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Author |
Jan, M.; Majeti, R. |
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Title |
Clonal evolution of acute leukemia genomes |
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Journal Article |
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Year |
2012 |
Publication |
Oncogene |
Abbreviated Journal |
Oncogene |
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Abstract |
In large part, cancer results from the accumulation of multiple mutations in a single cell lineage that are sequentially acquired and subject to an evolutionary process where selection drives the expansion of more fit subclones. Owing to the technical challenge of distinguishing and isolating distinct cancer subclones, many aspects of this clonal evolution are poorly understood, including the diversity of different subclones in an individual cancer, the nature of the subclones contributing to relapse, and the identity of pre-cancerous mutations. These issues are not just important to our understanding of cancer biology, but are also clinically important given the need to understand the nature of subclones responsible for the refractory and relapsed disease that cause significant morbidity and mortality in patients. Recently, advanced genomic techniques have been used to investigate clonal diversity and evolution in acute leukemia. Studies of pediatric acute lymphoblastic leukemia (ALL) demonstrated that in individual patients there are multiple genetic subclones of leukemia-initiating cells, with a complex clonal architecture. Separate studies also investigating pediatric ALL determined that the clonal basis of relapse was variable and complex, with relapse often evolving from a clone ancestral to the predominant de novo leukemia clone. Additional studies in both ALL and acute myeloid leukemia have identified pre-leukemic mutations in some individual cases. This review will highlight these recent reports investigating the clonal evolution of acute leukemia genomes and discuss the implications for clinical therapy.Oncogene advance online publication, 20 February 2012; doi:10.1038/onc.2012.48. |
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Address |
1] Department of Medicine, Division of Hematology, Cancer Institute, Stanford University School of Medicine, Palo Alto, CA, USA [2] Stanford Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Palo Alto, CA, USA [3] Program in Cancer Biology, Cancer Institute, Stanford University School of Medicine, Palo Alto, CA, USA |
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0950-9232 |
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PMID:22349821 |
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CBM.UAM @ ccobaleda @ |
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236 |
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Author |
Meyer, J.A.; Wang, J.; Hogan, L.E.; Yang, J.J.; Dandekar, S.; Patel, J.P.; Tang, Z.; Zumbo, P.; Li, S.; Zavadil, J.; Levine, R.L.; Cardozo, T.; Hunger, S.P.; Raetz, E.A.; Evans, W.E.; Morrison, D.J.; Mason, C.E.; Carroll, W.L. |
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Title |
Relapse-specific mutations in NT5C2 in childhood acute lymphoblastic leukemia |
Type |
Journal Article |
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Year |
2013 |
Publication |
Nature Genetics |
Abbreviated Journal |
Nat Genet |
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Relapsed childhood acute lymphoblastic leukemia (ALL) carries a poor prognosis, despite intensive retreatment, owing to intrinsic drug resistance. The biological pathways that mediate resistance are unknown. Here, we report the transcriptome profiles of matched diagnosis and relapse bone marrow specimens from ten individuals with pediatric B-lymphoblastic leukemia using RNA sequencing. Transcriptome sequencing identified 20 newly acquired, novel nonsynonymous mutations not present at initial diagnosis, with 2 individuals harboring relapse-specific mutations in the same gene, NT5C2, encoding a 5'-nucleotidase. Full-exon sequencing of NT5C2 was completed in 61 further relapse specimens, identifying additional mutations in 5 cases. Enzymatic analysis of mutant proteins showed that base substitutions conferred increased enzymatic activity and resistance to treatment with nucleoside analog therapies. Clinically, all individuals who harbored NT5C2 mutations relapsed early, within 36 months of initial diagnosis (P = 0.03). These results suggest that mutations in NT5C2 are associated with the outgrowth of drug-resistant clones in ALL. |
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1] New York University Cancer Institute, New York University Langone Medical Center, New York, New York, USA. [2] Department of Pathology, New York University Langone Medical Center, New York, New York, USA |
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1061-4036 |
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PMID:23377183 |
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CBM.UAM @ ccobaleda @ |
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239 |
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Holmfeldt, L.; Wei, L.; Diaz-Flores, E.; Walsh, M.; Zhang, J.; Ding, L.; Payne-Turner, D.; Churchman, M.; Andersson, A.; Chen, S.-C.; McCastlain, K.; Becksfort, J.; Ma, J.; Wu, G.; Patel, S.N.; Heatley, S.L.; Phillips, L.A.; Song, G.; Easton, J.; Parker, M.; Chen, X.; Rusch, M.; Boggs, K.; Vadodaria, B.; Hedlund, E.; Drenberg, C.; Baker, S.; Pei, D.; Cheng, C.; Huether, R.; Lu, C.; Fulton, R.S.; Fulton, L.L.; Tabib, Y.; Dooling, D.J.; Ochoa, K.; Minden, M.; Lewis, I.D.; To, L.B.; Marlton, P.; Roberts, A.W.; Raca, G.; Stock, W.; Neale, G.; Drexler, H.G.; Dickins, R.A.; Ellison, D.W.; Shurtleff, S.A.; Pui, C.-H.; Ribeiro, R.C.; Devidas, M.; Carroll, A.J.; Heerema, N.A.; Wood, B.; Borowitz, M.J.; Gastier-Foster, J.M.; Raimondi, S.C.; Mardis, E.R.; Wilson, R.K.; Downing, J.R.; Hunger, S.P.; Loh, M.L.; Mullighan, C.G. |
