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Prepublished online as a Blood First Edition Paper on January 16, 2003; DOI 10.1182/blood-2002-09-2873.
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Blood, 15 May 2003, Vol. 101, No. 10, pp. 3849-3856
CLINICAL OBSERVATIONS, INTERVENTIONS, AND THERAPEUTIC TRIALS
Continuous absence of metaphase-defined cytogenetic
abnormalities, especially of chromosome 13 and hypodiploidy,
ensures long-term survival in multiple myeloma treated with Total
Therapy I: interpretation in the context of global gene
expression
John Shaughnessy,
Joth Jacobson,
Jeff Sawyer,
Jason McCoy,
Athanasios Fassas,
Fenghuang Zhan,
Klaus Bumm,
Joshua Epstein,
Elias Anaissie,
Sundar Jagannath,
David Vesole,
David Siegel,
Raman Desikan,
Nikhil Munshi,
Ashraf Badros,
Erming Tian,
Maurizio Zangari,
Guido Tricot,
John Crowley, and
Bart Barlogie
From the Myeloma Institute for Research and Therapy,
University of Arkansas for Medical Sciences, Little Rock, AR; Cancer
Research and Biostatistics (CRAB), Seattle, WA;
Universitats-HNO-Klinik, Erlangen, Germany; St Vincent Comprehensive
Cancer Center, New York, NY; Medical College of Wisconsin, Milwaukee,
WI; Hackensack University Medical Center, Hackensack, NJ; Dana Farber
Cancer Center, Harvard Medical Center, Boston, MA; and Greenebaum
Cancer Center, University of Maryland, Baltimore, MD.
Metaphase cytogenetic abnormalities (CAs), especially of chromosome
13 (CA 13), confer a grave prognosis in multiple myeloma even
with tandem autotransplantations as applied in Total Therapy I, which
enrolled 231 patients between 1989 and 1994. With a median follow-up of
almost 9 years, the prognostic implications of all individual
CAs, detected prior to treatment and at relapse, were investigated. Among all CAs and standard prognostic factors examined prior to therapy, only hypodiploidy and CA 13 (hypo-13 CA), alone or
in combination, were associated with shortest event-free survival and
overall survival (OS). The shortest postrelapse OS was observed with hypo-13 CA, which was newly detected in 18 of all 28 patients presenting with this abnormality at relapse. Superior prognosis was
associated with the absence of any CA at both diagnosis and relapse
(10-year OS, 40%). The lack of independent prognostic implications of
other CAs points to a uniquely aggressive behavior of hypo-13 CA
(present in 16% of patients at diagnosis). With the use of microarray
data in 146 patients enrolled in Total Therapy II,
overexpression of cell cycle genes distinguished CA from no CA,
especially in cases of del(13) detected by interphase
fluorescence in situ hybridization (FISH). FISH 13, resulting
in a haploinsufficiency of RB1 and other genes mapping to
chromosome 13, as well as activation of IGF1R, appears to
have an amplifying effect on cell cycle gene expression, thus providing
a molecular explanation for the dire outcome of patients with CA 13 compared with those with other CAs.
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