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Sökning: WFRF:(Johansson Per Olov) > Iodine-131 induces ...

LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
00003661naa a2200433 4500
001oai:DiVA.org:umu-21104
003SwePub
008090402s2008 | |||||||||||000 ||eng|
024a https://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-211042 URI
024a https://doi.org/10.1089/cbr.2007.04712 DOI
040 a (SwePub)umu
041 a engb eng
042 9 SwePub
072 7a ref2 swepub-contenttype
072 7a art2 swepub-publicationtype
100a Eriksson, Davidu Umeå universitet,Immunologi/immunkemi,Stigbrand4 aut0 (Swepub:umu)daer0001
2451 0a Iodine-131 induces mitotic catastrophes and activates apoptotic pathways in HeLa Hep2 cells
264 c 2008-11-05
264 1b Mary Ann Liebert Inc,c 2008
338 a print2 rdacarrier
520 a Iodine-131 (131I) has been used both in unconjugated form and conjugated to antibody derivates (i.e., radioimmunotherapy; RIT) to treat malignant diseases. The mechanisms by which 131I-irradiation causes growth retardation are, however, inadequately understood. The aim of this study was to elucidate the sequential molecular and cellular events that initiate cell death in HeLa Hep2 cells exposed to 131I. In this paper, HeLa Hep2 cells were found to display a transient G2-M arrest following irradiation, but then reentered the cell cycle still containing unrepaired cellular damage. An increase of multipolar mitotic spindles, as well as a significant increase in centrosome numbers from 8.8% +/- 1.9% in controls to 54.7% +/- 2.2% in irradiated cells, was observed (p < 0.0001). A subsequent failure of cytokinesis caused the cells to progress into mitotic catastrophe. This was accompanied by the formation of giant cells with multiple nuclei, multilobulated nuclei, and an increased frequency of polyploidy cells. A fraction of the cells also displayed apoptotic features, including the activation of initiator caspases-2, -8, -9, and effector caspase-3, as well as cleavage of poly(ADP-ribose) polymerase, a cell-death substrate for active caspase-3. These findings demonstrate that mitotic catastrophes and the activation of a delayed type of apoptosis might be important mechanisms involved in cell death following the RIT of solid tumors with -emitting radionuclides, such as 131I.
650 7a MEDICIN OCH HÄLSOVETENSKAPx Medicinska och farmaceutiska grundvetenskaperx Immunologi inom det medicinska området0 (SwePub)301102 hsv//swe
650 7a MEDICAL AND HEALTH SCIENCESx Basic Medicinex Immunology in the medical area0 (SwePub)301102 hsv//eng
653 a iodine-131
653 a mitotic catastrophe
653 a apoptosis
653 a caspases
653 a centrosomes
653 a radioimmunotherapy
700a Blomberg, Jeanetteu Umeå universitet,Institutionen för molekylärbiologi (Medicinska fakulteten)4 aut0 (Swepub:umu)jebl0001
700a Lindgren, Theresu Umeå universitet,Immunologi/immunkemi,Stigbrand4 aut0 (Swepub:umu)thslin02
700a Löfroth, Per-Olovu Umeå universitet,Radiofysik4 aut
700a Johansson, Lennartu Umeå universitet,Radiofysik4 aut0 (Swepub:umu)lejo0023
700a Riklund, Katrineu Umeå universitet,Diagnostisk radiologi4 aut0 (Swepub:umu)kaah0001
700a Stigbrand, Torgnyu Umeå universitet,Immunologi/immunkemi,Stigbrand4 aut0 (Swepub:umu)tost0001
710a Umeå universitetb Immunologi/immunkemi4 org
773t Cancer Biotherapy and Radiopharmaceuticalsd : Mary Ann Liebert Incg 23:5, s. 541-549q 23:5<541-549x 1084-9785x 1557-8852
8564 8u https://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-21104
8564 8u https://doi.org/10.1089/cbr.2007.0471

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