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 Blood, 5 February 2009, Vol. 113, No. 6, pp. 1294-1303.
Prepublished online as a Blood First Edition Paper on October 15, 2008; DOI 10.1182/blood-2008-05-158865.

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LYMPHOID NEOPLASIA

Novel genomic alterations and clonal evolution in chronic lymphocytic leukemia revealed by representational oligonucleotide microarray analysis (ROMA)

Vladimir Grubor1, Alex Krasnitz1, Jennifer E. Troge1, Jennifer L. Meth1, B. Lakshmi1, Jude T. Kendall1, Boris Yamrom1, Garrick Alex1, Deepa Pai1, Nicholas Navin1, Lisa A. Hufnagel1, Yoon-Ha Lee1, Kerry Cook1, Steven L. Allen2,3, Kanti R. Rai2,4, Rajendra N. Damle2, Carlo Calissano2, Nicholas Chiorazzi2,3, Michael Wigler1, and Diane Esposito1

1 Cold Spring Harbor Laboratory, NY; 2 The Feinstein Institute for Medical Research and 3 North Shore University Hospital, North Shore–Long Island Jewish Health System, Manhasset, NY; and 4 Long Island Jewish Medical Center, North Shore–Long Island Jewish Health System, New Hyde Park, NY

We examined copy number changes in the genomes of B cells from 58 patients with chronic lymphocytic leukemia (CLL) by using representational oligonucleotide microarray analysis (ROMA), a form of comparative genomic hybridization (CGH), at a resolution exceeding previously published studies. We observed at least 1 genomic lesion in each CLL sample and considerable variation in the number of abnormalities from case to case. Virtually all abnormalities previously reported also were observed here, most of which were indeed highly recurrent. We observed the boundaries of known events with greater clarity and identified previously undescribed lesions, some of which were recurrent. We profiled the genomes of CLL cells separated by the surface marker CD38 and found evidence of distinct subclones of CLL within the same patient. We discuss the potential applications of high-resolution CGH analysis in a clinical setting.


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Related Article in Blood Online:

ROMA illuminates CLL genomic lesions
Federico Caligaris-Cappio
Blood 2009 113: 1209-1210. [Full Text] [PDF]





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