alexa Advances in the understanding of MYC-induced lymphomagenesis.


Journal of Blood Disorders & Transfusion

Author(s): Klapproth K, Wirth T

Abstract Share this page

Abstract Up to 70\% of all human malignancies show elevated expression of MYC. MYC is a pleiotropic transcription factor involved in many aspects of cellular development and physiology. Besides direct regulation of target genes involved in proliferation and growth MYC is implicated in controlling the complex networks of microRNAs and apoptosis mediators. The mode of MYC deregulation varies between different tumor entities. In most types of cancer high MYC levels are secondary to alterations in cell signalling pathways, leading to enhanced proliferation of the transformed cells. In some haematological malignancies, like Burkitt lymphoma (BL) and subsets of diffuse large B-cell lymphomas, elevated MYC levels are a direct consequence of genomic aberrations involving the MYC locus. BL is considered the prime example for MYC-induced lymphomagenesis. In comparison to other haematological malignancies it has the highest MYC-expression and is often connected to Epstein-Barr virus (EBV) infection. Over the past five decades BL has provided an invaluable tool for the entire discipline of oncology, helping to decipher many aspects of tumor biology. This review summarizes recent advances in the research on MYC-induced lymphomagenesis, focusing on the regulation of microRNAs and apoptosis, and possible contributions of EBV for lymphoma development. This article was published in Br J Haematol and referenced in Journal of Blood Disorders & Transfusion

Relevant Expert PPTs

Relevant Speaker PPTs

Recommended Conferences

Relevant Topics

Peer Reviewed Journals
Make the best use of Scientific Research and information from our 700 + peer reviewed, Open Access Journals
International Conferences 2017-18
Meet Inspiring Speakers and Experts at our 3000+ Global Annual Meetings

Contact Us

© 2008-2017 OMICS International - Open Access Publisher. Best viewed in Mozilla Firefox | Google Chrome | Above IE 7.0 version