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BioMed Research International - Volume 2015 2015, Article ID 205247, 6 pages -

Research Article

New Experimental Therapeutics Branch, National Cancer Center, Goyang-si, Gyeonggi-do 410-769, Republic of Korea

Supercomputing R&D Center, Korea Institute of Science and Technology Information KISTI, Daejeon 305-806, Republic of Korea

Bioscience Advising, Indianapolis, IN 46227, USA

Korean Bioinformation Center KOBIC, Korea Research Institute of Bioscience and Biotechnology, Daejeon 305-806, Republic of Korea

Received 17 December 2014; Revised 16 February 2015; Accepted 16 February 2015

Academic Editor: Junwen Wang

Copyright © 2015 Sungjin Park et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Recently, a large clinical study revealed an inverse correlation of individual risk of cancer versus Alzheimer’s disease AD. However, no explanation exists for this anticorrelation at the molecular level; however, inflammation is crucial to the pathogenesis of both diseases, necessitating a need to understand differing signaling usage during inflammatory responses distinct to both diseases. Using a subpathway analysis approach, we identified numerous well-known and previously unknown pathways enriched in datasets from both diseases. Here, we present the quantitative importance of the inflammatory response in the two disease pathologies and summarize signal transduction pathways common to both diseases that are affected by inflammation.

Autor: Sungjin Park, Seok Jong Yu, Yongseong Cho, Curt Balch, Jinhyuk Lee, Yon Hui Kim, and Seungyoon Nam



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