Disease: Multiple Myeloma ×
Source: ALL
Disease Score gda Association Type Type Original DB Sentence supporting the association PMID PMID Year
CUI: C0026764
Disease: Multiple Myeloma
Multiple Myeloma 		0.100 Biomarker disease BEFREE Together, our results have established the role of PTEN, but not SHIP and SHIP2, in negatively regulating the PI3K/Akt cascade and in myeloma leukemogenesis. 12149650 2002
CUI: C0026764
Disease: Multiple Myeloma
Multiple Myeloma 		0.100 Biomarker disease BEFREE Since PTEN-null myeloma lines exhibited much stronger Akt activation than PTEN-expressing cells in response to insulin-like growth factor I stimulation, we determined whether Akt could be responsible for PI3K-mediated cell survival and growth of PTEN-null myeloma lines. 13679867 2003
CUI: C0026764
Disease: Multiple Myeloma
Multiple Myeloma 		0.100 GeneticVariation disease BEFREE These findings suggest that PI3K/AKT mutations may not play a major role in multiple myeloma. 20022634 2010
CUI: C0026764
Disease: Multiple Myeloma
Multiple Myeloma 		0.100 Biomarker disease BEFREE PI3K/p110{delta} is a novel therapeutic target in multiple myeloma. 20505158 2010
CUI: C0026764
Disease: Multiple Myeloma
Multiple Myeloma 		0.100 Biomarker disease BEFREE The Pim inhibitor (Z)-5-(4-propoxybenzylidene) thiazolidine-2, 4-dione and the PI3K inhibitor LY294002 cooperatively enhance MM cell death. 21475253 2011
CUI: C0026764
Disease: Multiple Myeloma
Multiple Myeloma 		0.100 Biomarker disease BEFREE We have identified a robust cytogenetic biomarker for response to PI3K/mTOR inhibition--these results will inform the design and prioritisation of clinical studies with novel inhibitors in genetic subgroups of myeloma. 22415553 2012
CUI: C0026764
Disease: Multiple Myeloma
Multiple Myeloma 		0.100 AlteredExpression disease BEFREE A transcriptional-dependent (TFEB) and independent (PI3K/mTORC1) activation of autophagy mediated FK866 MM cytotoxicity. 22955917 2012
CUI: C0026764
Disease: Multiple Myeloma
Multiple Myeloma 		0.100 Biomarker disease BEFREE These results suggest that oncogenic RAS is a predictor of sensitivity to combination treatment with PI3K/Akt and MEK/MAPK inhibitors and that such an approach might therefore be beneficial for this genetically well-defined subgroup of MM patients. 22985491 2012
CUI: C0026764
Disease: Multiple Myeloma
Multiple Myeloma 		0.100 Biomarker disease BEFREE The PI3K/Akt/mTOR signal transduction pathway plays a central role in multiple myeloma (MM) disease progression and development of therapeutic resistance. mTORC1 inhibitors have shown limited efficacy in the clinic, largely attributed to the reactivation of Akt due to rapamycin induced mTORC2 activity. 23185517 2012
CUI: C0026764
Disease: Multiple Myeloma
Multiple Myeloma 		0.100 Biomarker disease BEFREE We show p110 α and β are the predominant PI3K catalytic subunits in MM and that a highly selective class I PI3K inhibitor, GDC-0941, has robust activity as a single agent to induce cell cycle arrest and apoptosis of both MM cell lines and patient myeloma cells. 23318440 2014
CUI: C0026764
Disease: Multiple Myeloma
Multiple Myeloma 		0.100 Biomarker disease BEFREE We tested the effect of pan-class I PI3K inhibition by siRNA silencing or pharmacologic inhibition with buparlisib on MM cell survival, apoptosis and cell cycle in vitro and tumor growth and mobilization of MM cells in vivo. 25060991 2014
CUI: C0026764
Disease: Multiple Myeloma
Multiple Myeloma 		0.100 AlteredExpression disease BEFREE Cancers like multiple myeloma (MM), which display elevated activity in key translation regulatory nodes, such as the PI3K/mammalian target of rapamycin and MYC-eukaryotic initiation factor (eIF) 4E pathways, are predicted to be particularly sensitive to therapeutic strategies that target this process. 25197055 2014
CUI: C0026764
Disease: Multiple Myeloma
