Novel technology for detection of genomic and transcriptional alterations in pancreatic cancer.
OBJECTIVE
The present review summarizes our strategies aimed at identifying and characterizing genetic alterations occurring at the transcriptional and chromosomal level in pancreatic cancer.


METHODS
To study transcriptional alterations we have used a number of techniques including modified versions of differential hybridizations and cDNA-RDA (representational difference analysis). Comparative genomic hybridization (CGH) was used to study chromosomal aberrations occurring in pancreatic cancer tissues.


RESULTS
The study of transcriptional alterations led to the identification of more than 500 genes with differential expression in pancreatic cancer. The sum of these alterations represented the first expression profile characteristic for pancreatic tumors. The CGH analysis allowed the identification of a number of chromosomal regions containing putative tumor suppressor genes or oncogenes. These regions are presently being characterized at the molecular level. In a first approach the myb-oncogene was identified as the relevant oncogene of an amplification on 6q occurring in up to 10% of pancreatic cancer patients.


CONCLUSIONS
Genes isolated in both approaches represent potential new disease genes for pancreatic cancer and are at present being characterized by individual or serial analysis.
Wallrapp
C
C
Universität Ulm, Abteilung Innere Medizin I, Germany.
Müller-Pillasch
F
F
Micha
A
A
Wenger
C
C
Geng
M
M
Solinas-Toldo
S
S
Lichter
P
P
Frohme
M
M
Hoheisel
J D
JD
Adler
G
G
Gress
T M
TM
D002869:Chromosome Aberrations; D019941:Cyclin-Dependent Kinase Inhibitor p16 / Q000235:genetics; D018628:Gene Dosage; D015972:Gene Expression Regulation, Neoplastic; D016147:Genes, Tumor Suppressor; D006801:Humans; D009693:Nucleic Acid Hybridization; D009857:Oncogenes; D010190:Pancreatic Neoplasms / Q000235:genetics*; D014158:Transcription, Genetic
D019941:Cyclin-Dependent Kinase Inhibitor p16