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Outgrowth of Stable Class I Major Histocompatibility Complex‐Expressing Subsets From Immunogenic Variants of a Murine Mammary Carcinoma: Association with a Differentially Staining Region on Chromosome 9
Author(s) -
Elliott Bruce E.,
Xu Wei,
Brissette Louise,
Deeley Roger G.,
Mudrik Kevin,
Marshall John,
Vekemans Michel,
Holden Jeanette J. A.
Publication year - 1991
Publication title -
genes, chromosomes and cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.754
H-Index - 119
eISSN - 1098-2264
pISSN - 1045-2257
DOI - 10.1002/gcc.2870030605
Subject(s) - major histocompatibility complex , biology , mhc class i , mhc restriction , phenotype , cd8 , genetics , mhc class ii , microbiology and biotechnology , immunology , antigen , gene
We have examined interactions among intratumor subpopulations during the rejection of immunogenic variants of a murine mammary carcinoma (SPI) and in the outgrowth of tumorigenic “revertant” subsets. Analysis of subclones isolated during the early phase of rejection of one immunogenic variant revealed extensive cellular heterogeneity of tumor‐forming ability and class I major histocompatibility complex (MHC) expression. Two main categories of subclones were identified. One set expressed high levels of class I MHC (MHC H ) and grew poorly or not at all in normal syngeneic mice. The second set of clones expressed generally low levels of class I MHC (MHC L ) and exhibited progressive growth in vivo, similar to the parent tumor. The steady‐state mRNA levels for class I MHC and β2‐microglobulin were constitutively elevated in MHC H clones compared to MHC L clones or the parent tumor. However, in vivo tumorigenic outgrowths from immunogenic variants always expressed the MHC H phenotype. A cytogenetic analysis was carried out to determine the clonal origin and lineage relationship of in vivo selected tumor outgrowths. Surprisingly, tumor outgrowths from mixtures of karyotypically distinct MHC H and MHC L subclones were derived from one lineage within the MHC H subset, despite the fact that MHC H subclones exhibited slower growth in vivo than MHC L subsets when analyzed individually. These results suggest that in polyclonal populations the various subsets sometimes interact in a way that overrides the influence of immunogenic and MHC phenotypes of individual subclones.