Multiple Myeloma 		0.100 Biomarker disease BEFREE Furthermore, our results demonstrated that the enforced expression of miR-145 in H929 cells profoundly decreased the levels of p-AKT and p-PI3K, which may contribute to some extent to the inhibition of MM cell proliferation and survival. 25369735 2015
CUI: C0026764
Disease: Multiple Myeloma
Multiple Myeloma 		0.100 AlteredExpression disease BEFREE Previously we showed that tetraspanin overexpression in MM cell lines attenuated mTOR and PI3K cascades, induced protein synthesis, activated unfolded protein response (UPR), and caused autophagic death, all suggesting breach of proteostasis. 25422161 2015
CUI: C0026764
Disease: Multiple Myeloma
Multiple Myeloma 		0.100 AlteredExpression disease BEFREE Multiple myeloma (MM) is a generally fatal plasma cell cancer that often shows activation of the phosphoinositide 3-kinase/Akt (PI3K/Akt) pathway. 25837824 2015
CUI: C0026764
Disease: Multiple Myeloma
Multiple Myeloma 		0.100 Biomarker disease BEFREE Moreover, the novel specific PI3K/Akt/mTOR signaling inhibitor S14161 displayed its prowess as a potential therapeutic agent by targeting MM SP cells. 25915427 2015
CUI: C0026764
Disease: Multiple Myeloma
Multiple Myeloma 		0.100 Biomarker disease BEFREE These results indicate that CIP2A modulates myeloma cell proliferation and apoptosis via PI3K/AKT/mTOR signaling and suggest that it can potentially serve as a drug target for the treatment of multiple myeloma. 27144172 2016
CUI: C0026764
Disease: Multiple Myeloma
Multiple Myeloma 		0.100 Biomarker disease BEFREE However, bortezomib activates the phosphatidylinositol 3-kinase/AKT (PI3K/AKT) pathway (which is essential to the development of myeloma), often resulting in drug resistance and disease recurrence. 27439454 2017
CUI: C0026764
Disease: Multiple Myeloma
Multiple Myeloma 		0.100 AlteredExpression disease BEFREE Myeloma-secreted 2DDR bound to integrin αVβ3/α5β1 in the progenitors, activated PI3K (phosphoinositide 3-kinase)/Akt signaling, and increased DNMT3A (DNA methyltransferase 3A) expression, resulting in hypermethylation of RUNX2, osterix, and IRF8 This study elucidates an important mechanism for myeloma-induced bone lesions, suggesting that targeting TP may be a viable approach to healing resorbed bone in patients. 27559096 2016
CUI: C0026764
Disease: Multiple Myeloma
Multiple Myeloma 		0.100 Biomarker disease BEFREE These results collectively demonstrate that acid activates the TRPV1-PI3K-Akt-Sp1 signaling in MM cells while inducing HDAC-mediated gene repression, and suggest that a positive feedback loop between acid sensing and the PI3K-Akt signaling is formed in MM cells, leading to MM cell response to acidic bone lesions. 27626482 2016
CUI: C0026764
Disease: Multiple Myeloma
Multiple Myeloma 		0.100 Biomarker disease BEFREE Concomitant pan-Raf/PI3K inhibition was also effective in carfilzomib- and lenalidomide-resistant MM models underscoring that this attractive therapeutic anti-MM strategy is suitable for immediate clinical translation. 27686868 2017
CUI: C0026764
Disease: Multiple Myeloma
Multiple Myeloma 		0.100 Biomarker disease BEFREE We report that PI3Kδ and PI3Kγ isoforms have distinct functions in MM and that combined PI3kδ/γ isoform inhibition has anti-MM activity. 28282033 2017
CUI: C0026764
Disease: Multiple Myeloma
Multiple Myeloma 		0.100 Biomarker disease BEFREE The Role of PI3K Isoforms in Regulating Bone Marrow Microenvironment Signaling Focusing on Acute Myeloid Leukemia and Multiple Myeloma. 28350342 2017
CUI: C0026764
Disease: Multiple Myeloma
Multiple Myeloma 		0.100 AlteredExpression disease BEFREE Oscillating expression of interleukin-16 in multiple myeloma is associated with proliferation, clonogenic growth, and PI3K/NFKB/MAPK activation. 28512269 2017
CUI: C0026764
Disease: Multiple Myeloma
Multiple Myeloma 		0.100 Biomarker disease BEFREE Endoplasmic reticulum stress induces autophagy and apoptosis while inhibiting proliferation and drug resistance in multiple myeloma through the PI3K/Akt/mTOR signaling pathway. 28977849 2017