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MHC imbalance and metastatic spread in Lewis lung carcinoma clones
Author(s) -
Eisenbach Lea,
Segal Shraga,
Feldman Michael
Publication year - 1983
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/ijc.2910320118
Subject(s) - clone (java method) , phenotype , cancer research , retinoic acid , lewis lung carcinoma , biology , metastasis , population , microbiology and biotechnology , cancer , gene , medicine , genetics , environmental health
Imbalance in the K b and D b region encoded molecules is observed in Lewis lung carcinoma clones. The uncloned metastatic population and the D122 high‐metastatic clone show no expression of H‐2K b products, while the non‐metastatic A9 clone expresses K b products. Twenty‐nine new subclones of 3LL and A9 were analyzed for D‐end and K‐end membrane expression, primary growth rate and metastatic spread. We show that the imbalance in H‐2K b to H‐2D b is correlated with metastatic properties of a given clone, but local tumor growth is not. A “low K b /low D 9 ” phenotype is nonmetastatic as is a “high K b /high D b ” phenotype; a “low K b /high D b ” is highly metastatic and a “medium K b /high D b ” is moderately metastatic. We find support for this notion of imbalance in experiments on MHC modulation by interferon and retinoic acid. Interferon increases both K b and D b expression of A9 and D122 clones yet the net increase of D b was greater than K b . This was associated with an increase in metastasis formation. Retinoic acid increases the expression of the D b gene product on the nonmetastatic A9, clone, without apparent changes in K b expression. This treatment shifts the A9 to a high‐metastatic phenotype. The significance of this imbalance to the tumor — host relationship is discussed.