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Involvement of Dopamine with Various Cancers
Published in Nira Ben-Jonathan, Dopamine, 2020
Analysis of DAR expression in paired HCC specimens and adjacent normal tissue showed up-regulation of D1R and down-regulation of D5R in the HCC samples; other DAR were low to undetectable [57]. Treatment with thioridazine caused dose-dependent suppression of cell viability and sphere formation in SNU449, LM3, and Huh7 HCC cell lines. The effects of thioridazine were mediated by induction of G0/G1 cell cycle arrest and suppression of stemness genes CD133, OCT4, and EpCam. Thioridazine also inhibited cell migration by suppressing epithelial–mesenchymal transition-related genes such as twist2 and E-cadherin. Injection of thioridazine to mice bearing LM3 cell-derived xenografts suppressed tumor growth. The authors concluded that thioridazine has a potential role in the treatment of HCC.
Ocular adnexal phenotype and management of a patient with mosaic expression of a mutation in TWIST2
Published in Orbit, 2022
Matthew A. De Niear, James J. Law, Ty W. Abel, Louise A. Mawn
Whole-exome sequencing of the patient’s DNA revealed a heterozygous variant in coding exon 1 of the TWIST2 gene, c.223 G > A, resulting in glutamic acid (E) to be replaced by lysine (K) at amino acid position 75 in the TWIST2 (twist family bHLH transcription factor 2) protein (p.E75K), the particular variant in the TWIST2 protein is known to be associated with AMS.1 Analysis of the TWIST2 gene in the patient’s mother and father revealed that neither parent carried the c.223 G > A variant, indicating the mutation observed in patient likely developed de novo (although germline mosaicism could also account for the variant). Additional sequencing of the patient’s TWIST2 gene by a separate laboratory confirmed the c.223 G > A variant; however, the peak of the A allele was lower than expected with typical heterozygosity, suggesting the patient was mosaic for this variant.
Identification of Two Subgroups of FOLFOX Resistance Patterns and Prediction of FOLFOX Response in Colorectal Cancer Patients
Published in Cancer Investigation, 2021
Sun Tian, Fulong Wang, Shixun Lu, Gong Chen
The resistant mechanism suggested by enriched function analysis of genes in the signature Table S2(B)). Overall, the downregulation of genes such as SPOCK1, TGFB1I1, WISP1, TWIST1, TWIST2 in nonresponders in the signature 31). The activation of mesenchymal phenotype was reported to resist chemotherapy (6,32). Here, the suppression of the mesenchymal phenotype is observed positively associated with the resistance to FOLFOX. This observation does not mean that suppression of the mesenchymal phenotype is the cause of resistance to FOLFOX, rather, the observed suppression of the mesenchymal phenotype is likely to be the effect of functional DNA damage repair proteins. The scores of FOFOX nonresponders predicted by signature BRCA1 and low level of BRCA1 inactivator CAVIN3, suggesting tumor cells in signature BRCA1 to repair double strand breaks induced by oxaliplatin (yellow box, Figure 4(C,D)). The pattern of activated BRCA1 is consistent with the absence of a mesenchymal phenotype as BRCA1 is known to suppress epithelial to mesenchymal transition and stem cell dedifferentiation (33). In addition, the FOLFOX nonresponders predicted by signature TYMP (yellow box, Figure 4(E)), suggesting tumor cells in signature
CD24 as a Novel Predictive Biomarker in Patients with Hepatocellular Carcinoma: Friend or Foe?
Published in Journal of Investigative Surgery, 2020
Nikolaos Machairas, Diamantis I. Tsilimigras, Demetrios Moris
Liver is an immunoprivileged organ biased to tolerance. There are many theories for this vital property. First, tolerance could be attributed to continuous exposure to antigens via portal vein, that promotes the expression of a set of cytokines, antigen-presenting molecules and co-stimulatory signals that impose T-cell inactivation, partly via effects on liver antigen presenting cells [12–14]. This property facilitates the organ to maintain homeostasis with a concomitant price being paid; that of vulnerability to viral infections, autoimmune diseases and carcinogenesis [15,16]. There is an increasing body of literature supporting the role of cluster of differentiation (CD) 24 as a biomarker for cancer diagnosis and prognosis. It seems that CD24 is overexpressed in many types of tumor tissues, including hematopoietic (B-cell lymphomas) as well as solid organ malignancies such as esophageal squamous cell carcinoma, HCC, cholangiocarcinoma, and pancreatic adenocarcinoma [17]. Interestingly, CD24 expression is significantly higher in invasive carcinoma than in precancerous lesions [18]. The causative role of CD24 in liver carcinogenesis is not fully understood; nevertheless, it seems that the epithelial-mesenchymal transition (EMT) and Notch1 signaling activations mediated by CD24 are potential mechanisms favoring the development of HCC [19]. In addition, Twist2-CD24-STAT3-Nanog pathway seems to play a critical role in regulating liver cancer stem-like cell self-renewal [20].