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"Efficacy and safety of a specific
inhibitor of the BCR-ABL tyrosine kinase in chronic myeloid leukemia,"
by Brian J. Druker and 10 others, New England Journal of Medicine,
344(14): 1031-7, 5 April 2001.
[Oregon Health Sciences University, Portland;
University of Texas M.D. Anderson Cancer Center, Houston; Novartis
Pharmaceutical, East Hanover, NJ, and Basel, Switzerland; University of
California, Los Angeles]
Abstract: "Background
BCR-ABL is a constitutively activated tyrosine kinase that causes chronic
myeloid leukemia (CML). Since tyrosine kinase activity is essential to the
transforming function of BCR-ABL, an inhibitor of the kinase could be an
effective treatment for CML. Methods We conducted a phase 1
dose-escalating trial of STI571 (formerly known as CGP57148B), a specific
inhibitor of the BCR-ABL tyrosine kinase. STI571 was administered orally to 83
patients with CML in the chronic phase in whom treatment with inteferon alfa
had failed. Patients were successively assigned to 1 to 14 doses ranging from
25 to 1000 mg per day. Results Adverse effects of STI571 were minimal;
the most common were nausea, myalgias, edema, and diarrhea. A maximal
tolerated dose was not identified. Complete hematologic responses were
observed in 53 of 54 patients treated with daily doses of 300 mg or more and
typically occurred in the first four weeks of therapy. Of the 54 patients
treated with doses of 300 or more, cytogenetic responses occurred in 29,
including 17 (31 percent of the 54 patients who received this dose) with major
responses (0 to 35 percent of cells in metaphase positive for the Philadelphia
chromosome); 7 of these patients had complete cytogenetic remissions. Conclusions
STI571 is well tolerated and has significant antileukemic activity in patients
with CML in whom treatment with interferon alpha had failed. Our results
provide evidence of the essential role of BCR-ABL tyrosine kinase activity in
CML and demonstrate the potential for the development of anticancer drugs
based on the specific molecular abnormality present in a human cancer."
This 2001 report in the New England Journal of Medicine was cited 53
times in current journal articles indexed by ISI during
September-October 2002. After a slight dip in its previous citation count for
July-August, the paper now reclaims its spot as the most-cited medicine paper
published in the last two years, aside from reviews. Prior to the most recent
bimonthly count, citations to the paper have accrued as follows:
July-August 2002: 37 citations
May-June 2002: 58
March-April 2002: 45
January-February 2002: 43
November-December 2001: 29
September-October 2001: 28
July-August 2001: 8
May-June 2001: 3
March-April 2001: 3
Total citations to date: 307
SOURCE: Hot
Papers Database (Included with a subscription to the ISI print newsletter Science
Watch®, available from the ISI
Research Services Group. Packaged on a CD-ROM that is mailed with each Science
Watch issue, the Hot
Papers Database contains data on hundreds of highly cited papers published
during the last two years. User interface permits searching by author,
organization, journal, field, and more. Total citations, as well as citations
accrued during successive bimonthly periods, can be assessed and graphed. An
updated CD containing the most recent bimonthly data is mailed with every new
issue of Science
Watch,
six times a year. The CD also includes an electronic version of the Science
Watch
issue in HTML format, for personal desktop access.)
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