Anastasiadou Ema
Investigator (Lecturer Level)
Instit.: BRFAA
Tel: (+30) 210-6597063
Personal Web Page: http://www.bioacademy.gr/Faculty/investigators_details_new.php?id=2&inv=0&ovr=0
Short Bio:
Dr. Ema Anastasiadou received her diploma in Biology from University of Athens, Greece. Her thesis, a prerequisite for the degree, was focused on the analysis of the chromosomal protein HMG 17 in chronic myelogenic leukaemia. She continued her studies at University of Cambridge, Institute of Biotechnology, UK in Dr. Jim Murray's laboratory where she obtained the Ph.D. degree. During her graduate studies she was introduced into various molecular and cellular biology techniques but her primary focus was developing a methodology for large scale manipulation of the mammalian genome and regulating the expression of specific genes. She also gained experience in stem cell technology and mouse genetics.
She continued her research at Harvard Medical School, Boston, at the Human Institute of Medicine, Department of Genetics, Division of Hematology/Oncology in the laboratory of Dr. Gary Gilliland. Her research was sponsored by the Howard Hughes Medical Institute where as a postdoctoral fellow,she applied her expertise to generate mice with conditional expression of specific genes as models for hematopoietic malignancies. Since December 2002 she is a member of BRFAA where as a Researcher (Lecturer Level) investigates genes and pathways that are involved in hematopoiesis and leukemogenesis.
Her main interest is the functional analysis of TEL and AML1 genes in hematopoietic development. TEL/AML1 is a chimeric product of a chromosomal translocation (12;21) (p12;q22) involving two transcription factors, TEL and AML1. It is the most common event in pediatric cancers; 25-30% of children with acute lymphoblastic leukemia (ALL) shows this specific translocation and demonstrates a blockage during the pre-B cell stage in hematopoietic development. The goal of this laboratory is to study/analyze the pathways that TEL and AML1 are involved and uncover the mechanisms, through which TEL/AML1 alters their function. Our target is to determine the specific events that blocks normal hematopoietic differentiation and lead to leukemogenesis and define molecules as potential targets for therapeutic purposes.

Sitemap | Contact | Credits | Rss
National and Kapodistrian University of Athens Department of Informatics and Telecommunications