alexa Chromosomal Instability, Inflammation, Plasmacytic Neoplasms, Elevated Stem Cell Antigen 1 Expression In Mice Deficient In Rrm2b Gene
ISSN: 2155-9864

Journal of Blood Disorders & Transfusion
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2nd International Conference on Hematology & Blood Disorders
September 29-October 01, 2014 DoubleTree by Hilton Baltimore-BWI Airport, USA

Lufen Chang
Accepted Abstracts: J Blood Disorders Transf
DOI: 10.4172/2155-9864.S1.008
Abstract
Chronic inflammation has a tight cause-and-effect relationship with DNA damage by inflicting tissue damage and increasing cancer risk. Stem-cell recruitment by chronic inflammation to injury sites may potentiate tumorigenesis. Rrm2b , a key enzyme in de novo deoxyribonucleotide synthesis, is involved in DNA damage repair. Rrm2b gene loss leads to severe numerical and structural chromosome abnormalities that cause ATM activation, inducing p-Ser85 IKK γ NEMO and I κ B kinase (IKK). NF-kB consequently induced by IKK triggered sustained IL-6 expression that constitutively activates STAT3 in Rrm2b -deficient cells. Rrm2b-/- mice developed dysfunctional immunologic and hematopoietic systems (high serum IL-6, splenic hemorrhage, abnormal IgM and IgG levels, lymphocytosis, neutrophilia, and thrombocytosis). 30-40% of aged Rrm2b heterozygous knockout mice developed plasma cell neoplasms and suffered from progressive splenomegaly and ascites. The genetic ablation of IL-6 suppressed STAT3 induction and delayed hematologic disorders and mortality from renal failure in Rrm2b-/- mice. Rrm2b protein levels were found inversely correlated with IL-6 expression in bone marrows of multiple myeloma patients. Stem Cell Antigen 1 positive (SCA-1+) small stem cell populations (≤6 μ m in diameter) which are termed spore-like cells, blastomere-like stem cells (BLSCs), or very-small embryonic-like stem cells (VSELs), Blastomere-like stem cells (BLSCs) accumulated more than 4 folds in Rrm2b-/- than Rrm2b +/+ bone marrows. The functional mechanisms underlying SCA-1+ BLSCs in Rrm2b-/- bone marrows for tissue repairing and tumorigenesis are currently investigated.
Biography
Lufen Chang obtained her PhD from Department of Cell biology of Vanderbilt University in Nashville, Tennessee, and Postdoctoral studies with Dr. Michael Karinin Department of Pharmacology from University of California, San Diego. She is currently an Assistant Research Professor in Department of Molecular Pharmacology and a member of Comprehensive Cancer Center in City of Hope. She has published numerous papers in high impact journals including, Nature, Cell, Cell Reports, PNAS, JCO, and Immunity.
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