FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W1966255005> ?p ?o ?g. }

• W1966255005 endingPage "612" @default.
• W1966255005 startingPage "607" @default.
• W1966255005 abstract "Novel therapies in multiple myeloma (MM) target not only the tumor cell but also the bone marrow (BM) microenvironment. Thalidomide (Thal), as well as derivative immunomodulatory drugs (IMiDs), directly induce apoptosis or GI growth arrest in MM cell lines and patient's MM cells which are resistant to melphalan (Mel), doxorubicin (Dox), and dexamethasone (Dex). Although Thal and IMiDs do not alter adhesion of MM cells to bone marrow stromal cells (BMSCs), they inhibit the upregulation of interleukin-6 (IL-6) and vascular endothelial growth factor (VEGF) secretion triggered by the binding of MM cells to BMSCs. Proteasome inhibitors represent another potential anticancer therapy targeting the MM cell and the BM microenvironment. The proteasome inhibitor PS-341 directly inhibits proliferation and induces apoptosis in both human MM cell lines and freshly isolated patient's MM cells which are resistant to Mel, Dox, and Dex. PS-341 inhibits p44/42 mitogen-activated protein kinase (MAPK) growth signaling triggered by IL-6 and induces apoptosis, despite induction of p21 and p27, in p53 wild-type and p53 mutant MM cells. PS-341 adds to the anti-MM activity of dexamethasone and overcomes IL-6-mediated protection against dexamethasone-induced apoptosis. PS-341 blocks the paracrine growth of human MM cells by decreasing their adherence to BMSCs and related NF-κB-dependent induction of IL-6 secretion in BMSCs. Moreover, proliferation and MAPK growth signaling of those residual adherent MM cells is also inhibited. Tumor necrosis factor-α (TNF-α), which is produced by some MM cells, induces only low-level MM proliferation and MAPK activation in MM cells, but markedly upregulates IL-6 secretion from BMSCs and upregulates expression of adhesion molecules (VLA-4 and LFA-I) on MM cells and their receptors (VCAM-I and ICAM-I) on BMSCs, with resultant increased binding of MM cells to BMSCs. Inhibition of TNF-α-induced NF-κB activation with PS-341 inhibits both the upregulation of these molecules on MM cells and BMSCs and the resultant increased adhesion. Therefore, inhibiting TNF-α and its sequelae may be useful treatment strategies in MM. Our data show that VEGF causes proliferation and enhances migration of MM as well as plasma cell leukemia (PCL) cells. VEGF induced twofold activation of cell migration in MM cells and more than 100-fold activation of cell migration in PCL cells, suggesting an important role of VEGF in the progression of MM to PCL. These data indicate that VEGF plays a pivotal role not only in neoangiogenesis in MM BM but also in proliferation and migration of tumor cells." @default.
• W1966255005 created "2016-06-24" @default.
• W1966255005 creator A5006765393 @default.
• W1966255005 creator A5007023688 @default.
• W1966255005 creator A5027328800 @default.
• W1966255005 creator A5032464400 @default.
• W1966255005 creator A5043526996 @default.
• W1966255005 creator A5091207345 @default.
• W1966255005 date "2001-12-01" @default.
• W1966255005 modified "2023-10-17" @default.
• W1966255005 title "Novel therapies targeting the myeloma cell and its bone marrow microenvironment" @default.
• W1966255005 cites W1520422891 @default.
• W1966255005 cites W1528751727 @default.
• W1966255005 cites W1568733499 @default.
• W1966255005 cites W1580184585 @default.
• W1966255005 cites W1756723285 @default.
• W1966255005 cites W1777794242 @default.
• W1966255005 cites W1966598311 @default.
• W1966255005 cites W1983492903 @default.
• W1966255005 cites W1984996099 @default.
• W1966255005 cites W1985147506 @default.
• W1966255005 cites W2009296843 @default.
• W1966255005 cites W2024846074 @default.
• W1966255005 cites W2032454178 @default.
• W1966255005 cites W2032891189 @default.
• W1966255005 cites W2039839254 @default.
