Gender	Female
E-mail	luni.emdad@mountsinai.org
Education and Training	PH. D., Nagoya University Graduate School of Medicine
	Internship, Dhaka Medical College Hospital
	MBBS, Dhaka Medical College, Dhaka University
Awards	2005 - 2007 American Brain Tumor Association Research Fellowship
	1999 Japanese Soroptomistic Award
	1998 - 2001 Research Assistantship, Research Institute of Environmental Medicine, Nagoya University School of Medicine

Assistant Professor Luni Emdad, MD, PhD joined the Department of Neurosurgery in June 2008, coming from Virginia Commonwealth University in Richmond, Virginia, where she was an Assistant Professor in the Department of Human Genetics. Prior to that, she served as a Postdoctoral Research Scientist (12/2002-5/2006) and an Associate Research Scientist (5/2006-12/2007) in the Department of Pathology and Urology at Columbia University, College of Physicians and Surgeons. She will be working in the laboratory of Isabelle Germano, MD, investigating the effects of mouse and human embryonic stem cells-derived astrocytes conditionally expressing pro-apoptotic genes on human malignant glioma.

Education and Training	PH. D., Nagoya University Graduate School of Medicine
	Internship, Dhaka Medical College Hospital
	MBBS, Dhaka Medical College, Dhaka University

• Translational research for brain tumors
• The study of gene therapy for malignant brain tumors
• Evaluating stem cells for therapy of brain tumors

The focus of our laboratory is to investigate new delivery methods to carrying pro-apoptotic genes while sparing normal brain cells. Additionally, we are investigating the effects of substances that can enhance the effects of standard treatments such as ionizing radiations and temozolomide.

Research Overview
Malignant primary brain tumors occur in the adult and children population. In particular, Glioblastoma multiforme (GBM) is the most common and aggressive type of primary brain tumor. In children, it is the second most common malignancy following leukemia and represents the leading cause of cancer death in children under the age of 15. In adults, it accounts for approximately 50% of primary brain tumors.³ The extensive infiltrating growth pattern of these tumors is the cause of their recurrence within less than six months of treatment.

Aggressive multimodality treatments with surgery, radiation, and chemotherapy have led to some improvement in prognosis for patients with glioblastoma and high-grade gliomas. Recent Level IIb evidence supports the concept that aggressive surgical resection of GBM has a positive impact on survival. However, the five year survival rate for patients with GBM is less than 5%⁵ and a median survival rate of less than 12 months.  The futility of present treatments in combating this disease is in part due to their inability to address the highly invasive nature of these neoplasms. Glial tumor cells intersperse themselves with normal brain parenchyma and typically give rise to tumor recurrence within the operated surgical site.⁶ Targeting these tumor cells while sparing the normal cells may prove to be critical for the success of any potential therapeutic strategy.

The development of successful treatments for GBM needs to focus on how the intracranial disease left behind at the time of surgery can be eliminated. Residual brain tumor cells may be protected from conventional adjuvant therapies by intrinsic factors, such as resistance to alkylating agents, and extrinsic factors, such as the blood-brain barrier.

Lee SG, Su ZZ, Emdad L, Gupta P, Sarkar D, Borjabad A, Volsky DJ, Fisher PB. Mechanism of ceftriaxone induction of excitatory amino acid transporter-2 expression and glutamate uptake in primary human astrocytes. J Biol Chem 2008; 283(19): 13116-13123.

Sarkar D, Park ES, Emdad L, Lee SG, Su ZZ, Fisher PB. Molecular basis of nuclear factor-kappaB activation by astrocyte elevated gene-1. Cancer Res 2008 Mar 1; 68(5): 1478-1484.

Emdad L, Lebedeva IV, Su ZZ, Sarkar D, Dent P, Curiel DT, Fisher PB. Melanoma differentiation associated gene-7/interleukin-24 reverses multidrug resistance in human colorectal cancer cells. Mol cancer Ther 2007; 6(11): 2985-2994.

Emdad L, Sarkar D, Su ZZ, Lee SG, Kang DC, Bruce JN, Volsky DJ, Fisher PB. Astrocyte elevated gene-1: recent insights into a novel gene involved in tumor progression, metastasis and neurodegeneration. Pharmacol Ther 2007 May; 114(2): 155-170.

Emdad L, Lebedeva IV, Su ZZ, Gupta P, Sarkar D, Settleman J, Fisher PB. Combinatorial treatment of non-small-cell lung cancers with gefitinib and Ad.mda-7 enhances apoptosis-induction and reverses resistance to a single therapy. J Cell Physiol 2007 Feb; 210(2): 549-559.

Emdad L, Sarkar D, Lebedeva IV, Su ZZ, Gupta P, Mahasreshti PJ, Dent P, Curiel DT, Fisher PB. Ionizing radiation enhances adenoviral vector expressing mda-7/IL-24-mediated apoptosis in human ovarian cancer. J Cell Physiol 2006 Aug; 208(2): 298-306.

Lee SG, Su ZZ, Emdad L, Sarkar D, Fisher PB. Astrocyte elevated gene-1 (AEG-1) is a target gene of oncogenic Ha-ras requiring phosphatidylinositol 3-kinase and c-Myc. Proc Natl Acad Sci U S A 2006 Nov 14; 103(46): 17390-17395.

Emdad L, Sarkar D, Su ZZ, Randolph A, Boukerche H, Valerie K, Fisher PB. Activation of the NF-kB pathway by Astrocyte Elevated Gene (AEG)-1: implications for tumor progression and metastasis. Cancer Res 2006 Feb 1; 66(3): 1509-1516.

Su ZZ, Emdad L, Sarkar D, Yacoub A, Dent P, Fisher PB. Potential molecular mechanism for rodent tumorigenesis: mutational generation of progression elevated gene-3 (PEG-3). Oncogene 2005 Mar 24; 24(13): 2247-2255.

Su ZZ, Sarkar D, Emdad L, Duigou GJ, Young CH, Ware J, Randolph A, Valerie K, Fisher PB. Targeting gene expression selectively in cancer cells by using the progression-elevated gene-3 promoter. Proc. Natl. Acad. Sci. USA 2005 Jan 25; 102(4): 1059-1064.