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Human Molecular Genetics Advance Access published online on December 22, 2004
Human Molecular Genetics, doi:10.1093/hmg/ddi043
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Human Molecular Genetics, © Oxford University Press 2004; all rights reserved

Article

Involvement of multiple developmental genes on chromosome 1p in lung tumorigenesis

Cathie Garnis 1*, Jennifer Campbell 2, Jonathan J. Davies 2, Calum MacAulay 2, Stephen Lam 2, and Wan L. Lam 2

1 British Columbia Cancer Research Centre, 601 West 10th Avenue, Vancouver BC, Canada V5Z 1L3
2 British Columbia Cancer Research Centre, Vancouver BC, Canada V5Z 1L3

* To whom correspondence should be addressed.
Cathie Garnis, E-mail: cgarnis{at}bccrc.ca


  Abstract

Lung cancer is the leading cause of cancer death in the North America. Despite advances in lung cancer treatment, the overall 5 year survival rate for those diagnosed with the disease is bleak presumably due to the late stage of diagnosis. Due to the difficulty of early detection, preneoplastic specimens are rare. However, studying both preinvasive and invasive stages of disease is necessary to fully understand lung cancer progression. Aberration of chromosome arm 1p is common in lung and other cancers. In this study we used a genomic array with complete tiling coverage of 1p to profile preinvasive and invasive squamous non-small cell lung carcinoma samples. With this technology multiple novel submegabase alterations were identified. Three of the 1p alterations harbored genes belonging to gene families known to be involved in cancer development through either the Wnt or Notch developmental pathways. Our finding of a 0.4 Mb amplified region at 1p36.12 containing WNT4 in preinvasive lung cancer, coupled with the identification of three additional alterations in invasive tumors that also contain genes related to the Notch and Wnt pathways, strongly suggest an intricate role of these pathways in early and late stages of lung cancer development. Furthermore, ectopic expression of DVL1, LRP8, and Notch2 in malignant lung tissue validates the biological impact of these genetic alterations. Importantly, this implication of pathways known only to be activated in fetal lung development lends support to the proposed model of lung cancer ontology whereby tumors arise from dysregulated pleuripotent stem cells.


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