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Access through your institution Buy or subscribe Both primary central nervous system lymphomas (CNSLs) and secondary CNSLs derived from peripheral sites can occur in the brain, but it is not
clear how malignant lymphoma cells (LCs) invade and proliferate in the brain, especially as lymphoid cells are not typically present in this tissue. However, as chronic inflammation can
promote development of peripheral lymphomas, and as the inflammatory nuclear factor-κB (NF-κB) pathway is upregulated in CNSLs, O’Connor et al. hypothesized that chronic CNS inflammation
might contribute to CNSL development. Intravenous injection of GFAP-LTαβ mice or IKK2CA mice with B cell LCs expressing the oncoprotein MYC (Eµ-MYC cells) led to more neurological
disturbances and substantial LC colonization of the brain compared with wild-type mice. Similar results were observed with LCs expressing a different oncoprotein (TCL1). This is a preview of
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* Log in * Learn about institutional subscriptions * Read our FAQs * Contact customer support REFERENCES ORIGINAL ARTICLE * O’Connor, T. et al. Age-related gliosis promotes central nervous
system lymphoma through CCL19-mediated tumor cell retention. _Cancer Cell_ 36, 250–267 (2019) Article Google Scholar Download references AUTHOR INFORMATION AUTHORS AND AFFILIATIONS *
Nature Reviews Cancer http://www.nature.com/nrc/ Sarah Seton-Rogers Authors * Sarah Seton-Rogers View author publications You can also search for this author inPubMed Google Scholar
CORRESPONDING AUTHOR Correspondence to Sarah Seton-Rogers. RIGHTS AND PERMISSIONS Reprints and permissions ABOUT THIS ARTICLE CITE THIS ARTICLE Seton-Rogers, S. How the brain retains
lymphoma cells. _Nat Rev Cancer_ 19, 609 (2019). https://doi.org/10.1038/s41568-019-0214-9 Download citation * Published: 30 September 2019 * Issue Date: November 2019 * DOI:
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