PMID- 15860351
OWN - NLM
STAT- MEDLINE
DCOM- 20050609
LR  - 20211203
IS  - 0165-4608 (Print)
IS  - 0165-4608 (Linking)
VI  - 159
IP  - 1
DP  - 2005 May
TI  - AURKA amplification, chromosome instability, and centrosome abnormality in human 
      pancreatic carcinoma cells.
PG  - 10-7
AB  - To test the hypothesis that AURKA amplification contributes to pancreatic 
      tumorigenesis by increasing centrosome abnormality and chromosome instability, 
      the current study explored the associations between AURKA amplification, 
      chromosome instability, centrosome abnormality, and the expression of several 
      important proteins that are involved in cell proliferation (Ki-67), cell cycle 
      regulation (p53, p16), and apoptosis (survivin) in 12 human pancreatic carcinoma 
      cell lines. Using fluorescence in situ hybridization (FISH), we observed that 5 
      of the 12 cell lines had an AURKA amplification index (AI) (percentage of cells 
      with more than three signals) >60%. Both the AURKA AI and the average number of 
      signals per cell (ANSPC) were significantly associated with the copy number of 
      chromosome 9 but not chromosome 17. The AURKA ANSPC was positively associated 
      with the percentage of cells with the centrosome abnormality. Furthermore, 
      centrosome abnormality was significantly associated with the frequency of cells 
      with abnormal nuclei and abnormal mitotic figures, but no direct association was 
      detected between the frequency of centrosome abnormalities and chromosome 
      instabilities. The AURKA AI was also associated with a lower expression of Ki-67, 
      a higher expression of survivin, and the lack of expression of p16. These 
      associations support our hypothesis that AURKA amplification contributes to 
      pancreatic carcinogenesis by increasing chromosome instability and centrosome 
      abnormality.
FAU - Zhu, Jijiang
AU  - Zhu J
AD  - Department of Gastrointestinal Medical Oncology, The University of Texas M.D. 
      Anderson Cancer Center, Houston, TX 77030, USA.
FAU - Abbruzzese, James L
AU  - Abbruzzese JL
FAU - Izzo, Julie
AU  - Izzo J
FAU - Hittelman, Walter N
AU  - Hittelman WN
FAU - Li, Donghui
AU  - Li D
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PL  - United States
TA  - Cancer Genet Cytogenet
JT  - Cancer genetics and cytogenetics
JID - 7909240
RN  - 0 (BIRC5 protein, human)
RN  - 0 (Cyclin-Dependent Kinase Inhibitor p16)
RN  - 0 (Inhibitor of Apoptosis Proteins)
RN  - 0 (Ki-67 Antigen)
RN  - 0 (Microtubule-Associated Proteins)
RN  - 0 (Neoplasm Proteins)
RN  - 0 (Survivin)
RN  - 0 (Tumor Suppressor Protein p53)
RN  - EC 2.7.11.1 (AURKA protein, human)
RN  - EC 2.7.11.1 (Aurora Kinase A)
RN  - EC 2.7.11.1 (Aurora Kinases)
RN  - EC 2.7.11.1 (Protein Serine-Threonine Kinases)
SB  - IM
MH  - Aurora Kinase A
MH  - Aurora Kinases
MH  - *Centrosome
MH  - *Chromosomal Instability
MH  - Chromosomes, Human, Pair 17/genetics
MH  - Chromosomes, Human, Pair 3/genetics
MH  - Cyclin-Dependent Kinase Inhibitor p16/metabolism
MH  - *Gene Amplification
MH  - Humans
MH  - In Situ Hybridization, Fluorescence
MH  - Inhibitor of Apoptosis Proteins
MH  - Ki-67 Antigen/metabolism
MH  - Microtubule-Associated Proteins/metabolism
MH  - Neoplasm Proteins
MH  - Pancreatic Neoplasms/*genetics
MH  - Protein Serine-Threonine Kinases/*genetics
MH  - Survivin
MH  - Tumor Cells, Cultured
MH  - Tumor Suppressor Protein p53/metabolism
EDAT- 2005/04/30 09:00
MHDA- 2005/06/10 09:00
CRDT- 2005/04/30 09:00
PHST- 2004/05/17 00:00 [received]
PHST- 2004/09/13 00:00 [revised]
PHST- 2004/09/13 00:00 [accepted]
PHST- 2005/04/30 09:00 [pubmed]
PHST- 2005/06/10 09:00 [medline]
PHST- 2005/04/30 09:00 [entrez]
AID - S0165-4608(04)00426-1 [pii]
AID - 10.1016/j.cancergencyto.2004.09.008 [doi]
PST - ppublish
SO  - Cancer Genet Cytogenet. 2005 May;159(1):10-7. doi: 
      10.1016/j.cancergencyto.2004.09.008.