Skip Navigation

JNCI Journal of the National Cancer Institute 2002 94(22):1660-1661; doi:10.1093/jnci/94.22.1660
© 2002 by Oxford University Press
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
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 My Personal Archive
Right arrow Download to citation manager
Right arrow Request Permissions
Google Scholar
Right arrow Articles by Druker, B. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Druker, B. J.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Journal of the National Cancer Institute, Vol. 94, No. 22, 1660-1661, November 20, 2002
© 2002 Oxford University Press

EDITORIAL

Taking Aim at Ewing's Sarcoma: Is KIT a Target and Will Imatinib Work?

Brian J. Druker

Correspondence to: Brian J. Druker, M.D., Oregon Health & Science University Cancer Institute, L592, 3181 SW Sam Jackson Park Rd., Portland, OR 97239 (e-mail: drukerb@ohsu.edu).

The first 10% of the full text of this article appears below.

Ewing's sarcoma is the second most common primary bone tumor in children. Although the cure rate for localized disease is approximately 50%, it requires intensive multiagent chemotherapy, surgery, and radiation therapy. Patients with metastatic, recurrent, or refractory disease have a much poorer prognosis. In this issue of the Journal, Merchant et al. (1) evaluate the sensitivity of Ewing's sarcoma cell lines to imatinib. Ewing's sarcoma cells express the c-KIT tyrosine kinase and stem cell factor, the ligand for this receptor, thereby closing an autocrine growth stimulatory loop (2,3). Given that c-KIT is inhibited by imatinib (4,5), it is logical to determine whether this drug inhibits the growth of these . . . [Full Text of this Article]


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 JNCI J Natl Cancer InstHome page
T. Negri, G. M. Pavan, E. Virdis, A. Greco, M. Fermeglia, M. Sandri, S. Pricl, M. A. Pierotti, S. Pilotti, and E. Tamborini
T670X KIT Mutations in Gastrointestinal Stromal Tumors: Making Sense of Missense
J Natl Cancer Inst, February 4, 2009; 101(3): 194 - 204.
[Abstract] [Full Text] [PDF]

Home page
 Ann OncolHome page
S. Ahn, B. Park, D. Noh, S. Nam, E. Lee, M. Lee, S. Kim, K. Lee, S. Park, and Y. Yun
Health-related quality of life in disease-free survivors of breast cancer with the general population
Ann. Onc., January 1, 2007; 18(1): 173 - 182.
[Abstract] [Full Text] [PDF]

Home page
 Clin. Cancer Res.Home page
E. Tamborini, L. Bonadiman, A. Greco, A. Gronchi, C. Riva, R. Bertulli, P. G. Casali, M. A. Pierotti, and S. Pilotti
Expression of Ligand-Activated KIT and Platelet-Derived Growth Factor Receptor {beta} Tyrosine Kinase Receptors in Synovial Sarcoma
Clin. Cancer Res., February 1, 2004; 10(3): 938 - 943.
[Abstract] [Full Text] [PDF]

Home page
 J. Clin. Endocrinol. Metab.Home page
C. S. Mitsiades, D. Sykoutri, C. McMullan, V. Poulaki, and N. Mitsiades
Effect of Imatinib Mesylate (Gleevec) on Anaplastic Thyroid Carcinoma Cell Lines
J. Clin. Endocrinol. Metab., October 1, 2003; 88(10): 5043 - 5044.
[Full Text] [PDF]

Home page
 JNCI J Natl Cancer InstHome page
E. Tamborini, L. Bonadiman, V. Albertini, M. A. Pierotti, and S. Pilotti
Re: Potential Use of Imatinib in Ewing's Sarcoma: Evidence for In Vitro and In Vivo Activity
J Natl Cancer Inst, July 16, 2003; 95(14): 1087 - 1088.
[Full Text] [PDF]