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Is Tumor Cell Radiation Resistance Correlated with Metastatic Ability?¹

Department of Radiation Oncology, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts 02114 [H. S., A. A., J. E.]; Cross Cancer Institute, Edmonton, Alberta, Canada T6G 1Z2 [J. A-T., R. P.]; Division of Radiotherapy, University of Texas M. D. Anderson Cancer Center, Houston, Texas 77030 [W. B., N. H., L. M., L. P.]; Institut Gustave Roussy, Paris, France 94805 [T. G.]; Gray Laboratory, Mount Vernon Hospital, Northwood, London HA6 2JR [S. H.]; Paterson Institute for Cancer Research, Christie Hospital (N.H.S.) Trust, Manchester, United Kingdom M2O 9BX [C. W.]; Division of Experimental Pathology, Pennsylvania State University College of Medicine, M. S. Hershey Medical Center, Hershey, Pennsylvania 17033 [D. R. W.]

Patients who experience local failure following radiation treatment of epithelial malignancies exhibit a substantially higher rate of distant metastasis than those patients who achieve permanent local control. This fact has raised concern that the local failure to control the primary/regional tumor may serve as a marker of a particularly malignant neoplasm, i.e., high metastatic activity and radiation resistance. If this were true, there would be no gains in survival by increasing the efficacy of treating the primary/regional disease because the new local controls would develop distant metastasis. To investigate this concept, the relationship between distant metastasis probability and tumor cell radiation resistance has been studied by examining laboratory and clinical data (in vitro and in vivo assays) from six collaborating centers. TCD₅₀s (radiation dose which inactivates half of the irradiated tumors) and incidence of distant metastasis in mice with local control have been evaluated for 24 murine tumor systems. SF₂s (surviving fraction after 2 Gy) were determined in vitro for cell lines from 8 human, 13 mouse, and 15 rat tumors/tumor sublines and the metastatic activity assessed after injection of the cells into syngeneic murine hosts and xenogenic hosts for the human tumors. SF₂s of cells from carcinomas of the head/neck, cervix, and endometrium which were controlled locally by radiation ± surgery from four centers were compared for those which did and those which did not metastasize. The total number of patients studied was 222. The cumulative distributions of SF₂s of locally controlled tumors which did and did not metastasize were not different in each of the data sets. Similarly, there was no demonstrable relationship between TCD₅₀s and metastatic frequency in local control mice. Furthermore, the SF₂s of murine and human tumor cell lines did not track with metastatic activity. Radiation sensitivity of clinical and laboratory tumors did not correlate with metastatic activity in studies of data from six centers.

¹ This work was supported in part by grants from the National Cancer Institute, DHHS (CA 13311 to H. D. S.; CA 50192 to W. B.; and CA 06294 to L. P.); Alberta Cancer Board, Research Initiative program (to J. A-T. and R. P.); Association pour La Recherche contre le Cancer and La Ligue Francaise Nationale contre le Cancer (to T. G.); and United Kingdom Cancer Research Campaign (to S. H. and C. W.). Portions of the work by D. W. were performed at the Upjohn Research laboratories.

² To whom requests for reprints should be addressed.

Received 10/28/93. Accepted 1/31/94.

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