PMID- 15949564
OWN - NLM
STAT- MEDLINE
DCOM- 20050721
LR  - 20161124
IS  - 0165-4608 (Print)
IS  - 0165-4608 (Linking)
VI  - 160
IP  - 1
DP  - 2005 Jul 1
TI  - Molecular cytogenetic analysis of chromosomes 1 and 19 in glioma cell lines.
PG  - 1-14
AB  - Deletions of chromosome 1p and 19q arms are frequent genetic abnormalities in 
      primary human gliomas and are especially common in oligodendrogliomas. However, 
      the chromosome 1p and 19q status of many glioma cell lines has not been 
      established. Using homozygosity mapping, fluorescence in situ hybridization 
      (FISH), and comparative genomic hybridization to arrayed BAC (CGHa), we screened 
      17 glioma cell lines for chromosome 1 and 19 deletions. Sequence tagged site 
      polymorphisms were used to evaluate the cell lines for regions of chromosome 1p 
      and 19q homozygosity. Cell lines A172, U251, TP265, U118, SW1088, U87, SW1783, 
      and D32 contained significant regions of 19q homozygosity. In addition, A172, 
      U87, TP483, D37, U118, MO67, and TP265 contained significant regions of 1p 
      homozygosity. FISH probes localized to 1p36.32 and 19q13.33 as well as CGHa were 
      used to determine which cell lines had deletions of 1p and/or 19q. Cell lines 
      A172, U87, TP483, TP265, H4, U251, and D37 were deleted for portions of 1p. CGHa 
      and homozygosity mapping of these cell lines define a 700-kilobase (Kb) common 
      deletion region that is encompassed by a larger deletion region previously mapped 
      in sporadic gliomas. This common deletion region is localized at 1p36.31 and 
      includes CHD5, a putative tumor suppressor gene. Cell line A172 was observed to 
      have a deletion between 19q13.33 and 19q13.41, while U87 was observed to have a 
      smaller deletion of 19q13.33. Cell lines A172 and U87 contain 1p and 19q 
      deletions similar to those found in sporadic gliomas and will be useful cellular 
      reagents for evaluating the function of putative 1p and 19q glioma tumor 
      suppressor genes.
FAU - Law, Mark E
AU  - Law ME
AD  - Department of Laboratory Medicine and Pathology, Division of Laboratory Genetics, 
      Mayo Clinic and Foundation, 200 First Street SW, Rochester, MN 55905, USA.
FAU - Templeton, Kristen L
AU  - Templeton KL
FAU - Kitange, Gaspar
AU  - Kitange G
FAU - Smith, Justin
AU  - Smith J
FAU - Misra, Anjan
AU  - Misra A
FAU - Feuerstein, Burt G
AU  - Feuerstein BG
FAU - Jenkins, Robert B
AU  - Jenkins RB
LA  - eng
GR  - CA85799/CA/NCI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Cancer Genet Cytogenet
JT  - Cancer genetics and cytogenetics
JID - 7909240
RN  - 0 (Tumor Suppressor Proteins)
RN  - EC 3.1.3.2 (Phosphoric Monoester Hydrolases)
RN  - EC 3.1.3.67 (PTEN Phosphohydrolase)
RN  - EC 3.1.3.67 (PTEN protein, human)
SB  - IM
MH  - Cell Line, Tumor
MH  - *Chromosomes, Human, Pair 1
MH  - *Chromosomes, Human, Pair 19
MH  - Glioma/*genetics
MH  - Humans
MH  - In Situ Hybridization, Fluorescence
MH  - *Loss of Heterozygosity
MH  - PTEN Phosphohydrolase
MH  - Phosphoric Monoester Hydrolases/genetics
MH  - Polymerase Chain Reaction
MH  - Tumor Suppressor Proteins/genetics
EDAT- 2005/06/14 09:00
MHDA- 2005/07/22 09:00
CRDT- 2005/06/14 09:00
PHST- 2004/10/12 00:00 [received]
PHST- 2004/11/16 00:00 [revised]
PHST- 2004/11/19 00:00 [accepted]
PHST- 2005/06/14 09:00 [pubmed]
PHST- 2005/07/22 09:00 [medline]
PHST- 2005/06/14 09:00 [entrez]
AID - S0165-4608(04)00583-7 [pii]
AID - 10.1016/j.cancergencyto.2004.11.012 [doi]
PST - ppublish
SO  - Cancer Genet Cytogenet. 2005 Jul 1;160(1):1-14. doi: 
      10.1016/j.cancergencyto.2004.11.012.