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Expression of an ASCL2 related stem cell signature and IGF2 in colorectal cancer liver metastases with 11p15.5 gain
D E Stange1, F Engel, T Longerich
1Division of Molecular Genetics, German Cancer Research Center, Im Neuenheimer Feld 280, 69120 Heidelberg, Germany.
Gut
|May 19, 2010
Summary
Colorectal cancer liver metastases show striking genomic similarity to primary tumors, indicating metastasis occurs late. A subset exhibits an ASCL2 stem cell signature, potentially influencing metastatic behavior.
Area of Science:
- Oncology
- Genomics
- Molecular Biology
Background:
- Liver metastases are the primary cause of death in colorectal cancer patients.
- Understanding molecular aberrations in liver metastases is crucial for identifying new therapeutic targets.
Purpose of the Study:
- To investigate liver-metastasis-specific molecular aberrations in colorectal cancer.
- To gain insights into the biology of metastasis and identify potential therapeutic targets.
Main Methods:
- Comparative genomic hybridization and gene expression profiling of primary colorectal cancer (pCRC) and matched liver metastases (LMs).
- Analysis of 21 pCRC-LM pairs for genomic alterations and 18 pairs for gene expression.
- Validation using publicly available independent datasets.
Main Results:
- Genomic and expression profiles of pCRC and matched LMs were highly similar, with minimal differences observed.
- A specific gain on chromosome 11p15.5 was identified in a subset of LMs.
- Overexpression of Insulin-like Growth Factor 2 (IGF2) and ASCL2 (a stem cell transcription factor) was noted in LMs with the 11p15.5 gain.
- ASCL2 target genes, including OLFM4, were upregulated, suggesting a stem-cell-like signature in a subset of liver metastases.
Conclusions:
- Metastasis in colorectal cancer typically occurs after the primary tumor has fully matured, as evidenced by the conservation of genomic alterations.
- A distinct subset of liver metastases displays an ASCL2-driven stem cell signature, which may play a role in their metastatic behavior.
