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Basic Cell Biology
Published in Kedar N. Prasad, Handbook of RADIOBIOLOGY, 2020
To understand the radìation injury of cells, one must be thoroughly aware of their structures, kinetics, and functions. Therefore, a brief description of basic cell biology in its simplest form is presented in this chapter.
Bias, Conflict of Interest, Ignorance, and Uncertainty
Published in Ted W. Simon, Environmental Risk Assessment, 2019
The hallmarks of cancer provide a conceptual basis for the functional characteristics of tumor cells that have undergone malignant transformation. The purpose of identifying the hallmarks was to make sense of the complexity of tumorigenesis and the wide variety of tumor types. The goal was to advance the treatment of cancer:With holistic clarity of mechanism, cancer prognosis and treatment will become a rational science, … One day, we imagine that cancer biology and treatment—at present, a patchwork quilt of cell biology, genetics, histopathology, biochemistry, immunology, and pharmacology—will become a science with a conceptual structure and logical coherence that rivals that of chemistry or physics.18These hallmarks occur through basic cellular processes; three such processes associated with development of cancer hallmarks are: (1) epigenetic changes, including alterations of DNA methylation in critical portions of the genome, (2) epistasis or gene–gene interactions, and (3) dysregulation of cellular energetics.
The laboratory basis of medical genetics
Published in Peter S. Harper, The Evolution of Medical Genetics, 2019
A major difference between the disorders whose gene was isolated by positional cloning and those where a known protein was the starting point was that the workers involved usually had little or no clue until the very last minute what the nature of the protein defect might be. Having used DNA-based technology throughout the often prolonged positional cloning process, the emergence of the gene sequence could suddenly show that its role might be in any one of a number of quite different areas of cell biology; this might be one with already established techniques of its own and experienced scientists working in the area, or alternatively the gene sequence might give little or no indication of the protein's function. Either way the geneticists responsible for the gene isolation found themselves in a new world with difficult choices to make. Should they convert themselves into cell biologists in a strange area requiring a radical change of orientation, or confine themselves to the detailed analysis of the gene and its mutations?
Current perspectives on the clinical management of cryptogenic stroke
Published in Expert Review of Neurotherapeutics, 2023
Dixon Yang, Mitchell S. V. Elkind
Looking ahead, molecular cell biology and specialized imaging may be two areas that particularly hold promise. Several studies have examined cellular and histological clot compositions of large vessel occlusions extracted during endovascular thrombectomy. Quantifying the relative proportion of red blood cells, fibrin, platelets, and leukocytes may provide clues on the source of the thromboembolism in cryptogenic stroke [8,127]. In a similar thread, emerging data have suggested that RNA may serve as a precision biomarker in the determination of stroke etiology [128–130]. Various circulating cells that may contribute to thromboembolism formation in the peripheral blood can express different RNA signatures and these differences have been preliminarily applied to classify probable etiology of cryptogenic stroke in conjunction with neuroimaging [131]. On the imaging front, high-resolution MRI with vessel wall imaging has become increasingly popular as an adjunctive tool in the assessment of extra- and intracranial arterial stenosis as it offers information beyond the degree of luminal stenosis like markers of plaque vulnerability [132]. Advanced ultrasound techniques such as elastography may provide an alternative and cheaper avenue to assessing plaque vulnerability [133]. Together, these promising diagnostic modalities would need validation of their findings with pathology and demonstration of feasibility in routine clinical practice.
MiR-144-3p inhibits the proliferation, migration and invasion of lung adenocargen cancer cells by targeting COL11A1
Published in Journal of Chemotherapy, 2021
Yahong Sun, Zhihao Liu, Lifei Huang, Yan Shang
In order to verify the effect of miR-144-3p on the proliferation, migration and invasion of LUAD cells by targeting COL11A1, rescue experiments were carried out. First of all, the cells are divided into NC simulators plus oe-NC, miR-144-3p simulators with oe-NC and miR-144-3p simulators with oe-COL11A1 groups. QRT-PCR was performed to detect levels of miR-144-3p and COL11A1 mRNA in each treatment group. Figure 6A shown, as shown, miR-144-3p imitation plus oe-NC and miR-144-3p imitation plus oe-COL11A1 group miR-1 144-3p is significantly raised, and there is no difference between the significant miR-144-3p simulator plus oe-NC and the miR-144-3p simulator plus oe-COL11A1 group. At the same time, COL11A1 decreased significantly when miR-144-3p over-expressed, while COL11A1 increased slightly when miR-144-3p and COL11A1 over-expressed at the same time. In addition, cell biology behavior was evaluated through a series of experiments. CCK-8, wound healing test and Transwell invasive test showed that the cell proliferation, migration and invasive ability of miR-144-3p imitation plus oe-NC group decreased significantly compared to NC imitation plus oe-NC group, Figure 6B-D). Together, these results show that the over-expression of miR-144-3p inhibits the proliferation, migration and invasion of LUAD cells, while the elevation of COL11A1 partially counteracts the inhibition of over-expression of miR-144-3p on cancer cells.
Ras-Mediated Activation of NF-κB and DNA Damage Response in Carcinogenesis
Published in Cancer Investigation, 2020
The regulation of the cell cycle is coupled to cell death, and has major significance in cell turnover and tumorigenesis. When cells are subjected to adverse (growth) conditions, complex signal transduction networks are initiated, regulated, and coordinated. The last few decades have seen an extraordinary increase in our understanding of proliferation and apoptosis, and its contribution to cancer therapy, but a sound understanding of underlying cancer cell biology likely to further enhance our knowledge and understanding. Several studies have underlined the association between DNA damage and development of different types of cancers like breast cancer, prostate cancer, colorectal cancer, renal cancer, lung cancer, nasopharyngeal cancer, melanoma, etc. (101–110). The genomic instability is the hallmark of cancer and is certain to contribute in changing the regulatory sequence regions that can enhance tumor progress. The transcription factors undergo mutations which lead to tumor development and overexpression of transcription factors can manipulate the core regulating machinery of the cell (111,112).