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Role of Tumor Cell Membrane in Hyperthermia
Published in Leopold J. Anghileri, Jacques Robert, Hyperthermia In Cancer Treatment, 2019
Malignant cell transformation is characterized by changes in the structure of glycoproteins and glycolipids of the plasma membrane.106–115 These modifications affect several types of cellular processes. The increased content of sialic acid of the plasma membrane is one of the characteristics of cells in mitosis.116 The impairment of intercellular contact gives a certain autonomy to the transformed cells, and this freedom of movement is reflected by their capacity to metastasize.117,118 In addition, the immune reactivity of the tumor cell is greatly influenced by the sugar chains of the glycoproteins.119,120 Coincidentally, the carcinoembryonal protein, alpha1-fetoprotein, as well as the carcinoembryonal antigen are related to transformation in glycoprotein synthesis, and their content of sialic acid (especially of the alpha1-fetoprotein) appears to determine the immunosuppressive characteristics of the protein.121,122 This behavior, which is similar to the corresponding to the fetal organism, seems to be a defensive reaction of the tumor cell for escaping immune surveillance. It is likely that the sialic acid in the glycoprotein and glycolipid acts to mask the corresponding antigens.123–125
Multistep Carcinogenesis and Human Epithelial Cells
Published in George E. Milo, Bruce C. Casto, Charles F. Shuler, Transformation of Human Epithelial Cells: Molecular and Oncogenetic Mechanisms, 2017
It is now widely accepted that cancer arises in a multistep fashion and that environmental exposure, particularly to physical, chemical, and biological agents, is a major etiological factor.1,2 Besides chemicals, irradiation, and viruses, other influences (e.g., genetic, hormonal, nutritional, and multifactor interactions) are also involved. While the majority of studies of carcinogenesis have relied on the use of rodent cells in culture, experimental models to define the role of carcinogenic agents in the development of human cancer must be established using human cells. Thus, the study of human cell transformation in vitro by carcinogenic agents is of particular importance for understanding the cellular and molecular mechanisms underlying human carcinogenesis. In keeping with the multistep development of human cancer in vivo, a stepwise approach to neoplastic transformation in vitro presents a reasonable strategy.
Antioxidants
Published in John Melford, Pocket Guide to Cancer, 2017
People who tan their skins using artificial UV rays are at a higher risk of developing skin cancer. The younger the age of exposure, the greater the risk. Welders and sheet metal workers may also have a higher risk of melanoma of the eye. Excessive UV exposure also can cause cataracts and suppression of the immune system. The chain of events leading to cell transformation starts with DNA damage caused by UV exposure, followed by the formation of DNA mutations at sites of damage, and then by the accumulation of driver mutations.
Pathogenicity and virulence of human T lymphotropic virus type-1 (HTLV-1) in oncogenesis: adult T-cell leukemia/lymphoma (ATLL)
Published in Critical Reviews in Clinical Laboratory Sciences, 2023
Sanaz Ahmadi Ghezeldasht, David J. Blackbourn, Arman Mosavat, Seyed Abdolrahim Rezaee
Many factors, such as viral and cellular factors, can act as cell transformation agents. For example, in the case of HTLV-1 BCL-xL, BAD expressions were up-regulated [176], but BIM gene expression was down-regulated in the ATLL cells to suppress apoptosis [177]. In our high-throughput studies, BCL2A1 [87] and BCL2L11 (BIM) genes were up-regulated and down-regulated [178], respectively. In the early stage of the infected cell transformation, apoptosis is inhibited by constitutive production of Bcl-xL, induced by Tax, and leads to leukemia promotion [179,180]. High throughput and gene expression studies in our laboratory had very controversial results in the up-regulation or down-regulation [85,89] of BIM in infected cancerous cells. However, Mühleisen et al. showed that Tax expressing cells became resistant to cell death by suppressing the expression of pro-apoptotic BH3-only proteins, BIM, and BID [181]. Overall, it can be suggested that the BIM expression, as an element of the intrinsic apoptosis pathway, does not have a pivotal role in ATLL cell transformation.
Hsa_circ_0044907 promotes acute myeloid leukemia progression through upregulating oncogene KIT via sequestering miR-186-5p
Published in Hematology, 2022
KIT is a trans-membrane receptor tyrosine kinase that binds the SCF ligand to activate MAPK, JAK/STAT, and PI3K pathways to facilitate cell survival [30]. It is implicated in cell transformation through overexpression or oncogenic mutation [31, 32]. A report from Hu et al. manifested that miR-137 decreased AML progression by targeting KIT [33]. Furthermore, TUG1 silencing induced AML cell apoptosis and curbed AML cell viability via targeting KIT [34]. Gao et al. showed that miR-193b restoration curbed AML cell growth through decreasing KIT expression [35]. Moreover, KIT upregulation frequently occurs in AML, resulting in promoting abnormal cell proliferation and poor outcomes [35, 36]. Here, KIT as a miR-186-5p target was identified. Moreover, KIT was overexpressed in AML patient-derived BM and AML cells, and KIT upregulation impaired miR-186-5p mimic mediated suppression on AML cell viability, proliferation, and cycle progression. Importantly, circ_0044907 could mediate KIT expression via interacting with miR-186-5p. Therefore, we concluded that circ_0044907 promoted AML progression via sequestering miR-186-5p and upregulating KIT.
Phenotype-Genotype Correlation of North Indian Progressive Familial Intrahepatic Cholestasis type2 Children Shows p.Val444Ala and p.Asn591Ser Variants and Retained BSEP Expression
Published in Fetal and Pediatric Pathology, 2020
Suvradeep Mitra, Ashim Das, Baburam Thapa, Rakesh Kumar Vasishta
Intracanalicular and intrahepatocytic cholestasis was present in eight (80%) and nine cases (90%), respectively. Feathery degeneration and pseudoacinar transformation was noted in eight (80%) and seven cases (70%) respectively. Giant cell transformation was present in five cases (50%). One case showed <33% involvement of the core area by the giant cells and one case showed involvement of nearly 80% of the core area (>67%) by the giant cells [Fig. 1d]. Three cases showed 34–66% core area involvement by the giant cells. Lobular inflammation was present in five cases (50%) and was mild in four patients and moderate in one patient. Lobular focus of extramedullary hematopoiesis was absent. However, one case (Case 7) showed portal collection of myeloid and erythroid precursor cells (10%). None of the cases showed steatosis. No dysplastic foci were noted (Table 5].