Skip Navigation

JNCI Journal of the National Cancer Institute 2004 96(9):642-643; doi:10.1093/jnci/djh153
© 2004 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 ISI Web of Science
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 Search for citing articles in:
ISI Web of Science (9)
Right arrow Request Permissions
Google Scholar
Right arrow Articles by Kitada, S.
Right arrow Articles by Reed, J. C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kitada, S.
Right arrow Articles by Reed, J. C.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© 2004 Oxford University Press

EDITORIALS

MCL-1 Promoter Insertions Dial-Up Aggressiveness of Chronic Leukemia

Shinichi Kitada, John C. Reed

Affiliations of authors: The Burnham Institute, La Jolla, CA.

Correspondence to: John C. Reed, The Burnham Institute, 10901 N. Torrey Pines Rd., La Jolla, CA 92037 (e-mail: reedoffice@burnham.org)

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

Chronic lymphocytic leukemia (CLL) is the most common form of leukemia in the western world, accounting for approximately 12 000 new cases annually, and a prevalence of about 50 000 to 60 000 patients in the United States alone. CLL is a quintessential example of a human malignancy caused predominantly by defective apoptosis, as opposed to accelerated cell division. The malignant lymphocytes that accumulate in patients with CLL are largely quiescent, noncycling cells that display prolonged lifespans due to failed programmed cell death (1). Normally, a delicate balance of anti-apoptotic and pro-apoptotic genes keeps cell lifespan in check, functioning analogous to an electrical rheostat to carefully adjust the body's cell flux dial that ensures the daily production of approximately 50–70 billion cells in humans that is offset by a commensurate amount of cell . . . [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
D. Iglesias-Serret, L. Coll-Mulet, A. F. Santidrian, A. Navarro-Sabate, A. Domingo, G. Pons, and J. Gil
Re: Prognostic Significance of a Short Sequence Insertion in the MCL-1 Promoter in Chronic Lymphocytic Leukemia
J Natl Cancer Inst, July 20, 2005; 97(14): 1090 - 1091.
[Full Text] [PDF]

Home page
 BloodHome page
J. C. Reed and M. Pellecchia
Apoptosis-based therapies for hematologic malignancies
Blood, July 15, 2005; 106(2): 408 - 418.
[Abstract] [Full Text] [PDF]

Home page
 BloodHome page
T. E. Battle, J. Arbiser, and D. A. Frank
The natural product honokiol induces caspase-dependent apoptosis in B-cell chronic lymphocytic leukemia (B-CLL) cells
Blood, July 15, 2005; 106(2): 690 - 697.
[Abstract] [Full Text] [PDF]