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A Call to Action for Acute Lymphoblastic Leukemia
by
Graubert, Timothy A
in
Acute lymphoblastic leukemia
/ Animals
/ BCR-ABL protein
/ Children
/ Children & youth
/ Cytokines
/ Female
/ Fusion protein
/ Gene expression
/ Humans
/ Kinases
/ Leukemia
/ Lymphatic leukemia
/ Lymphocytes B
/ Male
/ Mutation
/ Patients
/ Precursor B-Cell Lymphoblastic Leukemia-Lymphoma - genetics
/ Prognosis
/ Protein Kinase Inhibitors - therapeutic use
/ Protein-tyrosine kinase
/ Toxicity
/ Young adults
2014
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A Call to Action for Acute Lymphoblastic Leukemia
by
Graubert, Timothy A
in
Acute lymphoblastic leukemia
/ Animals
/ BCR-ABL protein
/ Children
/ Children & youth
/ Cytokines
/ Female
/ Fusion protein
/ Gene expression
/ Humans
/ Kinases
/ Leukemia
/ Lymphatic leukemia
/ Lymphocytes B
/ Male
/ Mutation
/ Patients
/ Precursor B-Cell Lymphoblastic Leukemia-Lymphoma - genetics
/ Prognosis
/ Protein Kinase Inhibitors - therapeutic use
/ Protein-tyrosine kinase
/ Toxicity
/ Young adults
2014
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Do you wish to request the book?
A Call to Action for Acute Lymphoblastic Leukemia
by
Graubert, Timothy A
in
Acute lymphoblastic leukemia
/ Animals
/ BCR-ABL protein
/ Children
/ Children & youth
/ Cytokines
/ Female
/ Fusion protein
/ Gene expression
/ Humans
/ Kinases
/ Leukemia
/ Lymphatic leukemia
/ Lymphocytes B
/ Male
/ Mutation
/ Patients
/ Precursor B-Cell Lymphoblastic Leukemia-Lymphoma - genetics
/ Prognosis
/ Protein Kinase Inhibitors - therapeutic use
/ Protein-tyrosine kinase
/ Toxicity
/ Young adults
2014
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Journal Article
A Call to Action for Acute Lymphoblastic Leukemia
2014
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Overview
The cure rates for precursor B-cell acute lymphoblastic leukemia (ALL) among children have improved, but the prognosis for older patients and children with relapsed disease remains poor. Risk stratification based on clinical features and disease characteristics can improve outcomes by enabling physicians to reduce the toxicity of therapy for patients with lower-risk disease and intensify therapy for patients with higher-risk disease. The negative prognosis associated with the t(9;22) translocation, which results in expression of the BCR–ABL1 activated kinase fusion protein, is attenuated by treatment that includes tyrosine kinase inhibitors, providing a paradigm for molecularly guided therapy in patients with precursor . . .
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