Autor: |
Perez-Andreu, Virginia, Roberts, Kathryn G., Harvey, Richard C., Yang, Wenjian, Cheng, Cheng, Pei, Deqing, Xu, Heng, Gastier-Fostier, Julie, E, Shuyu, Yew-Suang Lim, Joshua, Chen, I-Ming L., Fan, Yiping, Devidas, Meenakshi, Borowitz, Michael J., Smith, Colton, Neale, Geoffrey A., Burchard, Esteban Gonzalez, Torgerson, Dara G, Antillon, Federico, Rolando, Cesar, Winick, Naomi J., Camitta, Bruce, Raetz, Elizabeth A., Wood, Brent L., Yue, Feng, Carroll, William L., Larsen, Eric C., Bowman, William Paul, Loh, Mignon L., Dean, Michael, Bhojwani, Deepa, Pui, Ching-Hon, Evans, William E., Relling, Mary V., Hunger, Stephen P., Willman, Cheryl L., Mullighan, Charles G., Yang, Jun J. |
Zdroj: |
Blood; November 2013, Vol. 122 Issue: 21 p617-617, 1p |
Abstrakt: |
Recent genomic profiling of acute lymphoblastic leukemia (ALL) has identified a novel high-risk subtype with a gene expression signature similar to that of BCR-ABL1-positive (Ph+) ALL and a poor prognosis. This novel BCR-ABL1-like ALL subtype is characterized by genomic aberrations targeting lymphoid development, cytokine receptor, and tyrosine kinase signaling pathways, e.g., IKZF1deletion, CRLF2rearrangements, and JAKmutations. However, the role of the inherited genetic variation in the pathogenesis of BCR-ABL1-like ALL remains unknown. |
Databáze: |
Supplemental Index |
Externí odkaz: |
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