JTCS KCI
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to Personal Folders
Right arrow Download to citation manager
Right arrow Author home page(s):
Igor E. Konstantinov
Andrew N. Redington
Right arrow Permission Requests
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Konstantinov, I. E.
Right arrow Articles by Redington, A. N.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Konstantinov, I. E.
Right arrow Articles by Redington, A. N.
Related Collections
Right arrow Lung - cancer
Right arrow Pleura
Right arrow Molecular biology
Right arrow Myocardial protection
Right arrowRelated Article

J Thorac Cardiovasc Surg 2006;131:509-510
© 2006 The American Association for Thoracic Surgery

Letter to the Editor

From mesothelioma to cardiovascular protection via the phosphoinositide-3 kinase pathway: A new vista in cardiothoracic surgery

Igor E. Konstantinov, MD, PhD, Jia Li, MD, PhD, Andrew N. Redington, MD

Department of Cardiovascular Surgery and Cardiology, Hospital for Sick Children, Toronto, Ontario, Canada

The first 20% of the full text of this article appears below.

To the Editor:

We read with interest the article by Rascoe and colleagues 1 Go on the role of tyrosine kinase receptors and the phosphoinositide-3 kinase (PI3K) pathway in mesothelioma. The authors demonstrated differential involvement of 3 growth factor (GF) receptors—epidermal growth factor (EGF), insulin-like growth factor (IGF), and platelet-derived growth factor (PDGF) receptors—in PI3K-mediated survival of the malignant mesothelioma cells.

Survival of many cells under stress, particularly of myocytes, is dependent on PI3K pathway activation. 2 Go It is not often appreciated, however, that the PI3K pathway can be activated not only via tyrosine kinase receptors by GFs, but also via toll-like receptor by heat shock protein, bacterial lipopolysaccharide, and by tumor . . . [Full Text of this Article]


Related Article

Reply to the Editor
Philip A. Rascoe, Xiaobo Cao, Jonathan C. Daniel, Steven D. Miller, and W. Roy Smythe
J. Thorac. Cardiovasc. Surg. 2006 131: 510. [Extract] [Full Text] [PDF]





HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
ANN THORAC SURG ASIAN CARDIOVASC THORAC ANN EUR J CARDIOTHORAC SURG
J THORAC CARDIOVASC SURG ICVTS ALL CTSNet JOURNALS
Copyright © 2006 by The American Association for Thoracic Surgery.