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Targeted Therapy for Cancer Stem Cells
Published in Surinder K. Batra, Moorthy P. Ponnusamy, Gene Regulation and Therapeutics for Cancer, 2021
Rama Krishna Nimmakayala, Saswati Karmakar, Garima Kaushik, Sanchita Rauth, Srikanth Barkeer, Saravanakumar Marimuthu, Moorthy P. Ponnusamy
Cancer develops when the regular cellular growth control is disrupted; cells lose contact inhibition and develop resistance to cell death, leading to uncontrolled cellular proliferation and metastasis. The structure and composition of the tumor are incredibly complex with heterogeneous cell populations, which display a large number of mutations and consequent dysregulated gene expressions [1]. Cancer stem cells (CSCs) [2], by residing at the top of the cell hierarchy, can self-renew and undergo multi-lineage differentiation to produce heterogeneous cell population within the tumor [1].
General Biological Aspects of Oncogenesis
Published in Pimentel Enrique, Oncogenes, 2020
Normal cells growing in vitro put a stop to DNA synthesis and proliferation upon establishing intimate contact with neighbor cells. In contrast, in transformed cells growth is not arrested upon this contact, which determines the aforementioned disordered pattern of growth with “piling up” of a number of cells.65-67 The mechanisms involved in loss of contact inhibition of growth are not well understood but may depend on structural and/or functional alterations at the level of the cell surface, altered transmission of signals from the cell surface to the nucleus and/or altered response of the nucleus to these signals. Unfortunately, the cell surface structures and the chemical signals responsible for the phenomenon of contact inhibition of growth have not been identified.
Summary and Development of a New Approach to Senescence
Published in Nate F. Cardarelli, The Thymus in Health and Senescence, 2019
Basically, cancer arises from a change in the genome; such a change can be merely an alteration in a single nucleotide.94 A lack of regulation is implied — possibly in the DNA and/or RNA excision and repair mechanism. This defect must also be coupled with a decrease in immune capability. The fact that normal cells in culture die out after so many doublings while transformed cells become an established (i.e., immortal) line points to regulation in one case and a lack thereof in the other. Contact inhibition seen with normal cells in culture, and usually lacking or diminished with cancerous cells, points in the same direction. A common feature of malignant cells is a change in ploidy, usually from diploidy to heteroploidy. Chromosomal changes in themselves, however, do not necessarily cause transformation from normal to neoplastic. Cancer patients do not have an unusual tendency to heteroploidy. The relationship seen is that heteroploidy and cancer incidence increase with senescence.
Peters Anomaly: Novel Non-Invasive Alternatives to Penetrating Keratoplasty
Published in Seminars in Ophthalmology, 2023
Raksheeth Nathan Rajagopal, Merle Fernandes
The posterior stromal and endothelium-DM complex excavation characterizing PA is postulated to occur due to defective centripetal migration of neural crest cells.23,69 The peripheral normal endothelial cells are capable of enlargement and centripetal migration.70,71 Spontaneous migration and differentiation of these cells are prevented by strong contact inhibition. It is the breakage of this contact inhibition that facilitates migration of the peripheral endothelium and restoration of normal endothelial pump function.72–74 This forms the basis of SER, which was reported by Soh et al. to result in an excellent anatomical and visual outcome. Unlike surgical iridectomy, SER addresses the cause of the underlying abnormality in PA, and this resulted in a significant discernible reduction in the density and size of the corneal opacity.75 Though an option only in type I PA (where less extensive corneal involvement ensures at least some normal peripheral endothelium), SER will be a valuable alternative to PK in these cases, once validated by larger studies.
Recent advances in nanoscale targeted therapy of HER2-positive breast cancer
Published in Journal of Drug Targeting, 2022
Yadollah Omidi, Maha Mobasher, Ana M. Castejon, Morteza Mahmoudi
Cancer cells defy the normal rules of contact inhibition and divide limitlessly in a rapid manner by simultaneously suppressing the growth inhibitory and apoptotic signals. The main mechanism of most conventional anticancer cytotoxic chemotherapeutics is to suppress the rapid division and growth of cancer cells. However, because of non-specific functions, they can simultaneously inhibit the proliferation of rapidly dividing normal cells of the body, resulting in the inevitable emergence of side effects (e.g. alopecia, thrombocytopenia, anaemia, and gastrointestinal disturbances) and hence failure of therapy. To avoid such undesired off-target impacts on healthy cells, chemotherapy agents must be specifically/selectively delivered to the diseased cells using nanoscale delivery systems functionalised with a targeting agent. Such approaches might also minimise the emergence of drug resistance because of specific/selective toxicity in cancer cells [19]. As a result, many scientists have attempted to develop nanoscale multifunctional therapies to actively target cancer cells [15,20–31]. In this line, the passive and active targeting mechanisms via respectively enhanced permeability and retention (EPR) effect and direct targeting of clinically valid oncomarkers (e.g., HER2) have been widely explored.
Numerical modelling of osteocyte growth on different bone tissue scaffolds
Published in Computer Methods in Biomechanics and Biomedical Engineering, 2022
Concepción Paz, Eduardo Suárez, Christian Gil, Oscar Parga
The porosity and permeability of a scaffold can be modified using the proliferation of the cells, which invade and reduce the empty space of the porous scaffold structure. This reduction in the space remaining for the appearance of new cells associated with cell growth causes the contact inhibition phenomenon. The cell metabolism slows down as the cell density increases; hence, the cell proliferation greatly reduces or even ceases entirely when a critical cell density is reached (Huang and Ingber 2004). Typical bioreactor operations are carried out under controlled temperature; therefore, in this work, a constant temperature was assumed, and the possible temperature changes due to metabolic reactions were neglected. The different types of bone cells, the shape and size of the cells, cell detachment, and the cell ageing process, were not considered as hypotheses of the model. The density of the culture medium and the pH were considered to be constant (Coletti et al. 2006).