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Disorders of Growth and Differentiation
Published in Jeremy R. Jass, Understanding Pathology, 2020
Cell function is divided into three broad categories: (1) proliferation, (2) death, and (3) differentiation. Cell proliferation focuses on the cell cycle (mitogenesis) and the mechanisms that initiate and control this process. Cell death implies the programmed demise of individual cells known as apoptosis. The balance of cell generation and cell death will determine whether an organ grows, shrinks or remains the same size. Differentiation is concerned with the control of gene induction which will provide a cell with its repertoire of housekeeping requirements as well as its specialised functions. Although proliferation, death and differentiation must be studied in isolation, because each is extraordinarily complex, they are integrated not only at the level of the cell but also at the level of tissues. The global orchestration of proliferation, death and differentiation is encountered in its most dynamic and extraordinary form during embryological development. However the Hox genes, which are restricted to the animal kingdom and occur in clustered arrays for sequential activation of target genes during embryological development, also function in the stem cells of adult tissues. This is one of many examples of a single gene having multiple functions. The following account of the proliferation, death and differentiation of cells will include issues that are of particular interest to the anatomical pathologist because of their practical importance in tissue diagnosis.
Unified Theory on the Basic Mechanism of Normal Mitotic Control and Oncogenesis*
Published in Richard C. Niemtzow, Transmembrane Potentials and Characteristics of Immune and Tumor Cell, 2020
In conclusion of this section, the proposed system outlined herein for mitotic control by Em modulated metabolic feedback circuits and switching mechanisms, appears to be compatible with a range of experimental observations, and provides a unifying picture of some heretofore apparently unrelated mitogenic phenomena. Although necessarily based in some areas on meager and incomplete experimental data, the theory provides an effective basis for the design of further experiments to investigate its specific and general validity. Of particular significance are the prediction of a fundamental involvement of the cell surface in mitogenesis and the unifying explanation resulting therefrom of the relationships among the primary pathological features (invasiveness, metastasis, and unchecked proliferation) of malignant cells, all aspects of which are open to critical experimental investigation. If the present theory is to possess general applicability, it appears a necessary requirement that DNA synthesis and mitotic preparatory pathways and their regulation by ionic conditions, represented by Em be capable of relative dissociation (during G1 and S at least) from the more specific aspects of cell metabolism, since this latter factor is so grossly different in different cell types. There is good evidence that such is the case in that even many of the various mitotic preparatory pathways proceed independently in several respects.34
Kidney Microcirculation
Published in John H. Barker, Gary L. Anderson, Michael D. Menger, Clinically Applied Microcirculation Research, 2019
In infiltrative and remodeling disorders, the roles of factors that stimulate mitogenesis are of particular interest.18 Endothelial and non-endothelial vasoconstrictor agonists are known to be potent stimuli of smooth muscle cell growth and proliferation. Likewise, extracellular matrix deposition initiates vascular cell hyperplasia, as well as fibroblast infiltration.19 These remodeling effects are mediated through a variety of growth factors.20 In diabetes, the subintimal deposit of advanced glycosyation products may quench the vasodilatory and antimitogenic effects of nitric oxide leading to vasoconstriction and proliferative changes.21 Disorders of endothelial function promote thrombus formation.22 In addition, the role of endothelial adhesion molecules in thrombosis is currently being investigated.23
A review about the role of additives in nerve tissue engineering: growth factors, vitamins, and drugs
Published in Growth Factors, 2023
Mehrsa Nasiri, Javad Esmaeili, Amir Tebyani, Hojat Basati
As another growth factor, embedding FGFs in scaffolds could accelerate NTE progress by inducing angiogenesis to the injury site, and directly by promoting cell proliferation and axon outgrowth at the injury site. These growth factors are mainly expressed in the dorsal root ganglia and peripheral nerve. Because of the expression pattern and the effects after exogenous administration of basic FGF, it has a physiological role during nerve regeneration. FGF-2 mostly works in a coordinated way with other growth factors/co-factors during the cell differentiation process. Distinct functions of FGF-2 have been reported in the spinal ganglia and at the lesion site. It was reported that FGF-2 is potent to stimulate Schwann cell mitogenesis (Grothe and Nikkhah 2001). It was reported that higher proliferation was observed when FGF-2 has released and the main justification turns back to the reduction in the expression of RB2/P13. No changes were reported in the P16 protein levels when FGF-2 was released from hydrogels (Galderisi et al. 2013).
