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Accumulation of natural killer cells after hepatic artery embolisation in the midgut carcinoid syndrome.

Eleven patients with disseminated midgut carcinoid tumour disease were subjected to hepatic artery embolisation. In six patients, lymphocytosis with a predominance of NK cells occurred and the cytotoxic activity of isolated lymphocytes increased. A relation between NK cell accumulation and subsequen...

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Autores principales: Wängberg, B., Ahlman, H., Tylén, U., Nilsson, O., Hermodsson, S., Hellstrand, K.
Formato: Texto
Lenguaje:English
Publicado: Nature Publishing Group 1995
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2033616/
https://www.ncbi.nlm.nih.gov/pubmed/7880747
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author Wängberg, B.
Ahlman, H.
Tylén, U.
Nilsson, O.
Hermodsson, S.
Hellstrand, K.
author_facet Wängberg, B.
Ahlman, H.
Tylén, U.
Nilsson, O.
Hermodsson, S.
Hellstrand, K.
author_sort Wängberg, B.
collection PubMed
description Eleven patients with disseminated midgut carcinoid tumour disease were subjected to hepatic artery embolisation. In six patients, lymphocytosis with a predominance of NK cells occurred and the cytotoxic activity of isolated lymphocytes increased. A relation between NK cell accumulation and subsequent radiological and biochemical response was observed, and it is suggested that anti-tumour mechanisms other than ischaemia may contribute to the therapeutic response in these patients.
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spelling pubmed-20336162009-09-10 Accumulation of natural killer cells after hepatic artery embolisation in the midgut carcinoid syndrome. Wängberg, B. Ahlman, H. Tylén, U. Nilsson, O. Hermodsson, S. Hellstrand, K. Br J Cancer Research Article Eleven patients with disseminated midgut carcinoid tumour disease were subjected to hepatic artery embolisation. In six patients, lymphocytosis with a predominance of NK cells occurred and the cytotoxic activity of isolated lymphocytes increased. A relation between NK cell accumulation and subsequent radiological and biochemical response was observed, and it is suggested that anti-tumour mechanisms other than ischaemia may contribute to the therapeutic response in these patients. Nature Publishing Group 1995-03 /pmc/articles/PMC2033616/ /pubmed/7880747 Text en https://creativecommons.org/licenses/by/4.0/This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit https://creativecommons.org/licenses/by/4.0/.
spellingShingle Research Article
Wängberg, B.
Ahlman, H.
Tylén, U.
Nilsson, O.
Hermodsson, S.
Hellstrand, K.
Accumulation of natural killer cells after hepatic artery embolisation in the midgut carcinoid syndrome.
title Accumulation of natural killer cells after hepatic artery embolisation in the midgut carcinoid syndrome.
title_full Accumulation of natural killer cells after hepatic artery embolisation in the midgut carcinoid syndrome.
title_fullStr Accumulation of natural killer cells after hepatic artery embolisation in the midgut carcinoid syndrome.
title_full_unstemmed Accumulation of natural killer cells after hepatic artery embolisation in the midgut carcinoid syndrome.
title_short Accumulation of natural killer cells after hepatic artery embolisation in the midgut carcinoid syndrome.
title_sort accumulation of natural killer cells after hepatic artery embolisation in the midgut carcinoid syndrome.
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2033616/
https://www.ncbi.nlm.nih.gov/pubmed/7880747
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