PMID:  30482844

2. Addition of carbonic anhydrase 9 inhibitor SLC-0111 to temozolomide treatment delays glioblastoma growth in vivo.

Boyd NH, Walker K, Fried J, Hackney JR, McDonald PC, Benavides GA, Spina R, Audia A, Scott SE, Libby CJ, Tran AN, Bevensee MO, Griguer C, Nozell S, Gillespie GY, Nabors B, Bhat KP, Bar EE, Darley-Usmar V, Xu B, Gordon E, Cooper SJ, Dedhar S, Hjelmeland AB.

JCI Insight. 2017 Dec 21;2(24). pii: 92928. doi: 10.1172/jci.insight.92928.

PMID:  29263302

3. Disruption of the monocarboxylate transporter-4-basigin interaction inhibits the hypoxic response, proliferation, and tumor progression.

Voss DM, Spina R, Carter DL, Lim KS, Jeffery CJ, Bar EE.

Sci Rep. 2017 Jun 27;7(1):4292. doi: 10.1038/s41598-017-04612-w.

PMID:  28655889

4. Targetable T-type Calcium Channels Drive Glioblastoma.

Zhang Y, Cruickshanks N, Yuan F, Wang B, Pahuski M, Wulfkuhle J, Gallagher I, Koeppel AF, Hatef S, Papanicolas C, Lee J, Bar EE, Schiff D, Turner SD, Petricoin EF, Gray LS, Abounader R.

Cancer Res. 2017 Jul 1;77(13):3479-3490. doi: 10.1158/0008-5472.CAN-16-2347. Epub 2017 May 16.

PMID:  28512247

5. Atracurium Besylate and other neuromuscular blocking agents promote astroglial differentiation and deplete glioblastoma stem cells.

Spina R, Voss DM, Asnaghi L, Sloan A, Bar EE.

Oncotarget. 2016 Jan 5;7(1):459-72. doi: 10.18632/oncotarget.6314.

PMID:  26575950

6. Notch signaling activation in pediatric low-grade astrocytoma.

Brandt WD, Schreck KC, Bar EE, Taylor I, Marchionni L, Raabe E, Eberhart CG, Rodriguez FJ.

J Neuropathol Exp Neurol. 2015 Feb;74(2):121-31. doi: 10.1097/NEN.0000000000000155.

PMID:  25575134

7. Lateral inhibition of Notch signaling in neoplastic cells.

Lim KJ, Brandt WD, Heth JA, Muraszko KM, Fan X, Bar EE, Eberhart CG.

Oncotarget. 2015 Jan 30;6(3):1666-77.

PMID:  25557173

8. ZEB1 Promotes Invasion in Human Fetal Neural Stem Cells and Hypoxic Glioma Neurospheres.

Kahlert UD, Suwala AK, Raabe EH, Siebzehnrubl FA, Suarez MJ, Orr BA, Bar EE, Maciaczyk J, Eberhart CG.

Brain Pathol. 2015 Nov;25(6):724-32. doi: 10.1111/bpa.12240. Epub 2015 Feb 8.

PMID:  25521330

9. The polyamine catabolic enzyme SAT1 modulates tumorigenesis and radiation response in GBM.

Brett-Morris A, Wright BM, Seo Y, Pasupuleti V, Zhang J, Lu J, Spina R, Bar EE, Gujrati M, Schur R, Lu ZR, Welford SM.

Cancer Res. 2014 Dec 1;74(23):6925-34. doi: 10.1158/0008-5472.CAN-14-1249. Epub 2014 Oct 2.

PMID:  25277523

10. Hypoxia promotes uveal melanoma invasion through enhanced Notch and MAPK activation.

Asnaghi L, Lin MH, Lim KS, Lim KJ, Tripathy A, Wendeborn M, Merbs SL, Handa JT, Sodhi A, Bar EE, Eberhart CG.

PLoS One. 2014 Aug 28;9(8):e105372. doi: 10.1371/journal.pone.0105372. eCollection 2014.

PMID:  25166211

11. Inhibition of monocarboxylate transporter-4 depletes stem-like glioblastoma cells and inhibits HIF transcriptional response in a lactate-independent manner.

Lim KS, Lim KJ, Price AC, Orr BA, Eberhart CG, Bar EE.

Oncogene. 2014 Aug 28;33(35):4433-41. doi: 10.1038/onc.2013.390. Epub 2013 Sep 30.

PMID:  24077291

Research Interests

Glioblastoma is the most common and lethal of brain tumors claiming the lives of over 12,000 people each year in the U.S. alone. Median survival following diagnosis is approximately 15 months with maximal surgical resection, radiation, and temozolomide chemotherapy (standard of care). The challenges inherent in developing better and more effective treatments for glioblastoma are becoming increasingly clear. Glioblastomas are relentlessly invasive, resistance to standard treatments, genetically complex and molecularly adaptable, and contain subpopulations of cancer cells with phenotypic similarities to normal neural stem cells which are often referred to as glioma stem-like cells (GSC).

The microenvironment around cells is extremely rich in information. This includes localized signals from adjacent cells (cell-cell contact) and the surrounding extracellular matrix, as well as soluble molecules produced and secreted by distant cells and organs. Collectively, these signals constitute the tissue context, and the behavior of every cell is profoundly influenced by the precise combination of signals presented to it. Non neoplastic cells respond to these signals in ways that serve the body. In contrast, cancer cells react to their tissue context quite differently and in most cases,  they actively remodel the microenvironment to promote tumor progression and invasion.  

Awards and Affiliations

American Association for Cancer Research (AACR)

Society for Neuro-Oncology (SNO)

Research Projects

My laboratory is primarily focused on the identification and targeting of cancer-cell intrinsic signaling nodes which are activated by signals from the tumor microenvironment.

  1. Cellular adaptation to hypoxia and nutrient deprivation orchestrated by hypoxia inducible factors (HIFs) and the Monocarboxylate Transporter-4 (MCT4).We have recently reported that hypoxia increases the percentage of GSCs in GBM cultures and in primary tumors and implicated HIFs and MCT4 in this response. Hypoxia has also been shown to promote radiation resistance and tumor invasion, suggesting that an improved understanding of how reduced oxygenation and nutrient availability modulate the pathobiology of glioblastoma will be necessary if we are to effectively treat these universally fatal neoplasms. We are actively engaged in preclinical testing of pharmacological agents that target these pathways in glioblastoma.
  2. Crosstalk between microenvironmental factors and “stemness” signaling pathways.We have previously implicated Hedgehog, Notch, and other developmentally significant signaling pathways in the initiation and progression of Medulloblastoma and Glioblastoma. Increasing evidence suggest these pathways may be regulated not only by intrinsic but also by microenvironmental factors. Targeting microenvironmental factors which contribute to the induction of these pathways may lead to novel therapeutic approaches against glioblastomas and other tumors.
  3. Mechanisms of microenvironmentally acquired resistance to therapy. The goal of this project is to uncover the role of RNA binding proteins (RBPs) in mediating microenvironmental acquired therapy resistance.
  4. Mechanisms of drug resistance in low grade gliomas. Using array CGH technology, we showed that alterations activating the oncogene BRAF are common in pediatric low-grade gliomas (>60% of Pilocytic Astrocytomas). We are currently investigating mechanisms of drug resistance in this complex group of tumors.