Assessment of chromosome aberrations in large Japanese field mice (Apodemus speciosus) in Namie Town, Fukushima
Published in International Journal of Radiation Biology, 2022
Yohei Fujishima, Akifumi Nakata, Risa Ujiie, Kosuke Kasai, Kentaro Ariyoshi, Valerie Swee Ting Goh, Kojun Suzuki, Hirofumi Tazoe, Masatoshi Yamada, Mitsuaki A. Yoshida, Tomisato Miura
Spleen cell culture was performed to obtain metaphase spreads for chromosome aberration analysis. After spleen removal, the cells were isolated by gentle homogenization with RPMI 1640 medium, centrifugation (300 × g, 5 min, 4 °C) and resuspension to a concentration of 1.0 × 107 cells with RPMI 1640 medium (Thermo Fisher Scientific, Waltham, MA, USA) supplemented with 20% heat-inactivated fetal bovine serum (Sigma-Aldrich, MO, USA), 60 mg/ml kanamycin sulfate (Thermo Fisher Scientific, Waltham, MA, USA) in a 15 ml centrifuge tube. For lymphocyte mitogenesis induction, lipopolysaccharide (10 µg/ml, Sigma-Aldrich, MO, USA), concanavalin A (3 µg/ml, Sigma-Aldrich, MO, USA) and phytohemagglutinin (25 µg/ml, Remel Europe, Dartford, UK) were added. To obtain first-cycle metaphases, KaryoMAX colcemid solution (Thermo Fisher Scientific, Waltham, MA, USA) at a final concentration of 0.02 µg/ml was added 22 h before harvesting. Spleen cell cultures were maintained in a humidified 37 °C incubator with 5% CO2 for 46 h. Cultured cells were harvested with hypotonic treatment using 75 mM potassium chloride and fixed in cold fixative (3:1 methanol/glacial acetic acid). Fixed cell suspensions were stored at −30 °C.
Fibroblast growth factor receptor-like-1: a new therapeutic target and unfavorable prognostic indicator for rectal adenocarcinoma
Published in Journal of Receptors and Signal Transduction, 2020
Ru-Zhen Jia, Ji-Zhun Zhang, Chang-Qing Jing, Chen-Sheng Li, Hong-Qing Zhuo
Fibroblast growth factor receptor-like-1 (FGFRL1) is identified to be the fifth fibroblast growth factor receptor [9,10] which affects cell motility, being known as a target for the potential treatment of tumors [11]. The fibroblast growth factors can set in motion a set of downstream signals, ultimately influencing the mitogenesis and differentiation by interacting with the extracellular portion of proteins. According to previous studies, phosphorylated FGFRs can mediate many critical intracellular signaling pathways and the aberrant activity, which could result in organogenesis disruption, metabolic disorders and cancer [12]. So as a member of FGFRs, FGFRL1 was found to have important significances in cancers. For example, FGFRL1 as a target of miR-210 can promote cancer cell proliferation [13], invasion and migration in osteosarcoma [14]. Additionally, it has been reported to control tumor growth and metastasis of bladder cancer [15]. As a kind of tumor suppressor [16,17], the function of FGFRL1 is similar to cell adhesion protein that induces cell adhesion and treats ovarian carcinoma [9,18]. These evidences revealed that FGFRL1 has required influences on various kinds of cancers [14,15,17,18]. However, the function of FGFRL1 in rectal adenocarcinoma is still unknown.