Introduction of novel agents in the treatment of primary CNS lymphoma.
Adenine
/ analogs & derivatives
Agammaglobulinaemia Tyrosine Kinase
/ antagonists & inhibitors
Aminopyridines
/ therapeutic use
Antineoplastic Agents, Immunological
/ therapeutic use
Burkitt Lymphoma
/ drug therapy
Central Nervous System Neoplasms
/ drug therapy
Humans
Immunologic Factors
/ therapeutic use
Lenalidomide
/ therapeutic use
Lymphoma, Large B-Cell, Diffuse
/ drug therapy
Lymphoma, T-Cell
/ drug therapy
Morpholines
/ therapeutic use
Phosphatidylinositol 3-Kinases
Phosphoinositide-3 Kinase Inhibitors
/ therapeutic use
Piperidines
Protein Kinase Inhibitors
/ therapeutic use
Pyrazoles
/ therapeutic use
Pyrimidines
/ therapeutic use
Rituximab
/ therapeutic use
Salvage Therapy
TOR Serine-Threonine Kinases
Thalidomide
/ analogs & derivatives
Toll-Like Receptors
Tumor Escape
BTK
IMiD
PCNSL
immune checkpoint inhibition
targeted agents
Journal
Neuro-oncology
ISSN: 1523-5866
Titre abrégé: Neuro Oncol
Pays: England
ID NLM: 100887420
Informations de publication
Date de publication:
19 02 2019
19 02 2019
Historique:
pubmed:
14
11
2018
medline:
6
5
2020
entrez:
14
11
2018
Statut:
ppublish
Résumé
Novel insights into the pathophysiology of primary central nervous system lymphoma (PCNSL) have identified the B-cell receptor and Toll-like receptor pathway as well as immune evasion and suppressed tumor immune microenvironment as a key mechanism in the pathogenesis of PCNSL. Small molecules and novel agents targeting these aberrant pathways have been introduced into clinical trials targeting the recurrent or refractory PCNSL patient population. Agents like the Bruton tyrosine kinase (BTK) inhibitor ibrutinib or immunomodulatory drugs (IMiDs) like pomalidomide and lenalidomide have shown promising high response rates in the salvage setting. Here, we give an overview about the recent, exciting developments in PCNSL and summarize the results of clinical trials using novel agents in the recurrent and refractory salvage setting, which include immune checkpoint inhibitors, IMiDs, as well as BTK, phosphatidylinositol-3 kinase, and mammalian target of rapamycin inhibitors.
Identifiants
pubmed: 30423172
pii: 5180478
doi: 10.1093/neuonc/noy193
pmc: PMC6380407
doi:
Substances chimiques
Aminopyridines
0
Antineoplastic Agents, Immunological
0
Immunologic Factors
0
Morpholines
0
NVP-BKM120
0
Phosphoinositide-3 Kinase Inhibitors
0
Piperidines
0
Protein Kinase Inhibitors
0
Pyrazoles
0
Pyrimidines
0
Toll-Like Receptors
0
ibrutinib
1X70OSD4VX
Rituximab
4F4X42SYQ6
Thalidomide
4Z8R6ORS6L
pomalidomide
D2UX06XLB5
Agammaglobulinaemia Tyrosine Kinase
EC 2.7.10.2
TOR Serine-Threonine Kinases
EC 2.7.11.1
Lenalidomide
F0P408N6V4
Adenine
JAC85A2161
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
306-313Subventions
Organisme : NCI NIH HHS
ID : P30 CA008748
Pays : United States
Informations de copyright
© The Author(s) 2018. Published by Oxford University Press on behalf of the Society for Neuro-Oncology. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.
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