10.6084/m9.figshare.5442418.v1
Harada T.
Harada
T.
Chelala C.
Chelala
C.
Crnogorac-Jurcevic T.
Crnogorac-Jurcevic
T.
Lemoine N.R.
Lemoine
N.R.
Supplementary Material for: Genome-Wide Analysis of Pancreatic Cancer Using Microarray-Based Techniques
Karger Publishers
2017
Pancreatic ductal adenocarcinoma
array-based comparative genomic hybridisation
High-level amplification
Homozygous deletion
non-randomized genetic alterations
2017-09-26 13:59:27
Dataset
https://karger.figshare.com/articles/dataset/Supplementary_Material_for_Genome-Wide_Analysis_of_Pancreatic_Cancer_Using_Microarray-Based_Techniques/5442418
<p><i>Background/Aims:</i> Microarray-based comparative genomic
hybridisation (CGH) has allowed high-resolution analysis of DNA copy
number alterations across the entire cancer genome. Recent advances in
bioinformatics tools enable us to perform a robust and highly sensitive
analysis of array CGH data and facilitate the discovery of novel
cancer-related genes. <i>Methods:</i> We analysed a total of 29
pancreatic ductal adenocarcinoma (PDAC) samples (6 cell lines and 23
microdissected tissue specimens) using 1-Mb-spaced CGH arrays. The
transcript levels of all genes within the identified regions of genetic
alterations were then screened using our Pancreatic Expression Database.
<i>Results:</i> In addition to 238 high-level amplifications and 35
homozygous deletions, we identified 315 minimal common regions of
‘non-random’ genetic alterations (115 gains and 200 losses) which were
consistently observed across our tumour samples. The small size of these
aberrations (median size of 880 kb) contributed to the reduced number
of candidate genes included (on average 12 Ensembl-annotated genes). The
database has further specified the genes whose expression levels are
consistent with their copy number status. Such genes were <i>UQCRB</i>, <i>SQLE</i>, <i>DDEF1</i>, <i>SLA</i>, <i>ERICH1</i> and <i>DLC1</i>, indicating that these may be potential target candidates within regions of aberrations. <i>Conclusion:</i>
This study has revealed multiple novel regions that may indicate the
locations of oncogenes or tumour suppressor genes in PDAC. Using the
database, we provide a list of novel target genes whose altered DNA copy
numbers could lead to significant changes in transcript levels in PDAC.</p>