China
Africa
Explore chapters and articles related to this topic
Functions of Oncogene and Proto-Oncogene Protein Products
Published in Pimentel Enrique, Oncogenes, 2020
The v-myb oncogene apparently rose by transduction of several of the exons of a cellular gene, c-myb, which is present in the genome of a broad spectrum of vertebrate species.187-189 The chicken c-myb product is a 75,000-dalton protein, termed p45c-myb and the viral 45,000-dalton v-myb product is thus a truncated version of the cellular protein.190 In addition, p45v-myb and p45c-myb differ by the presence of several amino acid substitutions.191 Qualitative differences may be responsible for the oncogenic products as compared to the pl5c-myb cellular product. All three products are located in the nucleus,192,193 which indicates that the cellular localization is not sufficient to determine neoplastic transformation. DNA-binding activity is associated with the purified v-myb proteins from AMV and E26 ALV.194 Moreover, this activity is temperature-sensitive for E26 ts mutants.
The gastrointestinal system
Published in C. Simon Herrington, Muir's Textbook of Pathology, 2020
Sharon J. White, Francis A. Carey
The most common malignant salivary neoplasm is mucoepidermoid carcinoma (MEC) which may affect children as well as adults. Histologically it shows a variable mixture of squamoid, mucous, and intermediate cell types. The behaviour of mucoepidermoid carcinoma is variable with prognosis reflecting tumour grade. A t(11;19)(q21;p13) translocation and CRTC1-MAML2 gene fusion is found in most MECs. Adenoid cystic carcinoma tends to occur in older individuals and often shows a distinctive cribriform or ‘lace-like’ growth pattern (Figure 10.16). It has a particular tendency for perineural spread, thus making it very difficult to eradicate surgically. The majority of tumours have a t(6;9) translocation and MYB-NFIB gene fusion.
Gene Structure and Expression in Colon Cancer
Published in Leonard H. Augenlicht, Cell and Molecular Biology of Colon Cancer, 2019
Finally, other members of the myc gene family have also been investigated. The mybgene is both overexpressed and amplified in the colon neuroendocrine tumor cell line COLO 320 81 and in two lines, COLO 201 and 205, derived from a single colon tumor.82 In COLO 320, the amplified gene is present either in a homogeneously staining region (HSR) or in double minute (DM) chromosomes. We have found expression of the N-myc gene, previously suggested to be limited to neuroendocrine tissue, 83 in HT29 cells and in derivatives of this line differentiated along the lineages of mucin secretion and vectorial transport.38
Sickle cell disease in the era of precision medicine: looking to the future
Published in Expert Review of Precision Medicine and Drug Development, 2019
Martin H Steinberg, Sara Kumar, George J. Murphy, Kim Vanuytsel
MYB regulates the proliferation and maturation of erythroid cells and gene expression within the HBB gene cluster [24,26]. A 3 bp deletion polymorphism (rs66650371) is the probable functional variant of this QTL that affects γ-globin gene expression [27]. This SNP is highly associated with HbF in multiple populations. In its proximity are binding sites for multiple erythropoiesis-related transcription factors and it is in a locus with enhancer-like activity [28,29]. Downregulation of a long noncoding RNA, transcribed from this enhancer increased γ-globin gene mRNA 200-fold [30]. The frequency of rs66650371 in African and Saudi populations is low compared with its frequency in normal Europeans or Chinese with β thalassemia reducing the effect of this variant on HbF in sickle cell anemia.
c-MYB and DMTF1 in Cancer
Published in Cancer Investigation, 2019
Elizabeth A. Fry, Kazushi Inoue
Chromosomal translocations involving the c-MYB gene have been reported in other types of human tumors than leukemias. The t(6;9)(q22-23;p23-24) translocation was found in adenoid cystic carcinomas (ACCs) of the breast, head and neck, vulva, lacrimal gland and other tissues (17, 34, 36, 37), which consistently result in MYB-NF1B fusion transcripts consisting of c-MYB exon 14 linked to the last coding exon of nuclear factor 1B (NF1B). This leads to loss of c-MYB exon 15, which encodes the 3’-UTR, where several highly conserved target sites for microRNAs (miR15a/16 and miR-150) are located (Figure 3A). Thus, the translocation appears to deregulate c-MYB by removing the microRNA binding sites, and the product is different from that of wild type c-Myb.
Chitosan-gold nanoparticles mediated gene delivery of c-myb facilitates osseointegration of dental implants in ovariectomized rat
Published in Artificial Cells, Nanomedicine, and Biotechnology, 2018
Jyoti Shrestha Takanche, Ji-Eun Kim, Jeong-Seok Kim, Min-Ho Lee, Jae-Gyu Jeon, Il-Song Park, Ho-Keun Yi
The OVX rat model is accompanied by estrogen deficiency, reduced jawbone, periodontal bone and tooth loss [10]. c-myb is a transcription factor and member of the myoblastosis (MYB) family involved in the control of cell proliferation, differentiation, survival and death. c-myb plays a critical role in hematopoiesis and is most prevalent in bone marrow [11,12]. The analysis of various studies suggests that c-myb has a role in the cell developmental process including odontogenesis and osteogenesis [13–15]. Our previous study demonstrated that the gene delivery of c-myb increases bone formation around surrounding implants in a rat model [9]. However, the role of c-myb in osteoporosis is still poorly understood. Considering the possible benefit of gene delivery of c-myb for improving bone formation and supporting the osseointegration of implant and bone by Ch-GNP/c-myb-coated Ti implants, in this study we demonstrated the role of Ch-GNP/c-myb-coated Ti implants in osseointegration and bone formation in osteoporotic condition, as well as the possible molecular mechanism of c-myb in the OVX-induced osteoporosis rat model.