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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
1992-3-12
pubmed:abstractText
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 (MHCH) and grew poorly or not at all in normal syngeneic mice. The second set of clones expressed generally low levels of class I MHC (MHCL) and exhibited progressive growth in vivo, similar to the parent tumor. The steady-state mRNA levels for class I MHC and beta 2-microglobulin were constitutively elevated in MHCH clones compared to MHCL clones or the parent tumor. However, in vivo tumorigenic outgrowths from immunogenic variants always expressed the MHCH 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 MHCH and MHCL subclones were derived from one lineage within the MHCH subset, despite the fact that MHCH subclones exhibited slower growth in vivo than MHCL 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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
1045-2257
pubmed:author
pubmed:issnType
Print
pubmed:volume
3
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
433-42
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:1723292-Adenocarcinoma, pubmed-meshheading:1723292-Animals, pubmed-meshheading:1723292-Antigens, Neoplasm, pubmed-meshheading:1723292-Azacitidine, pubmed-meshheading:1723292-Chromosome Mapping, pubmed-meshheading:1723292-Clone Cells, pubmed-meshheading:1723292-Female, pubmed-meshheading:1723292-Genetic Markers, pubmed-meshheading:1723292-Graft Rejection, pubmed-meshheading:1723292-H-2 Antigens, pubmed-meshheading:1723292-Mammary Neoplasms, Experimental, pubmed-meshheading:1723292-Mice, pubmed-meshheading:1723292-Mice, Inbred BALB C, pubmed-meshheading:1723292-Mice, Inbred C3H, pubmed-meshheading:1723292-Mice, Inbred CBA, pubmed-meshheading:1723292-Mice, Nude, pubmed-meshheading:1723292-Neoplasm Transplantation, pubmed-meshheading:1723292-Phenotype, pubmed-meshheading:1723292-Tumor Markers, Biological
pubmed:year
1991
pubmed:articleTitle
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.
pubmed:affiliation
Cancer Research Laboratories, Queen's University, Kingston, Ontario, Canada.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't