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The Non-Hodgkin’s Lymphomas and Plasma Cell Dyscrasias
Published in Harold R. Schumacher, William A. Rock, Sanford A. Stass, Handbook of Hematologic Pathology, 2019
Lynne V. Abruzzo, L. Jeffrey Medeiros
Diffuse large B-cell lymphomas have clonal rearrangements of the Ig heavy and light chain genes. The TCR genes are usually in the germline configuration. A subset of cases have the t(14;18) by conventional cytogenetics or rearrangement of the bcl-2 oncogene by molecular diagnostic techniques. These lymphomas may represent histologic transformation of FCL. Patients with de-novo DLBCL with bcl-2 rearrangement have an increased tendency to relapse compared to histologically similar tumors without bcl-2 rearrangement, similar to the behavior of FCL. Another subset of DLBCL have translocations or other abnormalities that involve chromosome 3q27. This locus is the site of the bcl-6 gene, a zinc finger transcription factor and putative oncogene. The bcl-6 gene is rearranged in approximately one-third of these neoplasms, more often in those that arise in extranodal sites.
Chemical– and Drug–Receptor Interactions
Published in Frank A. Barile, Barile’s Clinical Toxicology, 2019
All nuclear receptors operate as ligand-activated zinc-finger transcription factors with a modular structure that comprises six domains. Figure 11.5 presents a schematic illustration of the structural and functional organization of nuclear receptors.
Epidemiology and genetic associations of neonatal tumors
Published in Prem Puri, Newborn Surgery, 2017
The Knudson model for WT has been validated through molecular identification of WT1 gene variation.117,118 The WT1 gene encodes a transcription factor that appears to act both as a tumor suppressor gene119 as well as an important regulator of renal embryological development. The deletion of this gene results in the development of a WT120 by encoding a zinc finger transcription factor, which binds GC-rich sequences and acts as either an activator or repressor of transcription for a number of growth factors (including Igf-2)121. This may be a possible explanation of the mechanism of action of WT1 in the pathogenesis of WT.
KLF5-mediated aquaporin 3 activated autophagy to facilitate cisplatin resistance of gastric cancer
Published in Immunopharmacology and Immunotoxicology, 2023
Xudong Dai, Yong Chen, Ning Chen, Jin Dou, Haiwen Zhuang, Jian Wang, Xin Zhao, Xiaoyu Zhang, Haijian Zhao
To further explore the mechanism underlying the effects of AQP3 on the resistance of GC to CDDP, bioinformatics analysis was performed and the potential targeting relationship between KLF5 and AQP3 was predicted, with the succeeding dual-luciferase reporter and ChIP assays revealing that KLF5 could positively modulate the transcription of AQP3 in CDDP-resistant GC cells. KLF5, a zinc-finger transcription factor, mediates essential functions in diverse cellular processes including invasion, proliferation and apoptosis [40,41]. Mechanically, KLF5 specifically binds to the promoter regions of its target genes to activate or restrain their transcription [42]. In addition, several reports have revealed the oncogenic role of KLF5 in GC [43–45]. In our study, it was worth noting that the KLF5 knockdown reversed overexpressed AQP3-induced effects on the autophagy, viability, invasion, migration and EMT in CDDP-resistant GC cells, which implied that KLF5-mediated AQP3 activated autophagy to facilitate CDDP resistance in GC.
Pluripotency inducing Yamanaka factors: role in stemness and chemoresistance of liver cancer
Published in Expert Review of Anticancer Therapy, 2021
Homa Fatma, Hifzur Rahman Siddique
Nio et al. [15] also reported c-MYC, which gives a malignant phenotype to HCC cells [15]. In another report, it was observed that lncRNA, testis-associated highly conserved oncogenic long non-coding RNA (THOR), regulates c-MYC via β-catenin and contributes to the dedifferentiation of HCC cells into HCC stem cells [68]. Another Yamanaka factor, OCT4, is responsible for the induction of CSC properties in HCC through the transactivation of c-JUN. OCT4 binds to the promoter of c-JUN and is an essential step for imparting CSC-like property in HepG2 cells [14]. OCT4 is a nucleocytoplasmic shuttling factor and regulates endothelial lineage transition of liver CSCs. Two isoforms of OCT4 are involved in the endothelial trans-differentiation phenomenon. Relative overexpression of nucleic isoform OCT4A facilitates trans-differentiation of liver CSCs in tumorigenic endothelial cells and maintains the pluripotent state of liver CSCs. On the other hand, downregulation of OCT4A and subsequent upregulation of cytoplasmic isoform OCT4B1 leads to the direct differentiation of liver CSCs into endothelium [69]. Although the Zinc finger transcription factor, ZIC2, is upregulated in liver cancers and liver CSCs, the expression level of ZIC2 is subsequently higher in CSCs HCC samples than the non-CSCs HCC samples. ZIC2 triggers stimulation of OCT4 in liver CSCs by recruiting NURF complex and maintains stemness [70].
Identification of key biomolecules in rheumatoid arthritis through the reconstruction of comprehensive disease-specific biological networks
Published in Autoimmunity, 2020
Recently, tissues with RA has been analyzed at the transcriptome level such as Ye et al. analyzed gene expression of CD4 positive T cells in healthy and diseased samples [11]. Their study showed that CD4 positive T cells highly related to the STAT3 signalling and Wnt signalling pathway in the RA pathogenesis. Also, their results suggest that ZEB1, ZNF292 and ZNF644, zinc finger transcription factors (TFs), may be taken an active role in development of RA. In another study, Ekwall et al. demonstrated that LBH is a key candidate gene in synovial tissues with RA and it is highly correlated with growth factors by using microarray techniques [12]. Ouyang et al. worked on five circular RNAs (092516, 003524, 103047, 104871 and 101873) via microarray screening in healthy individuals and patients with RA. It was determined that they were significantly elevated in peripheral blood mononuclear cells with RA [13].