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View the Table of Contents for the September 15 issue of Cancer Research.
Wang et al. Page 8158
Mouse is a valuable model for human lung cancer study. A series of linkage studies were previously conducted to identify quantitative trait loci (QTL) associated with chemically induced lung tumors. However, little is known of genetic susceptibility to spontaneously occurring lung tumorigenesis (SLT) in mice. Wang et al. performed a whole-genome linkage disequilibrium analysis for susceptibility to SLT in mice using the Roche SNP data. Five regions, SLT1 to SLT5, were mapped on chromosomes 6, 7, 8, 19, and X, respectively. These results for the first time provide an insight into the genetic control of spontaneously occurring lung tumorigenesis.
Brubaker et al. Page 8218
In response to the need for in vivo assessment of intratumor vasculature, Brubaker et al. utilized magnetic resonance angiography (MRA) to non-invasively evaluate vasculature of the genetically engineered mouse model, choroid plexus carcinoma (CPC). Their research indicated that consistent tumor vasculature properties can be determined by MRA. Such methods are critical for developing preclinical therapeutic testing and will help guide the development of human brain tumor analyses.
Tang et al. Page 8324
Activated H-RAS has been linked to the angiogenic phenotype of cancers but the mechanism underlying the relationship is not well understood. Tang et al. used the inducible Tyr/Tet-RAS Ink4a/Arf-/- model to show that loss of RAS activity in fully established melanomas led to an early impairment of vascular function before tumor volume decreased. This correlated with activation of apoptosis in host-derived endothelial cells as well as in tumor cells. Loss of vascular integrity upon inactivation of RAS is an active process, rather than a consequence of loss of tumor cell viability.
Wilderman et al. Page 8379
Non-small cell lung carcinoma (NSCLC) is the number one cancer killer in the U.S. and much of the world. Current therapies, however, are very suboptimal. Wilderman et al. have used a recently developed a transgenic orthotopic model of bronchogenic adenocarcinoma of the lung to evaluate the effects of an adenovirus expressing interferon-β. Two intrapulmonary doses of vector were well tolerated and led to markedly increased survival of tumor-bearing mice. Efficacy was due to direct antitumor effects in combination with stimulation of NK cell activity and generation of CD8+ cytotoxic T cells. These studies, showing remarkable antitumor activity in this orthotopic lung cancer model, provide strong preclinical support for a trial of Ad.IFNβ to treat human NSCLC.