BibSonomy :: publication ::

tag user group author concept BibTeX key search:all search:kanefendt

The blue social bookmark and publication sharing system.

entry of kanefendt:

(0)

This publication has not been reviewed yet.

rating distribution

average user rating

The average rating is computed over all reviews. However, some of them may be invisible to you due to the visibility setting chosen by the reviewers.

(0.0 of 5.0 based on 0 reviews)

Multiple circulating proangiogenic factors induced by sunitinib malate are tumor-independent and correlate with antitumor efficacy

by: J. M. Ebos, C. R. Lee, J. G. Christensen, A. J. Mutsaers, and R. S. Kerbel

In: Proc.Natl.Acad.Sci.U.S.A, Vol. 104, Nr. 43 (2007) , p. 17069-17074.

Resources (URL, PDF, PS...)

URL:	PM:17942672

Cancer patients treated with antiangiogenic multitargeted receptor tyrosine kinase RTK inhibitors show increased levels of plasma VEGF and placental growth factor and decreased levels of soluble VEGF receptor-2, thus implicating these overall changes as a possible class effect of such drugs and raising the possibility of their exploitation as surrogate biomarkers for pharmacodynamic drug activity/exposure and patient benefit. A postulated mechanism for these changes is that they are tumor-dependent, resulting from drug-induced decreases in vascular function, increases in tumor hypoxia, and changes in hypoxia-regulated genes. However, here we report that an identical pattern of change is observed in normal nontumor-bearing mice treated with SU11248/sunitinib, a small-molecule inhibitor of VEGF and PDGF RTKs. The changes were dose-dependent, plateaued after 4 days of consecutive treatment, reversed after discontinuation of therapy, and correlated with antitumor activity. Altered protei

BibTeX record

@article{Ebos.2007,
  abstract = {Cancer patients treated with antiangiogenic multitargeted receptor tyrosine kinase (RTK) inhibitors show increased levels of plasma VEGF and placental growth factor and decreased levels of soluble VEGF receptor-2, thus implicating these overall changes as a possible class effect of such drugs and raising the possibility of their exploitation as surrogate biomarkers for pharmacodynamic drug activity/exposure and patient benefit. A postulated mechanism for these changes is that they are tumor-dependent, resulting from drug-induced decreases in vascular function, increases in tumor hypoxia, and changes in hypoxia-regulated genes. However, here we report that an identical pattern of change is observed in normal nontumor-bearing mice treated with SU11248/sunitinib, a small-molecule inhibitor of VEGF and PDGF RTKs. The changes were dose-dependent, plateaued after 4 days of consecutive treatment, reversed after discontinuation of therapy, and correlated with antitumor activity. Altered protei},
  added-at = {2010-02-05T11:28:39.000+0100},
  author = {Ebos, J. M. and Lee, C. R. and Christensen, J. G. and Mutsaers, A. J. and Kerbel, R. S.},
  biburl = {http://www.bibsonomy.org/bibtex/2ef0f98aaa58251a4ab8b2c0be419ef9e/kanefendt},
  interhash = {f3ae59b27c9d7892da72bfc272b9d02b},
  intrahash = {ef0f98aaa58251a4ab8b2c0be419ef9e},
  journal = {Proc.Natl.Acad.Sci.U.S.A},
  keywords = {& A Administration Agents Angiogenesis Animals Antineoplastic Antitumor Assays Blood Cell Dose-Response Drug Endothelial Factor Female Growth Humans Hypoxia Indoles Inducing Line Mice Model Neoplasms Organ Outcome Placenta Pregnancy Proteins Pyrroles RANGE Receptor-2 Relationship Research Schedule Scid Specificity Treatment Tumor Tyrosine Vascular Xenograft administration blood dosage drug effects metabolism pathology pharmacology protein response therapy toxicity},
  number = 43,
  pages = {17069-17074},
  timestamp = {2010-02-05T11:28:39.000+0100},
  title = {Multiple circulating proangiogenic factors induced by sunitinib malate are tumor-independent and correlate with antitumor efficacy},
  url = {PM:17942672},
  volume = 104,
  year = 2007
}

Endnote record

%0 Journal Article
%1 Ebos.2007
%A Ebos, J. M.
%A Lee, C. R.
%A Christensen, J. G.
%A Mutsaers, A. J.
%A Kerbel, R. S.
%D 2007
%J Proc.Natl.Acad.Sci.U.S.A
%K 
%N 43
%P 17069-17074
%T Multiple circulating proangiogenic factors induced by sunitinib malate are tumor-independent and correlate with antitumor efficacy
%U PM:17942672
%V 104
%X Cancer patients treated with antiangiogenic multitargeted receptor tyrosine kinase (RTK) inhibitors show increased levels of plasma VEGF and placental growth factor and decreased levels of soluble VEGF receptor-2, thus implicating these overall changes as a possible class effect of such drugs and raising the possibility of their exploitation as surrogate biomarkers for pharmacodynamic drug activity/exposure and patient benefit. A postulated mechanism for these changes is that they are tumor-dependent, resulting from drug-induced decreases in vascular function, increases in tumor hypoxia, and changes in hypoxia-regulated genes. However, here we report that an identical pattern of change is observed in normal nontumor-bearing mice treated with SU11248/sunitinib, a small-molecule inhibitor of VEGF and PDGF RTKs. The changes were dose-dependent, plateaued after 4 days of consecutive treatment, reversed after discontinuation of therapy, and correlated with antitumor activity. Altered protei

BibSonomy :: publication ::

Multiple circulating proangiogenic factors induced by sunitinib malate are tumor-independent and correlate with antitumor efficacy

Resources (URL, PDF, PS...)

Abstract

BibTeX record

Endnote record