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[Cancer Research 46, 2442-2448, May 1, 1986]
© 1986 American Association for Cancer Research

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Characterization of Two Highly Metastatic Variants of Lewis Lung Carcinoma with Different Organ Specificities1

Pnina Brodt2

Department of Surgery, Division of Surgical Research, McGill University, Montreal, Quebec H3A 1A4, Canada

The biological properties and metastasis of two sublines of the Lewis lung carcinoma (3LL) which have maintained a stable pattern of organ-selective metastasis have been studied. Subline M-3LL, a lung-specific variant which originated from a lung metastasis of the parent line, metastasized only to the lung following injection of 104–106 tumor cells i.v. or s.c. Lymphatic metastases of this tumor were rarely detected. Subline H-3LL which was developed from a rare, spontaneous hepatic metastasis of the parent line metastasized primarily to the liver, but pulmonary metastases have also been observed. While it grew at local s.c. sites, this tumor metastasized to the regional lymph nodes draining the tumor site, as determined by histology and by bioassay of the lymph nodes following their grafting into new recipient animals. Histologically, the two lines were indistinguishable with the exception of a higher incidence of giant cells detected in tissue sections and culture monolayers of the liver-colonizing variant H-3LL. Ten clones derived from each of the variant lines were expanded in vitro and inoculated i.v. While none of the ten clones derived from line M-3LL gave rise to extrapulmonary metastasis, nine of ten clones derived from Tumor H-3LL gave rise to hepatic metastasis. Highly metastatic clones selected from each tumor were subsequently used to study the patterns of distribution and arrest of radiolabeled tumor cells following their inoculation i.v. No correlation could be found between the initial distribution of the radiolabeled tumor cells and the organ selectivity eventually noted in the site of the metastases.

1 Supported by grants from the Fonds de la Recherche en Santé du Québec and from the Cancer Research Society of Montreal; presented in part at the 75th and 76th Annual Meetings of the American Association for Cancer Research, May 1984 and May 1985 (1, 2).

2 Medical Research Council of Canada Scholar.

Received 8/ 6/85. Revised 12/ 5/85. Accepted 12/12/85.




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HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
Cancer Prevention Journals Portal Cancer Reviews Online
Annual Meeting Education Book Meeting Abstracts Online
Copyright © 1986 by the American Association for Cancer Research.