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Clonal growth of colorectal‐carcinoma cell lines transplanted to nude mice
Author(s) -
De Both Nico J.,
Vermey Marcel,
Groen Nicole,
Dinjens Winand N.,
Bosman Fred T.
Publication year - 1997
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/(sici)1097-0215(19970917)72:6<1137::aid-ijc32>3.0.co;2-z
Subject(s) - biology , metastasis , clone (java method) , viral vector , neomycin , cancer research , population , nude mouse , transplantation , colorectal cancer , cell culture , primary tumor , carcinoma , pathology , cancer , virology , gene , medicine , genetics , environmental health , recombinant dna , antibiotics
Abstract It is generally assumed that tumor progression is a micro‐evolutionary process in which increasingly aggressive clones, generated through genetic instability, emerge in an initially monoclonal lesion. The present study was undertaken to determine how rapidly a dominant clone will emerge from an initial polyclonal situation, and whether dominance of these clones is a prerequisite for the onset of metastasis. To this end, colon‐carcinoma cells were infected in culture with an amphotropic retroviral vector containing the neomycin‐phosphotransferase gene, which makes cells resistant to neomycin. A heterogeneous population of neomycin‐resistant cells carrying random retroviral integrations was xenografted to the subcutis and to the cecum of nude mice. The xenografts obtained, as well as the available metastases, were analyzed as to viral integrations by Southern blotting. The results show that, (i) clonal selection already takes place during growth of the primary tumor; (ii) dominant clones also generate metastases. The retroviral integration pattern of metastases turned out to be identical to that found in the primary xenografts. This pattern remained unchanged in tumors obtained after serial transplantations of cells cultured from metastases. Int. J. Cancer 72:1137–1141, 1997. © 1997 Wiley‐Liss, Inc.