PMID- 8830719
OWN - NLM
STAT- MEDLINE
DCOM- 19961104
LR  - 20190816
IS  - 0165-4608 (Print)
IS  - 0165-4608 (Linking)
VI  - 90
IP  - 2
DP  - 1996 Sep
TI  - Trisomy 12 and p53 deletion in chronic lymphocytic leukemia detected by 
      fluorescence in situ hybridization: association with morphology and resistance to 
      conventional chemotherapy.
PG  - 118-24
AB  - The incidence of trisomy 12 and p53 deletion was studied in a group of chronic 
      B-lymphocytic leukemia (B-CLL) patients, using fluorescence in situ hybridization 
      (FISH). Trisomy 12 was detected in eight of 50 patients (16%) and p53 deletion in 
      six of 38 cases analyzed (15.8%). A statistically significant difference was 
      observed between the incidence of trisomy 12 in patients with typical and 
      atypical morphology (3.03% versus 41.18%). No correlation was found between this 
      alteration and the rest of the clinical and biological parameters studied 
      (adenopathies, hepatomegaly, splenomegaly, lymphocyte count, staging, CD11c 
      expression, and resistance to chemotherapy). The p53 deletion was correlated with 
      the presence of hepatomegaly and splenomegaly, advanced stage of disease, and 
      resistance to conventional chemotherapy. The application of FISH to whole blood 
      cell nuclei, without prior manipulation or culture, showed a higher percentage of 
      cells with trisomy 12 than when the method was used following culture. We 
      conclude that 1) FISH is a simple and sensitive technique for the detection of 
      numerical and structural chromosome abnormalities; 2) Its application to 
      uncultured samples obviates the alteration of results originated by the probable 
      growth advantage of the normal or neoplastic cell population in vitro; 3) Trisomy 
      12 appears to define a B-CLL subgroup of atypical morphology; and 4) The p53 
      deletion is correlated with advanced stage of disease and resistance to 
      treatment.
FAU - Cano, I
AU  - Cano I
AD  - Department of Hematology and Hemotherapy, Hospital La Paz, Madrid, Spain.
FAU - Martinez, J
AU  - Martinez J
FAU - Quevedo, E
AU  - Quevedo E
FAU - Pinilla, J
AU  - Pinilla J
FAU - Martin-Recio, A
AU  - Martin-Recio A
FAU - Rodriguez, A
AU  - Rodriguez A
FAU - Castaneda, A
AU  - Castaneda A
FAU - Lopez, R
AU  - Lopez R
FAU - Perez-Pino, T
AU  - Perez-Pino T
FAU - Hernandez-Navarro, F
AU  - Hernandez-Navarro F
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Cancer Genet Cytogenet
JT  - Cancer genetics and cytogenetics
JID - 7909240
RN  - 5J49Q6B70F (Vincristine)
RN  - 8N3DW7272P (Cyclophosphamide)
RN  - VB0R961HZT (Prednisone)
RN  - COP protocol 2
SB  - IM
MH  - Aged
MH  - Aged, 80 and over
MH  - Antineoplastic Combined Chemotherapy Protocols/therapeutic use
MH  - *Chromosomes, Human, Pair 12
MH  - Cosmids
MH  - Cyclophosphamide/administration & dosage
MH  - Drug Resistance, Neoplasm/*genetics
MH  - Female
MH  - *Gene Deletion
MH  - *Genes, p53
MH  - Humans
MH  - In Situ Hybridization, Fluorescence
MH  - Interphase
MH  - Leukemia, Lymphocytic, Chronic, B-Cell/drug therapy/*genetics/pathology
MH  - Lymphocytes/cytology/pathology
MH  - Male
MH  - Middle Aged
MH  - Neoplasm Staging
MH  - Prednisone/administration & dosage
MH  - Reference Values
MH  - Reproducibility of Results
MH  - Retrospective Studies
MH  - *Trisomy
MH  - Vincristine/administration & dosage
EDAT- 1996/09/01 00:00
MHDA- 1996/09/01 00:01
CRDT- 1996/09/01 00:00
PHST- 1996/09/01 00:00 [pubmed]
PHST- 1996/09/01 00:01 [medline]
PHST- 1996/09/01 00:00 [entrez]
AID - S0165460896000635 [pii]
AID - 10.1016/s0165-4608(96)00063-5 [doi]
PST - ppublish
SO  - Cancer Genet Cytogenet. 1996 Sep;90(2):118-24. doi: 
      10.1016/s0165-4608(96)00063-5.