The DOI matches its Crossref record; 108 of the 108 references it cites were found in a registry or an index.
Redefining ALL classification: toward detecting high-risk ALL and implementing precision medicine
Open accessAbstract
Acute lymphoblastic leukemia (ALL) is the commonest childhood tumor and remains a leading cause of cancer death in the young. In the last decade, microarray and sequencing analysis of large ALL cohorts has revolutionized our understanding of the genetic basis of this disease. These studies have identified new ALL subtypes, each characterized by constellations of structural and sequence alterations that perturb key cellular pathways, including lymphoid development, cell-cycle regulation, and tumor suppression; cytokine receptor, kinase, and Ras signaling; and chromatin modifications. Several of these pathways, particularly kinase-activating lesions and epigenetic alterations, are logical targets for new precision medicine therapies. Genomic profiling has also identified important interactions between inherited genetic variants that influence the risk of leukemia development and the somatic genetic alterations that are required to establish the leukemic clone. Moreover, sequential sequencing studies at diagnosis, remission, and relapse have provided important insights into the relationship among genetic variants, clonal heterogeneity, and the risk of relapse. Ongoing studies are extending our understanding of coding and noncoding genetic alterations in B-progenitor and T-lineage ALL and using these insights to inform the development of faithful experimental models to test the efficacy of new treatment approaches.
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Cites
Recurrent Fusion of TMPRSS2 and ETS Transcription Factor Genes in Prostate Cancer
Tomlins, S. A., Rhodes, D. R., Perner, S., Dhanasekaran, S. M., Mehra, R., Sun, X.-W., Varambally, S., Cao, X., Tchinda, J., Kuefer, R., et al. (2005) · Science · doi:10.1126/science.1117679 · Cited by 3,846
Activating Mutations of NOTCH1 in Human T Cell Acute Lymphoblastic Leukemia
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Genome-wide analysis of genetic alterations in acute lymphoblastic leukaemia
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Self-citationThe genetic basis of early T-cell precursor acute lymphoblastic leukaemia
Zhang, J., Ding, L., Holmfeldt, L., Wu, G., Heatley, S. L., Payne-Turner, D., Easton, J., Chen, X., Wang, J., Rusch, M., et al. (2012) · Nature · doi:10.1038/nature10725 · Cited by 1,596 · cited 6×
“ETPALL is genetically heterogeneous,withmutation ofmultiple cellular pathways including (1) hematopoietic and lymphoid development (RUNX1, IKZF1, ETV6, GATA3, and EP300); (2) Ras, cytokine receptor, and kinase signaling (NRAS, IL7R, KRAS, JAK1, JAK3, NF1, PTPN11, and SH2B3); and (3) loss-of-function mutations targetin…”
BackgroundInfluentialSelf-citationDeletion of IKZF1 and Prognosis in Acute Lymphoblastic Leukemia
Mullighan, C. G., Su, X., Zhang, J., Radtke, I., Phillips, L. A. A., Miller, C. B., Ma, J., Liu, W., Cheng, C., Schulman, B. A., et al. (2009) · New England Journal of Medicine · doi:10.1056/nejmoa0808253 · Cited by 1,422
Self-citationTargetable Kinase-Activating Lesions in Ph-like Acute Lymphoblastic Leukemia
Roberts, K. G., Li, Y., Payne-Turner, D., Harvey, R. C., Yang, Y.-L., Pei, D., McCastlain, K., Ding, L., Lu, C., Song, G., et al. (2014) · New England Journal of Medicine · doi:10.1056/nejmoa1403088 · Cited by 1,377
Self-citationTreating Childhood Acute Lymphoblastic Leukemia without Cranial Irradiation
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Self-citationBCR–ABL1 lymphoblastic leukaemia is characterized by the deletion of Ikaros
Mullighan, C. G., Miller, C. B., Radtke, I., Phillips, L. A., Dalton, J., Ma, J., White, D., Hughes, T. P., Le Beau, M. M., Pui, C.-H., et al. (2008) · Nature · doi:10.1038/nature06866 · Cited by 1,072
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Cited by
Acute lymphoblastic leukemia: a comprehensive review and 2017 update
Terwilliger, T., & Abdul-Hay, M. (2017) · Blood Cancer Journal · doi:10.1038/bcj.2017.53 · Cited by 1,288
Jacoby, E., Nguyen, S. M., Fountaine, T. J., Welp, K., Gryder, B., Qin, H., Yang, Y., Chien, C. D., Seif, A. E., Lei, H., et al. (2016) · Nature Communications · doi:10.1038/ncomms12320 · Cited by 429
Metadata
- Authors
- Hunger, S. P., & Mullighan, C. G.
- Venue
- Blood
- Publisher
- American Society of Hematology
- Published
- 2015-06-25
- Volume
- 125
- Issue
- 26
- Pages
- 3977-3987
- ISSN
- 0006-4971 (ISSN-L)
- 1528-0020
- OpenAlex
- W1569839307
- Cited by
- 292
- References
- 108
- FWCI
- 30.09
- Type
- journal article
- Language
- en
- Open access
- green
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