PMID- 19887762
OWN - NLM
STAT- MEDLINE
DCOM- 20100610
LR  - 20151119
IS  - 1423-0194 (Electronic)
IS  - 0028-3835 (Linking)
VI  - 91
IP  - 2
DP  - 2010
TI  - Spectral karyotypic and comparative genomic analysis of the endocrine pancreatic 
      tumor cell line BON-1.
PG  - 131-41
LID - 10.1159/000254483 [doi]
AB  - BON-1 is a human serotonin-producing endocrine pancreatic tumor (EPT) cell line, 
      which has been used for various studies of tumorigenesis and treatment. Because 
      its genotype, phenotype and degree of differentiation may underlie events that 
      are instrumental to the development of endocrine tumors and, moreover, may vary 
      between labs and over time, we decided to comprehensively characterize the 
      chromosomal constitution of BON-1 by applying conventional GTG-banding, spectral 
      karyotyping (SKY), comparative genomic hybridization (CGH) and fluorescence in 
      situ hybridization (FISH). BON-1 cells proved to be hyperdiploid containing a 
      modal chromosome number of 57 (range 56-64). SKY identified a stemline containing 
      6 clonal aberrations including del(1p), t(9;12)del(9p)x2, der(10)t(5;10), 
      der(19)t(8;19), der(14)t(9;14)t(9;10), and a sideline harboring an additional 
      del(12q). CGH and FISH confirmed the SKY results and, in addition, highlighted 
      the chromosomal regions involved in the rearrangements. Moreover, they identified 
      a homozygous deletion of the key tumor suppressor genes CDKN2A and CDKN2B at 
      9p21.3, in accordance with absence of p16(INK4A) and p14(ARF) expression as 
      revealed by immunocytochemistry. Apart from deregulation of the cell cycle and 
      p53 pathway this finding indicates escape from replicative senescence (induced by 
      mutated NRAS) and detachment-induced apoptosis as molecular mechanisms underlying 
      the tumorigenesis of BON-1 cells. Immunostaining results for p53, MDM2 and pRb 
      expression were consistent with previously published data using Western analysis. 
      In conclusion, we provide here a comprehensive cytogenetic profile of BON-1. This 
      cell line harbors both numerical and structural genomic alterations indicative 
      for malignant EPTs.
CI  - Copyright 2009 S. Karger AG, Basel.
FAU - Lopez, Juan R
AU  - Lopez JR
AD  - Department of Medical Sciences, Uppsala University, Uppsala, Sweden.
FAU - Claessen, Sandra M H
AU  - Claessen SM
FAU - Macville, Merryn V E
AU  - Macville MV
FAU - Albrechts, Jozefa C M
AU  - Albrechts JC
FAU - Skogseid, Britt
AU  - Skogseid B
FAU - Speel, Ernst-Jan M
AU  - Speel EJ
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20091029
PL  - Switzerland
TA  - Neuroendocrinology
JT  - Neuroendocrinology
JID - 0035665
RN  - 0 (Biomarkers)
SB  - IM
MH  - Biomarkers/metabolism
MH  - Cell Cycle/genetics
MH  - Cell Line, Tumor
MH  - Chromosome Banding
MH  - Chromosome Breakage
MH  - *Comparative Genomic Hybridization
MH  - Endocrine Gland Neoplasms/*genetics
MH  - *Gene Expression Profiling
MH  - Gene Expression Regulation, Neoplastic
MH  - HeLa Cells
MH  - Humans
MH  - Immunohistochemistry
MH  - In Situ Hybridization, Fluorescence
MH  - Islets of Langerhans
MH  - Pancreatic Neoplasms/*genetics
MH  - *Spectral Karyotyping
MH  - Translocation, Genetic
EDAT- 2009/11/06 06:00
MHDA- 2010/06/11 06:00
CRDT- 2009/11/06 06:00
PHST- 2008/12/19 00:00 [received]
PHST- 2009/07/14 00:00 [accepted]
PHST- 2009/11/06 06:00 [entrez]
PHST- 2009/11/06 06:00 [pubmed]
PHST- 2010/06/11 06:00 [medline]
AID - 000254483 [pii]
AID - 10.1159/000254483 [doi]
PST - ppublish
SO  - Neuroendocrinology. 2010;91(2):131-41. doi: 10.1159/000254483. Epub 2009 Oct 29.