PMID- 11170283
OWN - NLM
STAT- MEDLINE
DCOM- 20010412
LR  - 20191025
IS  - 1045-2257 (Print)
IS  - 1045-2257 (Linking)
VI  - 30
IP  - 3
DP  - 2001 Mar
TI  - Isodicentric 7p, idic(7)(q11.2), in acute myeloid leukemia associated with older 
      age and favorable response to induction chemotherapy: a new clinical entity?
PG  - 261-6
AB  - Three adult de novo acute myeloid leukemias (AML M1, M2, and M4) with an 
      isochromosome 7p are presented. No additional abnormalities were detected by 
      G-band and multicolor, using combined binary ratio labeling, fluorescence in situ 
      hybridization (FISH) analyses, indicating that the i(7p) was the sole, i.e., the 
      primary, chromosomal aberration. Although the patients were elderly--68, 72, and 
      78 years old--they all responded very well to chemotherapy, achieving complete 
      remission lasting more than a year. Further FISH analyses, using painting, 
      centromeric, as well as 7q11.2-specific YAC probes, revealed that the i(7p) 
      contained two centromeres and that the breakpoints were located in 7q11.2. Thus, 
      the abnormality should formally be designated idic(7)(q11.2). The detailed 
      mapping disclosed a breakpoint heterogeneity, with the breaks in 7q11.2 varying 
      among the cases, being at least 1,310 kb apart. Furthermore, the breakpoints also 
      differed within one of the cases, being located on both the proximal and the 
      distal side of the most centromeric probe used. Based on our three patients, as 
      well as on a previously reported 82-year-old patient with AML M2 and idic(7)(q11) 
      as the only chromosomal change, we suggest that this abnormality, as the sole 
      anomaly, is associated with AML in elderly patients who display a good response 
      to induction chemotherapy and, hence, have a favorable prognosis. Furthermore, 
      the heterogeneous breakpoints in 7q11.2 suggest that the important functional 
      outcome of the idic(7)(q11.2) is the genomic imbalance incurred, i.e., gain of 7p 
      and loss of 7q material, rather than a rearrangement of a specific gene.
CI  - Copyright 2000 Wiley-Liss, Inc.
FAU - Johansson, B
AU  - Johansson B
AD  - Department of Clinical Genetics, Lund University Hospital, Sweden. 
      bertil.johansson@klingen.lu.se
FAU - Axelsson, P
AU  - Axelsson P
FAU - Billstrom, R
AU  - Billstrom R
FAU - Strombeck, B
AU  - Strombeck B
FAU - Arheden, K
AU  - Arheden K
FAU - Olofsson, T
AU  - Olofsson T
FAU - Cervin, A
AU  - Cervin A
FAU - Adriansson, M
AU  - Adriansson M
FAU - Tanke, H J
AU  - Tanke HJ
FAU - Mitelman, F
AU  - Mitelman F
FAU - Fioretos, T
AU  - Fioretos T
LA  - eng
PT  - Case Reports
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Genes Chromosomes Cancer
JT  - Genes, chromosomes & cancer
JID - 9007329
RN  - 0 (Antimetabolites, Antineoplastic)
RN  - 04079A1RDZ (Cytarabine)
RN  - FTK8U1GZNX (Thioguanine)
RN  - ZRP63D75JW (Idarubicin)
RN  - LAI regimen
SB  - IM
MH  - Aged
MH  - Aged, 80 and over
MH  - Aging/*genetics
MH  - Antimetabolites, Antineoplastic/therapeutic use
MH  - Antineoplastic Combined Chemotherapy Protocols/therapeutic use
MH  - Chromosome Banding
MH  - Chromosomes, Human, Pair 7/*genetics
MH  - Cytarabine/therapeutic use
MH  - Female
MH  - Humans
MH  - Idarubicin/therapeutic use
MH  - In Situ Hybridization, Fluorescence/methods
MH  - Isochromosomes/*genetics
MH  - Leukemia, Myeloid, Acute/*drug therapy/*genetics
MH  - Leukemia, Myelomonocytic, Acute/drug therapy/genetics
MH  - Male
MH  - Remission Induction
MH  - Thioguanine/therapeutic use
EDAT- 2001/02/15 11:00
MHDA- 2001/04/17 10:01
CRDT- 2001/02/15 11:00
PHST- 2001/02/15 11:00 [pubmed]
PHST- 2001/04/17 10:01 [medline]
PHST- 2001/02/15 11:00 [entrez]
AID - 10.1002/1098-2264(2000)9999:9999<::AID-GCC1087>3.0.CO;2-A [pii]
AID - 10.1002/1098-2264(2000)9999:9999<::aid-gcc1087>3.0.co;2-a [doi]
PST - ppublish
SO  - Genes Chromosomes Cancer. 2001 Mar;30(3):261-6. doi: 
      10.1002/1098-2264(2000)9999:9999<::aid-gcc1087>3.0.co;2-a.