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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.
[Authors' affiliations: 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 signficant 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 58 times in current journal articles indexed
by ISI during May-June 2002. Continuing its streak at the top of
the medicine rolls, this paper emerges after yet another two-month
tally as the most-cited medicine paper published in the last two
years, excluding reviews. Prior to the most recent bimonthly
count, citations to the paper have accrued as follows:
March-April 2002: 45 citations
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: 217
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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