Abstract
Quantitative aspects of the behaviour of B16 melanoma and Lewis lung carcinoma cells during the post-intravasation stages of metastasis were examined in relation to their spontaneous metastatic potential. Cancer cells were isolated from the blood of mice bearing i.m. tumours throughout tumour growth using a novel discontinuous gradient centrifugation technique. Four times more Lewis carcinoma cells than B16 melanoma cells were shed into the circulation, although the numbers of cells shed from either tumour were orders of magnitude more than the numbers of spontaneous pulmonary metastases which developed. Greater numbers of Lewis carcinoma cells were also shed as clumps and with leukocytes attached. However, although similar numbers of radiolabelled melanoma and Lewis carcinoma cells were arrested in the lungs after i.v. injection, fewer carcinoma cells were retained there and 12 times fewer Lewis carcinoma nodules developed in the lungs following injection of non-radiolabelled cells. It appears that the low lung colonization potential of the Lewis lung carcinoma is compensated for during spontaneous metastases by the numbers of cells shed from primary tumours as single cells and as clumps.
Highlights
Five minutes after cells were injected, similar numbers of melanoma and carcinoma cells were initially arrested in the lungs and the subsequent rates at which these cells were cleared from the pulmonary vasculature were similar over the following 6 h period
By 24 h post-injection there were more than twice as many melanoma as carcinoma cells still retained in the lungs
The only other quantitative experiments include those of Butler & Gullino (1975) which involved long-term cannulation of veins draining non-metastatic mammary carcinomas transplanted into the exteriorized ovaries of rats receiving concomitant transfusions of anticoagulated blood
Summary
The purpose of the present study is restricted to relating, in two distinct tumour types, the numbers of cancer cells released into the blood with the size of the primary tumours generating them and to seek correlation between the numbers of circulating cancer cells and metastatic status, as summarized in Table III
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