FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2800337568> ?p ?o ?g. }

• W2800337568 endingPage "3531" @default.
• W2800337568 startingPage "3522" @default.
• W2800337568 abstract "Abstract The development of myeloid and lymphoid neoplasms related to overexpression of FGFR1 kinases as a result of chromosome translocations depends on the promotion of a stem cell phenotype, suppression of terminal differentiation, and resistance to apoptosis. These phenotypes are related to the stem cell leukemia/lymphoma syndrome (SCLL), which arises through the effects of the activated FGFR1 kinase on gene transcription, which includes miRNA dysregulation. In a screen for miRNAs that are directly regulated by FGFR1, and which stimulate cell proliferation and survival, we identified miR-339-5p, which is highly upregulated in cells carrying various different chimeric kinases. Overexpression of miR-339-5p in SCLL cell types enhances cell survival and inhibition of its function leads to reduced cell viability. miR-339-5p overexpression protects cells from the consequences of FGFR1 inactivation, promoting cell-cycle progression and reduced apoptosis. Transient luciferase reporter assays and qRT-PCR detection of endogenous miR-339-5p expression in stably transduced cell lines demonstrated that BCR-FGFR1 can directly regulate miR-339-5p expression. This correlation between miR-339-5p and FGFR1 expression is also seen in primary human B-cell precursor acute lymphoblastic leukemia. In a screen to identify targets of miR-339-5p, we identified and verified the BCL2L11 and BAX genes, which can promote apoptosis. In vivo, SCLL cells forced to overexpress miR-339-5p show a more rapid onset of disease and poorer survival compared with parental cells expressing endogenous levels of miR-339-5p. Analysis of human primary B-cell precursor ALL shows a significant higher expression of miR339-5p compared with the two cohorts of CLL patient samples, suggesting direct roles in disease progression and supporting the evidence generated in mouse models of SCLL. Significance: Proapoptiotic genes that are direct targets of miR-339-5p significantly influence promotion and aggressive development of leukemia/lymphomas associated with FGFR1 overexpression. Cancer Res; 78(13); 3522–31. ©2018 AACR." @default.
• W2800337568 created "2018-05-17" @default.
• W2800337568 creator A5021944838 @default.
• W2800337568 creator A5027396734 @default.
• W2800337568 creator A5027726624 @default.
• W2800337568 creator A5027851192 @default.
• W2800337568 creator A5031988629 @default.
• W2800337568 creator A5035212537 @default.
• W2800337568 creator A5037132479 @default.
• W2800337568 creator A5055311322 @default.
• W2800337568 creator A5062917844 @default.
• W2800337568 creator A5079808476 @default.
• W2800337568 date "2018-07-01" @default.
• W2800337568 modified "2023-10-10" @default.
• W2800337568 title "miR-339 Promotes Development of Stem Cell Leukemia/Lymphoma Syndrome via Downregulation of the <i>BCL2L11</i> and <i>BAX</i> Proapoptotic Genes" @default.
• W2800337568 cites W114060563 @default.
• W2800337568 cites W1744683414 @default.
• W2800337568 cites W1884243320 @default.
• W2800337568 cites W2002037400 @default.
• W2800337568 cites W2019829976 @default.
• W2800337568 cites W2027657804 @default.
• W2800337568 cites W2027985469 @default.
• W2800337568 cites W2043761608 @default.
• W2800337568 cites W2044618451 @default.
• W2800337568 cites W2044867649 @default.
• W2800337568 cites W2054195724 @default.
• W2800337568 cites W2085908746 @default.
• W2800337568 cites W2088846648 @default.
• W2800337568 cites W2095600622 @default.
• W2800337568 cites W2109227959 @default.
• W2800337568 cites W2134629862 @default.
• W2800337568 cites W2137734450 @default.
• W2800337568 cites W2140710807 @default.
• W2800337568 cites W2149527737 @default.
• W2800337568 cites W2152276424 @default.
• W2800337568 cites W2154570280 @default.
• W2800337568 cites W2157740207 @default.
• W2800337568 cites W2287422180 @default.
• W2800337568 cites W2337882977 @default.
• W2800337568 cites W2470246776 @default.
• W2800337568 cites W2740607174 @default.
• W2800337568 cites W2793478791 @default.
• W2800337568 doi "https://doi.org/10.1158/0008-5472.can-17-4049" @default.
• W2800337568 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6052880" @default.
• W2800337568 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/29735550" @default.
• W2800337568 hasPublicationYear "2018" @default.
• W2800337568 type Work @default.
• W2800337568 sameAs 2800337568 @default.
• W2800337568 citedByCount "25" @default.
• W2800337568 countsByYear W28003375682018 @default.
• W2800337568 countsByYear W28003375682019 @default.
• W2800337568 countsByYear W28003375682020 @default.
• W2800337568 countsByYear W28003375682021 @default.
• W2800337568 countsByYear W28003375682022 @default.
• W2800337568 countsByYear W28003375682023 @default.
• W2800337568 crossrefType "journal-article" @default.
• W2800337568 hasAuthorship W2800337568A5021944838 @default.
• W2800337568 hasAuthorship W2800337568A5027396734 @default.
• W2800337568 hasAuthorship W2800337568A5027726624 @default.
• W2800337568 hasAuthorship W2800337568A5027851192 @default.
• W2800337568 hasAuthorship W2800337568A5031988629 @default.
• W2800337568 hasAuthorship W2800337568A5035212537 @default.
• W2800337568 hasAuthorship W2800337568A5037132479 @default.
• W2800337568 hasAuthorship W2800337568A5055311322 @default.
• W2800337568 hasAuthorship W2800337568A5062917844 @default.
• W2800337568 hasAuthorship W2800337568A5079808476 @default.
• W2800337568 hasBestOaLocation W28003375681 @default.
• W2800337568 hasConcept C104317684 @default.
• W2800337568 hasConcept C145059251 @default.
• W2800337568 hasConcept C190283241 @default.
• W2800337568 hasConcept C28328180 @default.
• W2800337568 hasConcept C502942594 @default.
• W2800337568 hasConcept C54355233 @default.
• W2800337568 hasConcept C62112901 @default.
• W2800337568 hasConcept C86803240 @default.
• W2800337568 hasConcept C95444343 @default.
• W2800337568 hasConceptScore W2800337568C104317684 @default.
• W2800337568 hasConceptScore W2800337568C145059251 @default.
• W2800337568 hasConceptScore W2800337568C190283241 @default.
• W2800337568 hasConceptScore W2800337568C28328180 @default.
• W2800337568 hasConceptScore W2800337568C502942594 @default.
• W2800337568 hasConceptScore W2800337568C54355233 @default.
• W2800337568 hasConceptScore W2800337568C62112901 @default.
• W2800337568 hasConceptScore W2800337568C86803240 @default.
• W2800337568 hasConceptScore W2800337568C95444343 @default.
• W2800337568 hasFunder F4320332161 @default.
• W2800337568 hasIssue "13" @default.
• W2800337568 hasLocation W28003375681 @default.
• W2800337568 hasLocation W28003375682 @default.
• W2800337568 hasLocation W28003375683 @default.
• W2800337568 hasLocation W28003375684 @default.
• W2800337568 hasLocation W28003375685 @default.
• W2800337568 hasOpenAccess W2800337568 @default.
• W2800337568 hasPrimaryLocation W28003375681 @default.
• W2800337568 hasRelatedWork W2060006898 @default.
• W2800337568 hasRelatedWork W2573992804 @default.
• W2800337568 hasRelatedWork W2605096019 @default.
• W2800337568 hasRelatedWork W2605667993 @default.

• next