Hemizygous p16INK4A deletion in pediatric acute lymphoblastic leukemia predicts independent risk of relapse

Blood

Volumn 97, Issue 2, 2001, Pages 572-574

  Carter, Tina L ^b   Watt, Paul M ^b   Kumar, Rolee ^b   Burton, Paul R ^b   Reaman, Gregory H ^b   Sather, Harland N ^b   Baker, David L ^b   Kees, Ursula R ^a  

^a UNIVERSITY OF WESTERN AUSTRALIA   (Australia)

^b NONE

Author keywords

[No Author keywords available]

Indexed keywords

PROTEIN P16;

ACUTE LYMPHOBLASTIC LEUKEMIA; ARTICLE; CANCER RECURRENCE; CHILD; CHROMOSOME 9P; DIAGNOSTIC ACCURACY; DIAGNOSTIC VALUE; EXON; FEMALE; GENE DELETION; GENE LOCUS; GENETIC RISK; HEMIZYGOTE; HUMAN; INFANT; MALE; POLYMERASE CHAIN REACTION; PRIORITY JOURNAL; PROGNOSIS; QUANTITATIVE ASSAY; RISK FACTOR; TREATMENT OUTCOME;

EID: 0035863837     PISSN: 00064971     EISSN: None     Source Type: Journal    
DOI: 10.1182/blood.V97.2.572     Document Type: Article

References (15)

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4. The INK4A/ARF locus and its two gene products
5. Homozygous deletion of the p16/MTS1 gene in pediatric acute lymphoblastic leukemia is associated with unfavorable clinical outcome
6. Review of alterations of the cyclin-dependent kinase inhibitor INK4 family genes p15, p16, p18 and p19 in human leukemia-lymphoma cells
7. The prognostic significance of altered cyclin-dependent kinase inhibitors in human cancer
8. Children's Cancer Group (CCG) Initiatives in Childhood Acute Lymphoblastic Leukemia
9. Prognostic importance of p15INK4B and p16INK4 gene inactivation in childhood acute lymphocytic leukemia
10. Detection of minimal disease in hematopoietic malignancies of the B-cell lineage by using third-complementarity-determining region (CDR-III)-specific probes
11. Sensitive detection of clonal antigen receptor gene rearrangements for the diagnosis and monitoring of lymphoid neoplasms by a polymerase chain reaction-mediated ribonuclease protection assay
12. Molecular genetics, natural history and the demise of childhood leukaemia
13. INK4a/ARF mutations accelerate lymphomagenesis and promote chemoresistance by disabling p53