Ercument Dirice, PhD

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DiriceEDiriceE 

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Advanced Postdoctoral

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 (Grant # 3-APF-2014-220-A-N) April 2014

Joslin Identifies Immune Cells That Promote Growth of Beta Cells in Type 1 Diabetes

 New Insights into Type 1 Diabetes Pathology

(Dirice E. Diabetes, 2014)

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Boston,
Sep 27, 2013

TEXT

VIDEO

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Beta Cell Regeneration in Type 1 Diabetes (Grant # 3-2010-474)   September 2010

Islet_Tx

Transplantation of isolated pancreatic islets. This work was performed by Dr. Sevim Kahraman Dirice, at Gene & Cell Therapy Center, Faculty of Medicine, Akdeniz University, TURKEY.

PancreaticBetaCellInfiltrationByTcells

Immunoflourescent staining of mononuclear cells infiltrating (blue) into pancreatic islets where insulin producing beta-cells (red) are localized. Infiltration induces pancreatic beta-cell replication rates (BrdU staining in green). Images were taken at Kulkarni Lab, Joslin Diabetes Center, Harvard Medical School, USA

Type1 diabetes

IProposed sheme for the pathogenesis of type 1 diabetes. Published in Islet Cell Growth Factors under the section Pathways Underlying beta-cell Regeneration in Type 1, Type 2 and Gestational Diabetes, 2011

Pacreatic Islets

Brightfield and Flourescent microscopy of AdEGFP transduced pancreatic islets.

I am currently working as a Postdoctoral Fellow in the section of Islet Cell & Regenerative Biology at Joslin Diabetes Center which is the worlds largest diabetes research center, diabetes clinic and provider of diabetes education. Since its founding in 1898, the Joslin Diabetes Center has constantly evolved to meet the ever-changing challenges of diabetes. The Joslin is an institution on the front lines of the world epidemic of diabetes, leading the battle to conquer diabetes in all of its forms through cutting-edge research.

I received my MSc degree in 2003 as a research assistant in Medical Genetics at the Department of Medical Biology and Genetics and Human Gene and Cell Therapy Center of Akdeniz University Faculty of Medicine. During my MSc education my project was focused on the identification of novel markers to follow up the progression of prostate cancer. This research revealed a putative connection between the down-regulation of a novel tumor suppressor gene namely PTEN and the progression of prostate carcinoma.

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After 2004, I studied as a PhD student in Medical Genetics. Our team was working on the role of Tumor Necrosis Factor-Releated Apoptosis Inducing Ligand (TRAIL) mechanism on cancer development.under the supervision of Prof. Dr. Salih Sanlioglu.  I have been studying the effect of TRAIL on rat/mouse pancreatic islet survival by using autoimmune diabetes mouse and rat models. My doctorate thesis was to develop novel gene therapy methods against type 1 diabetes. We have shown that the success of islet transplantation can be increased if complementary gene therapy modalities are employed prior to transplantation. My thesis named Adenovirus mediated TRAIL gene (Ad5hTRAIL) delivery into pancreatic islets prolongs normoglycemia in STZ-induced diabetic rats was  published by Human Gene Thearpy, official journal of European Society of Gene and Cell Therapy (ESGCT)(October 2009). In addition, the journal announced that October 2009 journal cover award has been given to our study. After completing my doctoral degree, I  was awarded the Novartis Research Award for Diabetes fellowship for postdoctoral training at Joslin Diabetes Center under the mentorship Rohit N. Kulkarni, M.D. PhD.(July, 2009).

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Dr. Kulkarni, M.D., Ph.D., focuses on understanding how beta cells grow in mice, and, by extension, in humans. Kulkarni Lab is examining unique genetically engineered mouse models that lack receptors or proteins in growth factor signaling pathways. Dr. Kulkarni is particularly interested in crosstalk among insulin/insulin-like growth factor 1 (IGF-1)-signaling and glucose-signaling pathways in regulating the development, replication and function of islet cells. One of his most important and unexpected findings is that insulin and IGF-1 play crucial roles in glucose sensing, which triggers insulin secretion, and compensate for each other to maintain the viability of beta cells.

