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Levels of E2F-1 Expression Are Higher in Lung Metastasis of Colon Cancer As Compared with Hepatic Metastasis and Correlate with Levels of Thymidylate Synthase¹

Program of Molecular Pharmacology, Sloan Kettering Institute for Cancer Research [D. B., A. L., J. R. B], and Departments of Pediatrics [R. G.], Pathology [D. K. C. C-C.], Human Genetics [S. J.], Surgery [Y. F.], and Medicine [N. K.], Memorial Sloan-Kettering Cancer Center, New York, New York 10021, and Norris Comprehensive Cancer Center, University Of Southern California, Los Angeles, California 90033 [K. D., P. C. D., P. V. D.]

We recently reported that forced overexpression of the transcription factor E2F-1 in human HT-1080 fibrosarcoma cells resulted in corresponding high levels of thymidylate synthase (TS) and resistance to 5-fluoropyrimidines (D. Banerjee et al., Cancer Res., 58: 4292–4296, 1998). Because colorectal metastasis to the lung has higher TS levels than liver metastasis and is less responsive to treatment with 5-fluorouracil (R. Gorlick et al., J. Clin. Oncol., 16: 1465–1469, 1998), it was, therefore, of interest to measure E2F-1 expression in these tumors. In contrast to marginally increased levels of dihydrofolate reductase and topoisomerase I in lung metastasis as compared with liver metastasis, lung tumors had a 5-fold increase in E2F-1 expression as compared with liver tumors, corresponding to the relative levels of TS in these metastases. These data indicate that there exists a close correlation between E2F-1 and TS levels and provide a rationale for targeting this transcription factor, i.e., E2F-1, for the treatment of certain cancers.

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