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Introduction to Cancer, Conventional Therapies, and Bionano-Based Advanced Anticancer Strategies
Published in D. Sakthi Kumar, Aswathy Ravindran Girija, Bionanotechnology in Cancer, 2023
The genetic theory of carcinogenesis is the most common theory. It states that normal cells become neoplastic due to mutations in the DNA [21]. The gene mutation theory predicts the spontaneous appearance of diploid polyclonal cancer cells following the accumulation of a sufficient number of transforming genes. The oncogenes of retroviruses are a class of genes that meet the predictions of the gene mutation theory because transformation takes place within one or limited cell generations, and the transformation depends on the continued role of viral proteins. Furthermore, the tumors seem to be diploid, or at least at the beginning [22].
Genetics and exercise: an introduction
Published in Adam P. Sharples, James P. Morton, Henning Wackerhage, Molecular Exercise Physiology, 2022
Claude Bouchard, Henning Wackerhage
It is important to understand the distinction between germ cells and somatic cells. Male and female germ cells, sperm and oocyte, respectively, are termed gametes. A mature germ cell has only 22 autosomes plus one sex chromosome (i.e. 23 chromosomes in total) in its nucleus instead of the full complement of 46 chromosomes seen in somatic cells (i.e. body cells or non-germ cells). A germ cell containing 23 chromosomes is said to be “haploid”, whereas normal somatic cells contain a “diploid” set of chromosomes. When a haploid sperm and a haploid oocyte fuse, they form a diploid, fertilized oocyte, termed zygote, which is the first cell of the new organism. It has 2 × 22 autosomes plus either two X chromosomes (XX, a female) or an X and a Y (XY, a male) chromosome.
Transforming Growth Factor-α and Epidermal Growth Factor
Published in Jason Kelley, Cytokines of the Lung, 2022
To summarize these studies, it appears that two distinct events, one resulting in growth factor production, the other resulting in EGF receptor over-expression, are necessary to establish an autocrine pathway leading to cellular transformation of this immortalized cell line. The relevance of these results to malignant transformation of diploid cells is uncertain. It is conceivable that deregulated expression of the EGF receptor and either TGF-α or EGF by pulmonary parenchymal cells could initiate transformation to one or more of the non-small-cell lung cancer phenotypes. Regardless of whether these changes actually initiate malignant transformation, overexpression of the EGF receptor and secretion of its ligand are likely to confer a selective growth advantage on these tumor cells through an autocrine mechanism. Thus, TGF-α, EGF, and the EGF receptor may contribute to the neoplastic process in two ways; (1) by initiating cellular transformation and (2) by promoting growth of the subpopulation of cells expressing the transformed phenotype. Additional studies utilizing heterologous recombination of diploid cells may help to clarify these issues.
Multifaceted applications of pre-mature chromosome condensation in radiation biodosimetry
Published in International Journal of Radiation Biology, 2020
Usha Yadav, Nagesh Nagabhushana Bhat, Kapil Bansidhar Shirsath, Utkarsha Sagar Mungse, Balvinder Kaur Sapra
G0-PCC spreads were identified by the presence of darkly stained metaphase chromosomes of CHO and lightly stained prematurely condensed human G0 chromosomes. PCC bodies were counted in both mock and irradiated samples, and chromosomal bodies in excess of 46 were considered as excess fragments. In general, G0-PCCs prepared from most of the mock-irradiated cells showed 46 chromosome bodies. In contrast, G0-PCCs prepared from irradiated lymphocytes displayed more than 46 chromosome bodies (Figure 1) and the frequency of excess chromosome fragments showed a linear increase with radiation dose. In addition to excess fragments, ring chromosomes were also observed in the irradiated cells. Hypo-diploid cells with chromosomes less than 46 were also observed occasionally but these were excluded from analysis.
A case of placental hydatid changes in third trimester of pregnancy
Published in Journal of Obstetrics and Gynaecology, 2020
Bai Yun, Zhao Xiang-Zhai, Guo Zhao-Jun, Pang Yi-Cun, Wang Jian
We searched published articles on ‘placental chimaera’ and found two cases with similar genotypes; however, the clinical manifestations were different. Zhang et al. (2000) reported a patient with a 20–week pregnancy who was diagnosed with foetal heart failure and severe preeclampsia. The foetus was a diploid (46XX) female, while the genotype of the vesicular part of the placenta was the same diploid and triploid chimaera, as in our case. The non-vesicular part of the placenta was triploid. The serum HCG of this patient was higher (311837 IU/L) than in our case, and serum AFP was not measured. The authors speculate that the principle of karyotype formation may be such that a whole set of haploid chromosomes are lost from triploid embryos and diploid cells develop into foetuses, but how this whole set of chromosomes is lost is hard to explain. Another possible explanation is that the embryo would be the product of fertilisation between a pack of egg cells containing polar nuclei and sperm. When the embryo precursor forms a placenta, the pentaploid divides into diploid and triploid sets of chromosomes.
Thiol/Disulfide Homeostasis in Patients with Molar Pregnancies
Published in Fetal and Pediatric Pathology, 2020
Meryem Kuru Pekcan, Aytekin Tokmak, Nazli Topfedaisi Ozkan, Gulnur Ozaksit, Arzu Kosem, Ozcan Erel, Mutlu Meydanli
PHM and CHM are identified through histopathologic examination of molar tissue, presence or absence of fetal or embryonic tissue, as well as genetic studies. It is well known that all chromosomes in CHM are diploid (46 XX/46 XY) and paternal in origin. Similarly, in PHM, the extra sets of chromosomes are generally paternal in origin and triploidy is present (69XXY/69XYY/69XXX) [2]. Although the genetic basis of the disease is well known, there may be also environmental factors that disturb the oocyte and/or sperm structurally or functionally, such as OS. Perhaps the imbalance between the oxidant/antioxidant defense systems during the pre-pregnancy period may potentiate the development of molar pregnancies by disrupting the physiologic mechanisms that occur during the fertilization and post-fertilization periods.