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Ann Thorac Surg 1991;52:732-737
© 1991 The Society of Thoracic Surgeons
Departments of Surgery and Pathology, University of California at Davis, Sacramento, California USA
* Address reprint requests to Dr Benfield, UC Davis, 4301 X St, Rm 2310, Sacramento, CA 95817.
In our hamster model of focal, chemically induced non-small cell lung cancer (NSCLC), we studied metastases in autochthonous hamster hosts (n = 300) and in syngeneic hamster and nude mice recipients (n = 230) of serial tumor transplants. Metastases in autochthonous hosts and transplant recipients occurred in regional lymph nodes, liver, and adrenals. In autochthonous host hamsters no metastases were noted from microinvasive (n = 112) or visible cancer less than 3.0 mm in diameter (n = 66); the incidence of metastasis was 8.2% ( [equation]) from 3- to 10-mm cancers and 22% ( [equation]) from cancers 10 mm in diameter or larger (p < 0.05). Serial transplants were used to evaluate the metastatic propensity of 20 primary and six metastatic NSCLCs. Six primary NSCLCs that metastasized in the autochthononous host ana six metastatic NSCLCs all metastasized promptly in recipients. This expression of metastatic potential was significantly different (p < 0.05) from 14 primary cancers without autochthonous host metastases. Eight of the 14 caused no metastases in recipients, even after 5 to 11 tumor growth cycles; metastases occurred from the other six primary NSCLC after 3 to 12 tumor growth cycles in transplant recipients. Primary hamster NSCLCs metastasize in the autochthonous host with a frequency and a distribution pattern similar to human NSCLCs. A new model to study serially the cellular changes that govern the process of metastasis in NSCLC has been developed.
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