Absence of mutations in the CDKN2 binding site of CDK4 in childhood acute lymphoblastic leukemia

Leukemia and Lymphoma

Volumn 40, Issue 3-4, 2001, Pages 413-417

  Einsiedel, H G V ^a   Taube, T ^a   Beyermann, B ^a   Dragon, S ^a   Moricke A ^a   Kebelmann Betzig, C ^a   Kochling J ^a   Henze, G ^a   Seeger, K ^a  

^a CHARITÉ UNIVERSITÄTSMEDIZIN BERLIN   (Germany)

Author keywords

CDK4 gene; Childhood ALL; Cyclin dependent kinase inhibitor genes; Mutations

Indexed keywords

CYCLIN DEPENDENT KINASE 4; CYCLIN DEPENDENT KINASE INHIBITOR; CYCLIN DEPENDENT KINASE INHIBITOR 2; PROTEIN P15; PROTEIN P16; PROTEIN P19; RETINOBLASTOMA PROTEIN; UNCLASSIFIED DRUG;

ACUTE LYMPHOBLASTIC LEUKEMIA; ARTICLE; BINDING SITE; CELL CYCLE; CELL LINE; CHILDHOOD LEUKEMIA; CHRONIC MYELOID LEUKEMIA; CONTROLLED STUDY; ENZYME PHOSPHORYLATION; EXON; GEL ELECTROPHORESIS; GENE DELETION; GENE DISRUPTION; GENE MUTATION; HEMATOLOGY; HOMOZYGOSITY; HUMAN; HUMAN CELL; POINT MUTATION; POLYMERASE CHAIN REACTION; PRIORITY JOURNAL; PROTEIN PHOSPHORYLATION; SINGLE STRAND CONFORMATION POLYMORPHISM;

EID: 0035037933     PISSN: 10428194     EISSN: None     Source Type: Journal    
DOI: 10.3109/10428190109057941     Document Type: Article

References (28)

1. Cancer cell cycles
2. The retinoblastoma protein and cell cycle control
3. The E2F transcription factor is a cellular target for the RB protein
4. p15INK4B is a potential effector of TGF-beta-induced cell cycle arrest
5. Frequent inactivation of the retinoblastoma anti-oncogene is restricted to a subset of human tumor cells
6. Amplification and expression of the human cyclin D gene in esophageal cancer
7. CDKN2 (p16/MTS1) gene deletion or CDK4 amplification occurs in the majority of glioblastomas
8. CDK4 amplification is an alternative mechanism to p16 gene homozygous deletion in glioma cell lines
9. Novel mutations in the p16/CDKN2A binding region of the cyclin-dependent kinase-4 gene
10. Deletions of the cyclin-dependent kinase-4 inhibitor gene in multiple human cancers
11. A cell cycle regulator potentially involved in genesis of many tumor types
12. p16 gene in uncultured tumours
13. Multiple tumor-suppressor gene 1 inactivation is the most frequent genetic alteration in T-cell acute lymphoblastic leukemia
14. Analysis of a family of cyclin-dependent kinase inhibitors: P15/MTS2/INK4B, p16/MTS1/INK4A, and p18 genes in acute lymphoblastic leukemia of childhood
15. p15ink4B and p16ink4 gene inactivation in acute lymphocytic leukemia
16. Frequent and selective methylation of p15 and deletion of both p15 and p16 in T-cell acute lymphoblastic leukemia
17. Hypermethylation-associated inactivation indicates a tumor suppressor role for p15INK4B
18. Review of alterations of the cyclin-dependent kinase inhibitor INK4 family genes p15, p16, p18 and p19 in human leukemia-lymphoma cells
19. Germline mutations in the p16INK4a binding domain of CDK4 in familial melanoma
20. A p16INK4a-insensitive CDK4 mutant targeted by cytolytic T lymphocytes in a human melanoma
21. Complete scanning of the CDK4 gene by denaturing gradient gel electrophoresis: A novel missense mutation but low overall frequency of mutations in sporadic metastatic malignant melanoma
22. Prevalence of p16 and CDK4 germline mutations in 48 melanoma-prone families in France
23. Chemotherapy in 998 unselected childhood acute lymphoblastic leukemia patients. Results and conclusions of the multicenter trial ALL-BFM 86
24. Six-year experience with a comprehensive approach to the treatment of recurrent childhood acute lymphoblastic leukemia (ALL-REZ BFM 85). A relapse study of the BFM group
25. Multiplex PCR for simultaneous detection of the most frequent T cell receptor-delta gene rearrangements in childhood ALL
26. Prevalence of germ-line mutations in p16, p19ARF, and CDK4 in familial melanoma: Analysis of a clinic-based population
27. Analysis of the CDKN2A, CDKN2B and CDK4 genes in 48 Australian melanoma kindreds
28. p16/CDKN2 and CDK4 gene mutations in sporadic melanoma development and progression