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Angiography and Pharmacoangiography in Human and Experimental Tumors
Published in Hans-Inge Peterson, Tumor Blood Circulation: Angiogenesis, Vascular Morphology and Blood Flow of Experimental and Human Tumors, 2020
Experimental tumors may also be investigated by in vivo angiography. The rat is widely used in experimental cancer research, but until recently no technique has been available for the angiographic study of these tumors. In 1970 Ekelund and Olin11 developed a technique for selective arterial catheterization in the rat. The catheterization is performed under general ether anesthesia, the radiopaque catheter (OPP 10, Portex, England, O.D./I.D. 0.65/0.25 mm), being introduced from the femoral artery by a cutdown technique. With the aid of magnification fluoroscopy, the preformed tip of the catheter can be directed into most branches of the aorta, e.g., the renal, celiac, or superior mesenteric artery, as well as the carotid or vertebral artery. A small film changer for industrial film is used to obtain serial angiograms. With this technique it is possible to obtain films of high quality; at a selective renal angiography, it is thus possible to visualize the glomeruli. Using this technique, various experimental tumors have been investigated, including renal, urinary bladder, and hepatic neoplasm.12,13,14 Renal tumors were induced by dimethylnitrosamine. The best time to examine these tumors by angiography appeared to be 6 to 8 months after the introduction of carcinogen. These neoplasms were often anaplastic and, angiographically, appeared hypovascular, but well-differentiated tumors presenting as hypervascular lesions at angiography were also seen (Figure 3).
Biochemical Aspects of Fatty Liver
Published in Robert G. Meeks, Steadman D. Harrison, Richard J. Bull, Hepatotoxicology, 2020
Dimethylnitrosamine and diethylnitrosamine are also powerful alkylating, carcinogenic, and steatogenic substances. Fatty liver is evident in this case 5–6 h after treatment with 30–50 mg/kg b.w.t. Both substances are activated by the enzymes of the SER (Brouwers and Emmelot, 1960; Kawanishi et al., 1985; Magee, 1971). Induction of such enzyme by previous treatments strongly increases toxicity (Garner and McLean, 1969; Seawright and McLean, 1967), whereas previous feeding a protein-deficient diet results both in decrease in cytochrome P450 and in toxicity (McLean and McLean, 1969; Menzel et al., 1982).
Steroid Hormones, Hormone Secretion, and Steroid Receptors in Carcinogenesis
Published in Velibor Krsmanović, James F. Whitfield, Malignant Cell Secretion, 2019
Radmila Djordjević-Marković, Dušan T. Kanazir
The roles of these ectopically secreted steroids in carcinogenesis are unknown. They might cause different endocrine dysfunctions secondary to the secreting tumors, but they might also alter the metabolism of chemical carcinogens by increasing the activities of carcinogen-activatin enzymes (aryl monooxygenases), which convert chemical procarcinogens into potent carcinogens.17 This might be the cause of secondary tumors in cancerous patients, but there is no direct proof of this hypothesis. However, it has been demonstrated that two classes of procarcinogens are affected by hormonally influenced metabolism. Thus, for example, dimethylnitrosamine is converted to a short-lived metabolite with carcinogenic and mutagenic properties. This activation occurs in the kidney and is stimulated by testosterone and progestins.17,170 Thus, organs effective in forming active metabolites could be at risk for secondary tumor induction.
Protective Effects of Dietary Capsaicin on the Initiation Step of a Two-Stage Hepatocarcinogenesis Rat Model
Published in Nutrition and Cancer, 2021
Luis Manuel Sarmiento-Machado, Guilherme Ribeiro Romualdo, Joyce Regina Zapaterini, Mariana Baptista Tablas, Ana Angélica Henrique Fernandes, Fernando Salvador Moreno, Luís Fernando Barbisan
Although an increase in Grb2 mRNA and protein expression was reported as an initial event in preneoplastic and neoplastic liver lesions induced by dimethylnitrosamine (DMN) in mice (54), the Grb2 gene was downregulated after DEN-induced carcinogenic liver injury in our study. On the other hand, Grb2 is positively correlated to increased cell proliferation during the early events of hepatic regeneration in rats (44). Considering that 0.02% CPS intervention apparently protected rats from carcinogenic liver injury, Gbr2 upregulation could be interpreted as an initial regenerative stimulus for the hepatocytes. Nonetheless, further studies on the effects of dietary CPS on gene expression and reparative hepatocyte proliferation should be performed contemplating other timepoints after carcinogen injury.
Evolutionary Underpinnings of Innate-Like T Cell Interactions with Cancer
Published in Immunological Investigations, 2019
Maureen Banach, Jacques Robert
Since all multicellular organisms are susceptible to tumors, it is not surprising that a range of spontaneous tumors have been described in Xenopus (Robert, 2010; Stern et al., 2014). However, deriving tumor cell lines from these cancers has been met with little success. The induction of cancers with potent carcinogens, such as N-dimethylnitrosamine or N-methyl-N-nitrosourea, that in mice cause extensive DNA damage, have resulted in limited carcinogenesis in Xenopus (Balls et al., 1989, 1983). Reverse genetic methodologies to disable gene function have recently propelled the development of tumors in Xenopus. For instance, Transcription Activator-Like Effector Nucleases (TALEN)-mediated disruption of the tumor suppressor gene adenomatous polyposis coli apc gene in X. tropicalis was reported to lead to familial adenomatous polyposis, similar to mouse and human intestinal cancers (Van Nieuwenhuysen et al., 2015). Also, akin to pediatric tumors of retina, double knockouts of retinoblastoma 1 (rb1) and retinoblastoma-like 1 (rbl1) by the clustered regularly interspaced short palindromic and associated protein 9 nuclease (CRISPR/Cas9) technology initiated retinoblastoma in X. tropicalis (Naert et al., 2016).
Neuroimmunomodulation of adrenoblockers during liver cirrhosis: modulation of hepatic stellate cell activity
Published in Annals of Medicine, 2023
Mariana Yazmin Medina Pizaño, María de Jesús Loera Arias, Roberto Montes de Oca Luna, Odila Saucedo Cárdenas, Javier Ventura Juárez, Martin Humberto Muñoz Ortega
Leukocytes were initially found to express a group of cytokines known as ILs; however, it was later discovered that a wide variety of other cells, including CD4 T lymphocytes, monocytes, macrophages, and endothelial cells, were also capable of producing ILs [66]. Pro-fibrotic ILs: In response to liver tissue damage, KCs and SECs can quickly create ILs. As a result of IL-1's direct activation of HSCs and stimulation of their production of MMP-9, MMP-13, and TIMP-1, hepatic fibrogenesis occurs. In contrast, IL-1-receptor-deficient animals show reduced susceptibility to fibrosis development and liver injury [67]. Similarly, it was discovered that IL-1 receptor antagonists prevented dimethylnitrosamine-induced liver fibrosis in rats [68].