Matches in SemOpenAlex for { <https://semopenalex.org/work/W2018561279> ?p ?o ?g. }
- W2018561279 endingPage "311" @default.
- W2018561279 startingPage "303" @default.
- W2018561279 abstract "Classical Hodgkin's disease (HD) is a peculiar form of lymphoma characterized by a low frequency of tumor cells, the so-called Hodgkin (H) and Reed/Sternberg (RS) cells, embedded in a background of non-neoplastic (reactive) cells believed to be recruited and activated by H - RS cell-derived cytokines/chemokines. How these tumor cells can survive in such a seemingly hostile environment has confused researchers. We have previously identified interleukin (IL)-3 receptor (R) expression as a common feature of classical HD and unveiled the potential role of IL-3 as a growth and anti-apoptotic factor for H - RS cells. More then 90% of malignant cells of classical HD usually express the α chain of the IL-3R (IL-3Rα), as evidenced by immunostaining of frozen sections and cell suspensions from neoplastic lymph nodes. Consistently, HD-derived cell lines (L428, KMH2, HDLM2 and L1236) express the α and β chains that form IL-3R, both at the mRNA and protein level, with a molecular size of IL-3Rα identical (70 kDa) to that expressed by human myeloid cells. Exogenous IL-3 promotes the growth of cultured H - RS cells, such an effect being potentiated by IL-9 and stem cell factor (SCF) co-stimulation, and is able to partially rescue tumor cells from apoptosis induced by serum deprivation. Finally, cultured H - RS cells are able to increase the production of IL-3 by pre-activated T cells, suggesting an involvement of IL-3/IL-3R interactions in the cellular growth of HD through paracrine mechanisms. This review will outline the biological activity of IL-3 and summarize the evidence indicating IL-3 as a growth and anti-apoptotic factor for H - RS cells in classical HD." @default.
- W2018561279 created "2016-06-24" @default.
- W2018561279 creator A5006278471 @default.
- W2018561279 creator A5017907643 @default.
- W2018561279 creator A5018789268 @default.
- W2018561279 creator A5020652802 @default.
- W2018561279 creator A5033029228 @default.
- W2018561279 creator A5045745778 @default.
- W2018561279 creator A5061054780 @default.
- W2018561279 date "2005-01-01" @default.
- W2018561279 modified "2023-09-25" @default.
- W2018561279 title "The role of interleukin-3 in classical Hodgkin's disease" @default.
- W2018561279 cites W124601896 @default.
- W2018561279 cites W125310830 @default.
- W2018561279 cites W133636034 @default.
- W2018561279 cites W1495792176 @default.
- W2018561279 cites W1535220340 @default.
- W2018561279 cites W1560817952 @default.
- W2018561279 cites W1593158365 @default.
- W2018561279 cites W1617532721 @default.
- W2018561279 cites W1658400760 @default.
- W2018561279 cites W1699631922 @default.
- W2018561279 cites W1844161829 @default.
- W2018561279 cites W1969037609 @default.
- W2018561279 cites W1970842110 @default.
- W2018561279 cites W1972168709 @default.
- W2018561279 cites W1972922050 @default.
- W2018561279 cites W1974995599 @default.
- W2018561279 cites W1977911088 @default.
- W2018561279 cites W1977911898 @default.
- W2018561279 cites W1980364406 @default.
- W2018561279 cites W1986455568 @default.
- W2018561279 cites W1986858547 @default.
- W2018561279 cites W1987294733 @default.
- W2018561279 cites W1993216157 @default.
- W2018561279 cites W1995600281 @default.
- W2018561279 cites W1996994761 @default.
- W2018561279 cites W1999648081 @default.
- W2018561279 cites W2004216239 @default.
- W2018561279 cites W2008603529 @default.
- W2018561279 cites W2015788325 @default.
- W2018561279 cites W2016190362 @default.
- W2018561279 cites W2024512241 @default.
- W2018561279 cites W2032531389 @default.
- W2018561279 cites W2034470389 @default.
- W2018561279 cites W2045530045 @default.
- W2018561279 cites W2048589504 @default.
- W2018561279 cites W2053616455 @default.
- W2018561279 cites W2055907134 @default.
- W2018561279 cites W2057312986 @default.
- W2018561279 cites W2058589355 @default.
- W2018561279 cites W205984844 @default.
- W2018561279 cites W2063696920 @default.
- W2018561279 cites W2066338758 @default.
- W2018561279 cites W2066416336 @default.
- W2018561279 cites W2068025977 @default.
- W2018561279 cites W2069832306 @default.
- W2018561279 cites W2070125949 @default.
- W2018561279 cites W2074181523 @default.
- W2018561279 cites W2076918047 @default.
- W2018561279 cites W2078400068 @default.
- W2018561279 cites W2079722765 @default.
- W2018561279 cites W2082756328 @default.
- W2018561279 cites W2089577567 @default.
- W2018561279 cites W2090101693 @default.
- W2018561279 cites W2093628776 @default.
- W2018561279 cites W2094869608 @default.
- W2018561279 cites W2096142655 @default.
- W2018561279 cites W2097710494 @default.
- W2018561279 cites W2099031160 @default.
- W2018561279 cites W2102517064 @default.
- W2018561279 cites W2108296098 @default.
- W2018561279 cites W2109406287 @default.
- W2018561279 cites W2111220263 @default.
- W2018561279 cites W2112327624 @default.
- W2018561279 cites W2122748601 @default.
- W2018561279 cites W2146851451 @default.
- W2018561279 cites W2154758405 @default.
- W2018561279 cites W2156873654 @default.
- W2018561279 cites W2157235421 @default.
- W2018561279 cites W2160486077 @default.
- W2018561279 cites W2172257243 @default.
- W2018561279 cites W2267405788 @default.
- W2018561279 cites W2296158263 @default.
- W2018561279 cites W2314008482 @default.
- W2018561279 cites W2340068765 @default.
- W2018561279 cites W2344615469 @default.
- W2018561279 cites W2346836846 @default.
- W2018561279 cites W2412593438 @default.
- W2018561279 cites W2417601200 @default.
- W2018561279 cites W2436272293 @default.
- W2018561279 cites W2442004163 @default.
- W2018561279 cites W2474942244 @default.
- W2018561279 cites W3117022642 @default.
- W2018561279 cites W4231034519 @default.
- W2018561279 cites W4239413745 @default.
- W2018561279 cites W4241299256 @default.
- W2018561279 cites W4241400564 @default.