• W1966255005 cites W204363060 @default.
• W1966255005 cites W2056769035 @default.
• W1966255005 cites W2059873406 @default.
• W1966255005 cites W2070739194 @default.
• W1966255005 cites W2079007861 @default.
• W1966255005 cites W2100208042 @default.
• W1966255005 cites W2101759139 @default.
• W1966255005 cites W2105109537 @default.
• W1966255005 cites W2117834514 @default.
• W1966255005 cites W2119810076 @default.
• W1966255005 cites W2125559109 @default.
• W1966255005 cites W2133986577 @default.
• W1966255005 cites W2137651777 @default.
• W1966255005 cites W2138102966 @default.
• W1966255005 cites W2143356582 @default.
• W1966255005 cites W2151458137 @default.
• W1966255005 cites W2154374454 @default.
• W1966255005 cites W2159679541 @default.
• W1966255005 cites W2181009182 @default.
• W1966255005 cites W2292093022 @default.
• W1966255005 cites W2316160054 @default.
• W1966255005 cites W2324088026 @default.
• W1966255005 cites W2341526758 @default.
• W1966255005 cites W2410168620 @default.
• W1966255005 doi "https://doi.org/10.1016/s0093-7754(01)90033-8" @default.
• W1966255005 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/11740818" @default.
• W1966255005 hasPublicationYear "2001" @default.
• W1966255005 type Work @default.
• W1966255005 sameAs 1966255005 @default.
• W1966255005 citedByCount "175" @default.
• W1966255005 countsByYear W19662550052012 @default.
• W1966255005 countsByYear W19662550052013 @default.
• W1966255005 countsByYear W19662550052014 @default.
• W1966255005 countsByYear W19662550052015 @default.
• W1966255005 countsByYear W19662550052016 @default.
• W1966255005 countsByYear W19662550052017 @default.
• W1966255005 countsByYear W19662550052018 @default.
• W1966255005 countsByYear W19662550052019 @default.
• W1966255005 countsByYear W19662550052020 @default.
• W1966255005 countsByYear W19662550052022 @default.
• W1966255005 countsByYear W19662550052023 @default.
• W1966255005 crossrefType "journal-article" @default.
• W1966255005 hasAuthorship W1966255005A5006765393 @default.
• W1966255005 hasAuthorship W1966255005A5007023688 @default.
• W1966255005 hasAuthorship W1966255005A5027328800 @default.
• W1966255005 hasAuthorship W1966255005A5032464400 @default.
• W1966255005 hasAuthorship W1966255005A5043526996 @default.
• W1966255005 hasAuthorship W1966255005A5091207345 @default.
• W1966255005 hasConcept C126322002 @default.
• W1966255005 hasConcept C16930146 @default.
• W1966255005 hasConcept C170493617 @default.
• W1966255005 hasConcept C17991360 @default.
• W1966255005 hasConcept C190283241 @default.
• W1966255005 hasConcept C203014093 @default.
• W1966255005 hasConcept C2776364478 @default.
• W1966255005 hasConcept C2778367456 @default.
• W1966255005 hasConcept C2780007613 @default.
• W1966255005 hasConcept C502942594 @default.
• W1966255005 hasConcept C55493867 @default.
• W1966255005 hasConcept C57074206 @default.
• W1966255005 hasConcept C62478195 @default.
• W1966255005 hasConcept C71924100 @default.
• W1966255005 hasConcept C7876069 @default.
• W1966255005 hasConcept C86803240 @default.
• W1966255005 hasConcept C95444343 @default.
• W1966255005 hasConceptScore W1966255005C126322002 @default.
• W1966255005 hasConceptScore W1966255005C16930146 @default.
• W1966255005 hasConceptScore W1966255005C170493617 @default.
• W1966255005 hasConceptScore W1966255005C17991360 @default.
• W1966255005 hasConceptScore W1966255005C190283241 @default.
• W1966255005 hasConceptScore W1966255005C203014093 @default.
• W1966255005 hasConceptScore W1966255005C2776364478 @default.

• next