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Targetable Kinase-Activating Lesions in Ph-like Acute Lymphoblastic Leukemia

2014; Massachusetts Medical Society; Volume: 371; Issue: 11 Linguagem: Inglês

10.1056/nejmoa1403088

1533-4406

Kathryn G. Roberts, Yongjin Li, Debbie Payne-Turner, Richard C. Harvey, Yung‐Li Yang, Deqing Pei, Kelly McCastlain, Li Ding, Charles Lu, Guangchun Song, Jing Ma, Jared Becksfort, Michael Rusch, Shann-Ching Chen, John Easton, Jinjun Cheng, Kristy Boggs, Natalia Santiago-Morales, Ilaria Iacobucci, Robert S. Fulton, Ji Wen, Marcus Valentine, Cheng Cheng, Steven W. Paugh, Meenakshi Devidas, I‐Ming Chen, Shalini C. Reshmi, Amy Smith, Erin Hedlund, Pankaj Gupta, Panduka Nagahawatte, Gang Wu, Xiang Chen, Donald Yergeau, Bhavin Vadodaria, Heather L. Mulder, Naomi J. Winick, Eric Larsen, William L. Carroll, Nyla A. Heerema, Andrew J. Carroll, Guy H. Grayson, Sarah K. Tasian, Andrew S. Moore, Frank Keller, Melissa Frei‐Jones, James A. Whitlock, Elizabeth A. Raetz, Deborah L. White, Timothy P. Hughes, Jaime M. Guidry Auvil, Malcolm A. Smith, Guido Marcucci, Clara D. Bloomfield, Krzysztof Mrózek, Jessica Kohlschmidt, Wendy Stock, Steven M. Kornblau, Marina Konopleva, Elisabeth Paietta, Ching‐Hon Pui, Sima Jeha, Mary V. Relling, William E. Evans, Daniela S. Gerhard, Julie M. Gastier-Foster, Elaine R. Mardis, Richard K. Wilson, Mignon L. Loh, James R. Downing, Stephen P. Hunger, Cheryl L. Willman, Jinghui Zhang, Charles G. Mullighan,

Childhood Cancer Survivors' Quality of Life

Philadelphia chromosome–like acute lymphoblastic leukemia (Ph-like ALL) is characterized by a gene-expression profile similar to that of BCR–ABL1–positive ALL, alterations of lymphoid transcription factor genes, and a poor outcome. The frequency and spectrum of genetic alterations in Ph-like ALL and its responsiveness to tyrosine kinase inhibition are undefined, especially in adolescents and adults.