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Title |
The genomic landscape of hypodiploid acute lymphoblastic leukemia |
Type |
Journal Article |
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Year |
2013 |
Publication |
Nature Genetics |
Abbreviated Journal |
Nat Genet |
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The genetic basis of hypodiploid acute lymphoblastic leukemia (ALL), a subtype of ALL characterized by aneuploidy and poor outcome, is unknown. Genomic profiling of 124 hypodiploid ALL cases, including whole-genome and exome sequencing of 40 cases, identified two subtypes that differ in the severity of aneuploidy, transcriptional profiles and submicroscopic genetic alterations. Near-haploid ALL with 24-31 chromosomes harbor alterations targeting receptor tyrosine kinase signaling and Ras signaling (71%) and the lymphoid transcription factor gene IKZF3 (encoding AIOLOS; 13%). In contrast, low-hypodiploid ALL with 32-39 chromosomes are characterized by alterations in TP53 (91.2%) that are commonly present in nontumor cells, IKZF2 (encoding HELIOS; 53%) and RB1 (41%). Both near-haploid and low-hypodiploid leukemic cells show activation of Ras-signaling and phosphoinositide 3-kinase (PI3K)-signaling pathways and are sensitive to PI3K inhibitors, indicating that these drugs should be explored as a new therapeutic strategy for this aggressive form of leukemia. |
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1] Department of Pathology, St. Jude Children's Research Hospital, Memphis, Tennessee, USA. [2] |
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1061-4036 |
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PMID:23334668 |
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CBM.UAM @ ccobaleda @ |
Serial |
240 |
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Author |
Li, M.; Jones, L.; Gaillard, C.; Binnewies, M.; Ochoa, R.; Garcia, E.; Lam, V.; Wei, G.; Yang, W.; Lobe, C.; Hermiston, M.; Passegue, E.; Kogan, S.C. |
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Title |
Initially disadvantaged, TEL-AML1 cells expand and initiate leukemia in response to irradiation and cooperating mutations |
Type |
Journal Article |
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Year |
2013 |
Publication |
Leukemia : Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K |
Abbreviated Journal |
Leukemia |
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Address |
Helen Diller Family Comprehensive Cancer Center and Department of Laboratory Medicine, University of California, San Francisco, CA, USA |
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0887-6924 |
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PMID:23443342 |
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CBM.UAM @ ccobaleda @ |
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241 |
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Author |
Schuz, J.; Grell, K.; Kinsey, S.; Linet, M.S.; Link, M.P.; Mezei, G.; Pollock, B.H.; Roman, E.; Zhang, Y.; McBride, M.L.; Johansen, C.; Spix, C.; Hagihara, J.; Saito, A.M.; Simpson, J.; Robison, L.L.; Dockerty, J.D.; Feychting, M.; Kheifets, L.; Frederiksen, K. |
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Title |
Extremely low-frequency magnetic fields and survival from childhood acute lymphoblastic leukemia: an international follow-up study |
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Journal Article |
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Year |
2012 |
Publication |
Blood Cancer Journal |
Abbreviated Journal |
Blood Cancer J |
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2 |
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e98 |
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Abstract |
A previous US study reported poorer survival in children with acute lymphoblastic leukemia (ALL) exposed to extremely low-frequency magnetic fields (ELF-MF) above 0.3 muT, but based on small numbers. Data from 3073 cases of childhood ALL were pooled from prospective studies conducted in Canada, Denmark, Germany, Japan, UK and US to determine death or relapse up to 10 years from diagnosis. Adjusting for known prognostic factors, we calculated hazard ratios (HRs) and 95% confidence intervals (CI) for overall survival and event-free survival for ELF-MF exposure categories and by 0.1 muT increases. The HRs by 0.1 muT increases were 1.00 (CI, 0.93-1.07) for event-free survival analysis and 1.04 (CI, 0.97-1.11) for overall survival. ALL cases exposed to >0.3 muT did not have a poorer event-free survival (HR=0.76; CI, 0.44-1.33) or overall survival (HR=0.96; CI, 0.49-1.89). HRs varied little by subtype of ALL. In conclusion, ELF-MF exposure has no impact on the survival probability or risk of relapse in children with ALL. |
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1] Section of Environment and Radiation, International Agency for Research on Cancer (IARC), Lyon, France [2] Institute of Cancer Epidemiology, Danish Cancer Society, Copenhagen, Denmark |
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2044-5385 |
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PMID:23262804 |
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CBM.UAM @ ccobaleda @ |
Serial |
242 |
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