PMID- 8547131
OWN - NLM
STAT- MEDLINE
DCOM- 19960220
LR  - 20190705
IS  - 0007-1048 (Print)
IS  - 0007-1048 (Linking)
VI  - 91
IP  - 4
DP  - 1995 Dec
TI  - CDKN2 gene deletion is not found in chronic lymphoid leukaemias of B- and T-cell 
      origin but is frequent in acute lymphoblastic leukaemia.
PG  - 865-70
AB  - Homozygous deletions of the cyclin-dependent kinase 4 (CDK4) inhibitor gene CDKN2 
      (p16, MTS1) have been demonstrated to occur frequently in human cancer cell lines 
      of different origin. However, in most primary tumours the frequencies of CDKN2 
      deletions are not well defined. We studied primary samples of 100 patients with 
      lymphoid leukaemias [B-lineage acute lymphoblastic leukaemia (ALL), n = 23; 
      T-ALL, n = 7; B-cell chronic lymphocytic (B-CLL) or prolymphocytic (B-PLL) 
      leukaemia, n = 50; T-CLL/T-PLL, n = 20] using fluorescence in situ hybridization 
      (FISH) with eight overlapping cosmid clones covering the region on chromosome 
      band 9p21 containing CDKN2. We did not observe any CDKN2 deletions in the 70 
      patients with chronic lymphoid leukaemias of B- or T-cell origin. Of the 23 
      patients with B-lineage ALL, one (4%) exhibited a CDKN2 deletion: in this 
      patient, two clones were detected, one exhibiting a hemizygous and the other a 
      homozygous deletion. On chromosome banding analysis, four patients with B-lineage 
      ALL had a 9p aberration, whereas all CDKN2 copies were retained. In contrast, six 
      of the seven (86%) patients with T-ALL exhibited CDKN2 deletions (homozygous, n = 
      4; hemizygous, n = 2). We conclude that hemizygous or homozygous deletions of the 
      CDKN2 gene occur at high frequency in T-ALL and at low frequency in B-lineage 
      ALL, supporting the role of this gene as a tumour suppressor, especially in 
      T-ALL. However, from our data there is no evidence that CDKN2 is involved in the 
      pathogenesis of chronic lymphoid leukaemias of B- or T-cell origin.
FAU - Schroder, M
AU  - Schroder M
AD  - Medizinische Klinik und Poliklinik V, Universitat Heidelberg, Germany.
FAU - Mathieu, U
AU  - Mathieu U
FAU - Dreyling, M H
AU  - Dreyling MH
FAU - Bohlander, S K
AU  - Bohlander SK
FAU - Hagemeijer, A
AU  - Hagemeijer A
FAU - Beverloo, B H
AU  - Beverloo BH
FAU - Olopade, O I
AU  - Olopade OI
FAU - Stilgenbauer, S
AU  - Stilgenbauer S
FAU - Fischer, K
AU  - Fischer K
FAU - Bentz, M
AU  - Bentz M
AU  - et al.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Br J Haematol
JT  - British journal of haematology
JID - 0372544
RN  - 0 (Carrier Proteins)
RN  - 0 (Cyclin-Dependent Kinase Inhibitor p16)
RN  - 0 (Protein Kinase Inhibitors)
SB  - IM
MH  - Adolescent
MH  - Adult
MH  - Aged
MH  - Carrier Proteins/*genetics
MH  - Child
MH  - Child, Preschool
MH  - Cyclin-Dependent Kinase Inhibitor p16
MH  - Humans
MH  - Infant
MH  - Leukemia, B-Cell/genetics
MH  - Leukemia, T-Cell/genetics
MH  - Middle Aged
MH  - Precursor Cell Lymphoblastic Leukemia-Lymphoma/*genetics
MH  - *Protein Kinase Inhibitors
EDAT- 1995/12/01 00:00
MHDA- 1995/12/01 00:01
CRDT- 1995/12/01 00:00
PHST- 1995/12/01 00:00 [pubmed]
PHST- 1995/12/01 00:01 [medline]
PHST- 1995/12/01 00:00 [entrez]
AID - 10.1111/j.1365-2141.1995.tb05402.x [doi]
PST - ppublish
SO  - Br J Haematol. 1995 Dec;91(4):865-70. doi: 10.1111/j.1365-2141.1995.tb05402.x.