<i>SF3B1</i> and Other Novel Cancer Genes in Chronic Lymphocytic Leukemia

Lili Wang(Dana-Farber Cancer Institute), Michael S. Lawrence(Broad Institute), Youzhong Wan(Dana-Farber Cancer Institute), Petar Stojanov(Broad Institute), Carrie Sougnez(Broad Institute), Kristen Stevenson(Dana-Farber Cancer Institute), Lillian Werner(Dana-Farber Cancer Institute), Andrey Sivachenko(Broad Institute), David S. DeLuca(Broad Institute), Li Zhang(Dana-Farber Cancer Institute), Wandi Zhang(Dana-Farber Cancer Institute), Alexander R. Vartanov(Dana-Farber Cancer Institute), Stacey M. Fernandes(Dana-Farber Cancer Institute), Natalie R. Goldstein(Dana-Farber Cancer Institute), Eric G. Folco(Harvard University), Kristian Cibulskis(Broad Institute), Bethany Tesar(Dana-Farber Cancer Institute), Quinlan Sievers(Dana-Farber Cancer Institute), Erica Shefler(Broad Institute), Stacey Gabriel(Broad Institute), Nir Hacohen(Broad Institute), Robin Reed(Harvard University), Matthew Meyerson(Broad Institute), Todd R. Golub(Broad Institute), Eric S. Lander(Broad Institute), Donna Neuberg(Dana-Farber Cancer Institute), Jennifer R. Brown(Brigham and Women's Hospital), Gad Getz(Broad Institute), Catherine J. Wu(Brigham and Women's Hospital)
New England Journal of Medicine
December 12, 2011
Cited by 1,065Open Access
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Abstract

BACKGROUND: The somatic genetic basis of chronic lymphocytic leukemia, a common and clinically heterogeneous leukemia occurring in adults, remains poorly understood. METHODS: We obtained DNA samples from leukemia cells in 91 patients with chronic lymphocytic leukemia and performed massively parallel sequencing of 88 whole exomes and whole genomes, together with sequencing of matched germline DNA, to characterize the spectrum of somatic mutations in this disease. RESULTS: Nine genes that are mutated at significant frequencies were identified, including four with established roles in chronic lymphocytic leukemia (TP53 in 15% of patients, ATM in 9%, MYD88 in 10%, and NOTCH1 in 4%) and five with unestablished roles (SF3B1, ZMYM3, MAPK1, FBXW7, and DDX3X). SF3B1, which functions at the catalytic core of the spliceosome, was the second most frequently mutated gene (with mutations occurring in 15% of patients). SF3B1 mutations occurred primarily in tumors with deletions in chromosome 11q, which are associated with a poor prognosis in patients with chronic lymphocytic leukemia. We further discovered that tumor samples with mutations in SF3B1 had alterations in pre-messenger RNA (mRNA) splicing. CONCLUSIONS: Our study defines the landscape of somatic mutations in chronic lymphocytic leukemia and highlights pre-mRNA splicing as a critical cellular process contributing to chronic lymphocytic leukemia.


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