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| Status |
Public on Dec 01, 2010 |
| Title |
Normal prostate cells were immortalized and cultured for 650 days till several transformation hallmarks were observed |
| Organism |
Homo sapiens |
| Experiment type |
Expression profiling by array
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| Summary |
Duplication of chromosomal arm 20q occurs in prostate, cervical, colon, gastric, bladder, melanoma, pancreas and breast cancer, suggesting that 20q amplification may play a key causal role in tumorigenesis. According to an alternative view, chromosomal instabilities are mainly a common side effect of cancer progression. To test whether a specific genomic aberration might serve as a cancer initiating event, we established an in vitro system that models the evolutionary process of early stages of prostate tumor formation; normal prostate cells were immortalized and cultured for 650 days till several transformation hallmarks were observed. Gene expression patterns were measured and chromosomal aberrations were monitored by spectral karyotype analysis at different times. Several chromosomal aberrations, in particular duplication of chromosomal arm 20q, occurred early in the process and were fixed in the cell populations, while other aberrations became extinct shortly after their appearance. A wide range of bioinformatic tools, applied to our data and to data from several cancer databases, revealed that spontaneous 20q amplification can promote cancer initiation. Our computational model suggests that deregulation of some key pathways, such as MAPK, p53, cell cycle regulation and Polycomb group factors, in addition to activation of several genes like Myc, AML, B-Catenin and the ETS family transcription factors, are key steps in cancer development driven by 20q amplification. Finally we identified 13 cancer initiating genes, located on 20q13, which were significantly overexpressed in many tumors, with expression levels correlated with tumor grade and outcome; these probably play key roles in inducing malignancy via20q amplification.
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| Overall design |
33 samples were analysised, 12 were in replicate
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| Contributor(s) |
Kogan-Sakin I, Tabach Y, Buganim Y, Goldfinger N, Domany E, Rotter V |
| Citation(s) |
21297939, 20689556 |
| Submission date |
Jul 20, 2010 |
| Last update date |
Dec 06, 2018 |
| Contact name |
Yuval Tabach |
| E-mail(s) |
yuval.tabach@weizmann.ac.il
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| Phone |
972-8-9344985
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| Organization name |
Weizmann Institute of Science
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| Department |
Molecular Cell Biology
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| Street address |
Hativat Givaty 30
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| City |
Raanana |
| ZIP/Postal code |
43338 |
| Country |
Israel |
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| Platforms (1) |
| GPL571 |
[HG-U133A_2] Affymetrix Human Genome U133A 2.0 Array |
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| Samples (27)
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| GSM568587 |
hTERT immortalized cells passage 0 |
| GSM568588 |
hTERT immortalized cells passage 10 |
| GSM568589 |
hTERT immortalized cells passage 20 |
| GSM568590 |
hTERT immortalized cells, empty vector control, passage 30 |
| GSM568591 |
hTERT immortalized cells, empty vector control, passage 40 |
| GSM568592 |
hTERT immortalized cells, empty vector control, passage 50 |
| GSM568593 |
hTERT immortalized cells, empty vector control, passage 60 |
| GSM568594 |
hTERT immortalized cells, empty vector control, passage 70 |
| GSM568595 |
hTERT immortalized cells, empty vector control, passage 80 |
| GSM568596 |
hTERT immortalized cells, dominant negative peptide for p53 vector , passage 30 |
| GSM568597 |
hTERT immortalized cells, dominant negative peptide for p53 vector , passage 40 |
| GSM568598 |
hTERT immortalized cells, dominant negative peptide for p53 vector , passage 50 |
| GSM568599 |
hTERT immortalized cells, dominant negative peptide for p53 vector , passage 60 |
| GSM568600 |
hTERT immortalized cells, dominant negative peptide for p53 vector , passage 70 |
| GSM568601 |
hTERT immortalized cells, dominant negative peptide for p53 vector , passage 80 |
| GSM568602 |
hTERT immortalized cells, mutant p53 vector , passage 30 |
| GSM568603 |
hTERT immortalized cells, mutant p53 vector , passage 40 |
| GSM568604 |
hTERT immortalized cells, mutant p53 vector , passage 50 |
| GSM568605 |
hTERT immortalized cells, mutant p53 vector , passage 60 |
| GSM568606 |
hTERT immortalized cells, mutant p53 vector , passage 70 |
| GSM568607 |
hTERT immortalized cells, mutant p53 vector , passage 80 |
| GSM568608 |
hTERT immortalized cells, empty vector control + hRAS, passage 80, reps a and b |
| GSM568609 |
hTERT immortalized cells, dominant negative peptide for p53 vector + hRAS, passage 80, reps a and b |
| GSM568610 |
hTERT immortalized cells, mutant p53 vector + hRAS, passage 80, reps a and b |
| GSM568611 |
hTERT immortalized cells, passage 80, reps a and b |
| GSM568612 |
hTERT immortalized cells + dominant negative peptide for p53, passage 80, reps a and b |
| GSM568613 |
hTERT immortalized cells + mutant p53, passage 80, reps a and b |
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| Relations |
| BioProject |
PRJNA131175 |
| Supplementary file |
Size |
Download |
File type/resource |
| GSE23038_RAW.tar |
73.2 Mb |
(http)(custom) |
TAR (of CEL, CHP) |
| Processed data included within Sample table |
| Processed data provided as supplementary file |
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