
IndraLab
Statements
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"Interestingly, it has been observed in multiple studies that targeting NFκB signalling pathways when treating MM, reduces drug resistance to PIs xref , suggesting that the significantly increased abundance of Integrin β3 shown in this study may be leading to increased levels of NFκB signalling, causing CAM-DR to three of the five drugs."
| PMC
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"Given that the adhesion of MM cells to BMSC via VLA-4- VCAM-1 interaction confers CAM-DR in MM cells xref , xref , xref and osteoclastogenesis, xref these results suggested the therapeutic impact of TAK1 inhibition on CAM-DR as well as osteoclastogenesis induced by the MM-bone marrow interaction."
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"Several new drugs are developed to overcome de novo drug resistance, such as proteasome inhibitors and EZH2 inhibitors to overcome CAM-DR, and anti-IL-6 monoclonal antibodies and IGF-1R inhibitors to overcome SFM-DR, in a preclinical study, although several of those have not shown efficacy in clinical trials and thus are not available in clinical practice."
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"Drug resistance mediated by the MM BM microenvironment can be caused either by soluble factors or by direct physical cell–cell interactions mediated by cell adhesion molecules, termed soluble factor-mediated drug resistance (SFM-DR) and cell adhesion-mediated drug resistance (CAM-DR), respectively [ xref , xref , xref ]."
| PMC
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"By demonstrating that GBM cells can alternate from one form of CAM-DR (cell-substrate tethering) to another (homocellular cell-cell adhesion) and that inhibition of both forms is necessary for apoptosis sensitization, our findings not only have important implications for novel approaches to restore defective apoptosis programs, but also reveal a novel role of gap junctions in GBM."
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"So far, there is one study that has reported its relationship with head and neck cancer, indicating that ENO1 promotes transformation partly via chemokine CCL20 induction and can be regarded as a potential prognostic marker. xref Moreover, ENO1 participates in the process of lymphoma cell adhesion mediated drug resistance (CAM-DR), besides promoting tumor proliferation. xref ENO1 overexpression was also observed in pancreatic cancer, xref and ENO1 silencing could sensitize hypoxia-induced chemoresistance. xref Some Italian scholars used a genetic model of pancreatic carcinoma and observed the effects that vaccination with ENO1 DNA elicits."
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"Kikuchi et al. demonstrated that pharmacological and genetic inhibition of the IGF1R-PI3K-AKT pathway reverses CAM-DR by promoting enhancer of zeste homolog 2 (EZH2) dephosphorylation and H3K27 hypermethylation both in vitro and in refractory murine MM models, suggesting an epigenetic mechanism underlying CAM-DR [ xref ]."
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"Second, the TME might aid cancer cell survival and induce epithelial–mesenchymal transition (EMT) through the enhanced adhesion of cancer cells to the ECM, leading to therapeutic resistance, often described as cell adhesion-mediated drug resistance (CAM-DR) [ xref , xref , xref ]."
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"Both ectopic expression of miR-548m and knockdown of HDAC6 were able to disrupt the stroma-lymphoma adhesion and consequently induce cell apoptosis, suppress colony formation, sensitize B-lymphoma cells to the cytotoxic drug mitoxantrone, and abolishing the cell adhesion–mediated drug resistance acquisition (CAM-DR) [ xref ]."
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"MM cell adhesion to BMSC through the interaction between VLA-4 and its corresponding ligand, VCAM-1, is among the predominant mechanisms for cell adhesionmediated drug resistance (CAM-DR) in MM, xref , xref while enhancing the production of IL-6 30 and RANKL, an critical osteoclastogenic factor in MM. xref In addition to TAK1 activation in MM cells, TAK1 was found to be phosphorylated along with PIM2 upregulation in BMSC, when cocultured with MM cells ( xref )."
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"Furthermore, Wang et al. recently demonstrated that BTK induces CAM-DR through CXCR4 regulation degradation in MM [ xref ], promoting BTK expression induced MM cell adherence to the extracellular matrix and stromal cells in vitro and in vivo and increased drug resistance to bortezomib and doxorubicin in MM cells."
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"EMDR can be separated in two groups: EMDR due to soluble factors which is called Soluble Factor-Mediated Drug Resistance (SFM-DR), and EMDR due to adhesion process between the tumor cell receptors and extracellular matrix (ECM) proteins which is called Cell Adhesion-Mediated Drug Resistance (CAM-DR)."
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"Furthermore, we clarified that CD49d- and CD49e-mediated CAM-DR could be attributed to an increase in the expression of B cell leukemia-xL (Bcl-xL) and survivin proteins, and a decrease in the expression of Bcl-2 associated X (Bax), Bcl-2 interacting mediator (Bim) and p53 upregulated modulator of apoptosis (PUMA) proteins via nuclear factor kappaB (NF-κB) activation."
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"While we found alterations in other metabolism-associated genes (e.g. PKM2, CS, IDH1, ACO2, FH, MDH2, or HK1)), we focused on examining the functional significance of ENO1 in the present study since: (1) a significant induction of ENO1 was noted during pDC-MM interactions versus other molecules; (2) ENO1 is essential for maintaining tumor cell metabolism and represents a potential therapeutic target in cancer [ xref – xref ]; (3) ENO1 promotes tumor cell proliferation and cell adhesion-mediated drug-resistance (CAM-DR) [ xref ] characteristic of MM; and (4) ENO1 functions as an immunoregulatory molecule both in T-regulatory cell differentiation and dendritic cell function [ xref , xref ]."
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"The apoptosis-protective adhesion to stromal cells, termed cell adhesion-mediated drug resistance (CAM-DR), is another underlying mechanism of R-CHOP resistance in DLBCL.[ xref ]CAM-DR was revealed to correlate with rituximab resistance through ADAM metalloproteinase domain 12 ( ADAM-12 ) upregulation and phosphatidylinositol 3-kinase ( PI3K ) -Akt signaling modulation.[ xref ]However, as per findings reported by Lenz et al ,[ xref ]genetically identified non-malignant signatures of stromal-1 (fibrosis and myeloid infiltration) and stromal-2 (vessel formation) in pretreatment biopsies were found to be prognostically favorable and unfavorable for patients with DLBCL who received R-CHOP, respectively."