These findings have implications for treating patients with type 2 diabetes because most of these patients develop insulin resistance. Dr. Kulkarnis research suggests a vicious cycle: Not only is the beta cell producing insufficient insulin, but the cell itself is also resistant to insulin, which prevents glucose sensing and in turn lowers insulin secretion. To examine whether the problem begins in the insulin receptor itself, the Kulkarni laboratory is now examining the kinetics of turnover of insulin and C-peptide synthesis in mutant mice lacking insulin receptors in beta cells

This research also extends to the study of type 1 diabetes from a novel perspective. Rather than seeing beta cell death as the result of an autoimmune process (the usual theory about type 1 diabetes), our laboratory is working on the hypothesis that even before the autoimmune problem begins, there is dysfunction in insulin/IGF-1 signaling and increased vulnerability of beta cells to stress.In addition we are studying the pathways utilized by lymphocytes that allow regeneration in beta-cells in type 1 diabetes using NOD mice.

These studies will provide critical information on several fronts - first, it will allow us to gain greater insights into the fundamental physiological mechanisms that govern the normal growth and functioning of pancreatic islets; second, it will provide a physiological basis to identify targets in signaling pathways that would be useful to design potential therapeutic strategies to prevent beta cell death and to plan alternative approaches to generate new beta cells to prevent and/or cure type 1 and type 2 diabetes.

 

 

Scientific Contribution Award
50th National Diabetes Meeting
April 2014, Antalya-Turkiye
Ulusal Diyabet Odul 2014
Best Scientific Publication
46th National Diabetes Meeting
May 2010, Antalya-Turkiye
afis 46 diyabet kongresi
Research Award 1st place
11th Med.Biology&Genetics Meeting
November 2009, Kusadasi-Turkiye
Altan Gunalp-1
Cover Award
Human Gene Therapy,
October 2009
Large_HumanGeneTherapy_October_2009
Appreciation Letter
Rectorate of Akdeniz University
July 2009, Antalya, Turkiye
appreciation_letter
Young Investigator Award
11th Eur. Congress of Endocrinology   April 2009 Istanbul, Turkiye
ECE2009_Young_Investigator_Award_DiriceE
Novartis Science Award 2009
April 2009, Ankara-Turkiye
Novartis_2009_Science_Award
Best Poster Award
6th Metabolic Syndrome Symposium
April 2009 Antalya, Turkiye
6MetabolicSyndromeSymposium_PosterAward_1st_place_3

 

Update: May 1, 2014

Publications

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  • Joslin Diabetes Center
  • Harvard University
  • Boston

    100

    Boston is the capital of and the largest city in Massachussets, and is one of the oldest cities in the United States. The largest city in New England, Boston is regarded as the unofficial Capital of New England for its economic and cultural impact on the entire New England region.

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    Zakim Bridge

    Several early battles of the American Revolution, such as the Battle of Bunker Hill and the Siege of Boston, occurred within the city and surrounding areas. Through land reclamation and municipal annexation, Boston has expanded beyond the peninsula. After American independence was attained Boston became a major shipping port and manufacturing center,and its rich history now helps attract many tourists, with Faneuil Hall alone attracting over 20 million every year.

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    The city was the site of several firsts, including America's first public school, Boston latin School (1635), and the first subway system in the United States (1897). With many colleges and universities within the city and surrounding area, Boston is an international center of higher education and a center for medicine.

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    The city's economic base includes research, manufacturing, finance, and biotech. As a result, the city is a leading finance center, ranking 12th in the Z/Yen top 20 Global Financial Centers. The city was also ranked number one for innovation, both globally and in North America, for a variety of reasons.