Minh-Tuan Nguyen-Khac's research while affiliated with University of Liège and other places

... This limits its therapeutic applications, for example, in cancer treatment. For instance, a clinical trial in patients with glioblastoma had to be discontinued because there was no response in patients with malignant glioma and two patients died prematurely 49 . Sorafenib is an anticancer multikinase inhibitor approved by the US Food and Drug Administration (FDA) that purportedly induces cell death through system x c inhibition 13,50 . ...

... Many of these responses may be cancer-typedependent; studies have shown that CSNK2A1 activates phosphorylation of SIRT6 in breast cancer, the phosphoinositide 3-kinase (PI3K)-protein kinase B (Akt)-mammalian target of rapamycin (mTOR) pathway in gastric cancer, and nuclear factor kB (NF-kB) in glioblastoma, all contributing to poor patient prognosis. [48][49][50] In order to examine the effect of silencing CSNK2A1 expression on oncogenic activity in ovarian cancer cells, viability, scratch migration, and colonization assays were completed after treatment with DIV3W-siCSNK2A1 complexes. While we did not observe any significant loss of cell viability after a 48-h treatment with DIV3W-siCSNK2A1 complexes, other studies have also demonstrated that knocking down CSNK2A1 does not result in a loss in cell viability without including supplemental drug treatments due to the many roles of CSNK2A1 in cell communication pathways in different cell types. ...

... Enfin, se pose également la question d'un éventuel rôle de ces zones neurogéniques dans le déclenchement ou la pathogénie des gliomes de différents grades histologiques. Cet aspect fait cependant l'objet d'une revue connexe (33). ...

... Generally, connexins are considered to be tumor suppressive; however, recent studies using clinical samples indicate that connexins play a different role depending on the type of tumor. For example, connexin 30 expression inhibits the growth of malignant gliomas, but is protective against radiation treatment [5]. Furthermore, it has been observed that connexin 30.3 can enhance gastric cancer cell proliferation and migration through activation of the Wnt/CTNNB1 pathway [6]. ...

... CK2 is a ubiquitous cellular Ser/Thr-protein kinase that has downstream effects on cell proliferation, cell viability, modulation of DNA damage, contractility, and cellular invasion through the extracellular matrix (Pinna and Meggio 1997;Morales and Carpenter 2004;Kim et al., 2018;Suhas et al., 2018). Apigenin is well known for its ability to inhibit CK2 and has been used experimentally as a CK2 inhibitor (Ahmad et al., 2006;Kroonen et al., 2012;Jung et al., 2014;Kim et al., 2018;Suhas et al., 2018). However, it is uncertain that apigenin exerts its effect on cellular behaviours including regulation of interactions with the extracellular matrix, cellular contractility and the function of molecules including CD26 (Lefort and Blay 2011;Kim et al., 2018;Suhas et al., 2018) solely through CK2. ...

... Orbital roof fractures after blunt injury are rare: 1 -5% of orbital fractures [1]. In fact, post-traumatic brain hernias represent unusual complications, with only 25 cases been reported [2] they are caused by blunt trauma to the orbital column and are more common in children, especially before age 7, due to the lack of pneumatization of the frontal sinus [3]. Orbital roof fractures can widen over time. ...

... Further, we tested the ability of SiR in imaging intracellular Cys fluctuation induced by sulphasalazine (SAS), an inhibitor of system x c  , [56][57][58] which has also been evaluated in phase I clinical trial. 59 As shown in Fig. 2B, when HeLa cells were pretreated with increased concentrations of SAS for 48 hr and then treated with the increasing concentrations of SiR, a gradually decreased intracellular fluorescence was observed in a dose-dependent manner, consistent with previous report that SAS could deplete intracellular Cys by inhibiting the activity of system x c  . [56][57][58] Given that SAS and BSO both were reported to be able to sensitize cancer cells to chemotherapies, we subsequently wanted to know which is better. ...

... In this tumorigenic process, glioma stem cells exert a leading role (Uchida et al., 2000;Gaya et al., 2002;Kondo et al., 2004;Gürsel et al., 2011). Since glioma stem cells are able to selfpropagate, in order to avoid recurrence, it is fundamental to target specifically them (Kroonen et al., 2008). The new possibility to isolate GBM stem cells allows for new therapeutic approaches, among which are gene replacement, knockdown, or silencing (Kroonen et al., 2008). ...

... A dexamethasone-mediated disruption of the bystander effect of CN-2409 also has to be considered as playing a crucial role in this regard. 51 Also, pre-existing immunity against therapeutic virotherapies may also have an impact on local immunotherapies. 52 Cell viability and T-cell killing assays have shown that dexamethasone diminishes the effects of CAN-2409 treatment in vitro, with immune-mediated killing being the most affected. ...

... SSZ and its metabolites (sulfapyridine and 5-aminosalicylic acid) suppress lymphocyte activities and inhibit cytokine release. Preclinical studies showed that SSZ has an antineoplastic effect on lymphoma [100], breast cancer [101][102][103][104][105], colorectal cancer [106], gastric cancer [107], glioma [108][109][110], lung cancer [111], and prostate cancer. The mechanisms accounting for the antineoplastic effect of SSZ may include (a) inhibition of xccystine transporter [100,[110][111][112][113][114], (b) inhibition of matrix metalloproteinase-related genes [102], (c) increasing the accumulation of intracellular reactive oxygen species (ROS) [102], and (d) inhibition of NF-jB activation [108]. ...