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pubmed-article:8204946pubmed:abstractTextLymphokine Activated Killer (LAK) cells, stimulated by interleukin 2 (IL-2) have a pronounced antitumor effect in the therapy of melanoma and renal cancers. LAK cells were cultivated in presence of the nodules of the human breast adenocarcinoma cell line MCF-7 maintained in organotypic culture to study the interactions between lymphocytes and breast tumor cells. After two days of co-culture, the proliferation of MCF-7 nodules and that of LAK cells was diminished about five folds. The cytotoxic effect of the latter, appreciated by Chrome 51 release was unchanged after the coculture. In histological sections, the penetration of the LAK cells into the MCF-7 nodules was accompanied by an increase of tumor necrosis but also by a glandular differentiation of cancerous tissue. Polarized epithelial cell formations bording neoplasic lumens with intracytoplasmic vacuoles filled with mucus, appeared in the nodules. The immunohistochemistry underlines the presence of T lymphocytes marked by UCHL1 and CD3 antibodies and of Natural Killer (NK) cells marked by IOT10, located between the MCF-7 cancer cells. In electron microscopy, the membrane contacts were tight and were accompanied by the appearance of secondary lysosomes and nuclear alterations. The relatively low infiltration level of the nodules may lead to the supposition that an indirect mechanism will intervene in this dual action of a LAK cells: increase of necrosis, although partially, and development of glandular and functional differentiation.lld:pubmed
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pubmed-article:8204946pubmed:pagination659-65lld:pubmed
pubmed-article:8204946pubmed:dateRevised2009-11-11lld:pubmed
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pubmed-article:8204946pubmed:articleTitle[Effects of LAK cells activated by IL-2 on MCF-7 human breast cancer cell line maintained in organotypic culture].lld:pubmed
pubmed-article:8204946pubmed:affiliationInstitut d'oncologie cellulaire et moléculaire humaine (IOCMH), SDI 6098 CNRS 129, Bobigny, France.lld:pubmed
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pubmed-article:8204946pubmed:publicationTypeEnglish Abstractlld:pubmed