An 11-year-old male patient with the deletion of <i>IKZF1</i> (Ikaros family zinc finger 1) and positive Breakpoint Cluster Region-C-Abelson oncogene 1(<i>BCR-ABL1</i>) acute lymphoblastic leukemia developed mucositis, gastrointestinal toxicity, hepatotoxicity, myelosuppression, and severe dermatologic toxicity during the first and second courses of high-dose methotrexate.
By contrast, the MRD15 was higher in Ikaros family Zinc Finger Protein 1 (<i>IKZF1)</i>-deleted BCP-ALL patients than in BCP-ALL patients without <i>IKZF1</i> deletions [1.18% (0.06-12.0%) vs 0.33% (0.03-2.6%); p=0.003].
Intensifying Treatment of Childhood B-Lymphoblastic Leukemia With IKZF1 Deletion Reduces Relapse and Improves Overall Survival: Results of Malaysia-Singapore ALL 2010 Study.
Tumor suppressors BTG1 and IKZF1 cooperate during mouse leukemia development and increase relapse risk in B-cell precursor acute lymphoblastic leukemia patients.
Genetic alterations of the transcription factor IKZF1 ("IKAROS") are detected in around 15-30% of cases of <i>BCR-ABL</i>-negative B-cell precursor acute lymphoblastic leukemia.
The genomic profile of ETV6-ABL1 acute lymphoblastic leukemia resembled that of BCR-ABL1 and BCR-ABL1-like cases with 80% of patients having concurrent CDKN2A/B and IKZF1 deletions.
IKAROS family zinc finger 1/IKZF1 is a transcription factor important in lymphoid differentiation, and a known tumor suppressor in acute lymphoid leukemia.
We performed a comprehensive analysis of the impact of IKZF1(del) in a large cohort of children (n=1223) with BCR-ABL1-negative BCP-ALL treated in the EORTC-CLG trial 58951.