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Role of Hematopoietic Growth Factors in Human Leukemias: Implication of an Autocrine Process?
Published in Velibor Krsmanović, James F. Whitfield, Malignant Cell Secretion, 2019
Patrice Mannoni, Françoise Birg, Claude Mawas
The unregulated proliferation of a clonal population from hematopoietic tissue leads to leukemia. As a consequence, a progressive amplification of the leukemic clone is observed, which is characterized by a complete dissociation of the differentiation capability from the proliferative capability of the tumor cells. It has been said that leukemic cells were “frozen” at given stages of differentiation, analogous to their normal counterparts. It appears more appropriate to see this absence of differentiation as a consequence, rather than a cause, of the leukemic process. Indeed, the main abnormality of leukemic cells appears to be an increase in their proliferative capacity, as they progressively overgrow the normal populations. The identification of proto-oncogenes and genes coding for growth factors and growth factor receptors have brought new insights and new hypotheses.96,98 Thus activation of protooncogenes, either by mutation, chromosomal translocation, or provirus insertion, could lead to the synthesis of an abnormal protein involved in the regulation of cell proliferation.
SBA Answers and Explanations
Published in Vivian A. Elwell, Jonathan M. Fishman, Rajat Chowdhury, SBAs for the MRCS Part A, 2018
Vivian A. Elwell, Jonathan M. Fishman, Rajat Chowdhury
Mitochondria are found in all eukaryotic cells. They contain their own DNA and are thought to be symbiotic prokaryotes that have been assimilated into eukaryotic cells in our biological past (endosymbiotic theory). They replicate by mitosis to form a clonal population. All the mitochondrial DNA in humans is derived from the clonal population of the ovum and therefore are maternally inherited.
Introduction to Blood Cancers
Published in Tariq I Mughal, John M Goldman, Sabena T Mughal, Understanding Leukemias, Lymphomas, and Myelomas, 2017
Tariq I Mughal, John M Goldman, Sabena T Mughal
In contrast, cancer arises when proliferation consistently and aberrantly exceeds apoptosis in a single (clonal) population of cells. Research studies into the mechanisms underlying the precise nature of how normal cell proliferation becomes abnormal and chaotic and how these cells lose the ability to die at the prescribed time suggest that this process proceeds through multiple stages (e.g., cells developing pre-malignant changes—a phenomenon first suggested by Isaac Berenblum in 1947) that involves complex interactions with the host environment. Such interactions and changes include an ability to acquire a blood supply [angiogenesis, from the Greek words αγγειο (angio) for blood cell and γευεσιs (genesis) for birth, meaning to acquire a new blood supply] and production of enzymes and hormones (cytokines). These changes facilitate the invasion by the cancer cell across anatomical boundaries and spread of the cancer cell to distant organs (metastasis, from the Greek word μετ σταστς for migration). They also allow the cancer cell to evade the body’s normal immune responses.
Prevalence and significance of large granular lymphocytes in patients with immune thrombocytopenia
Published in Platelets, 2023
Caroline Gabe, Yang Liu, Joanne Duncan, Melanie St John, Kayla J. Lucier, David Kimmel, John G. Kelton, Donald M. Arnold
We collected 139 flow cytometry tests (n = 120 patients); 120 tests (86.3%) were done as part of screening or reflex testing, and 19 (13.7%) were specifically requested by the physician. In the ITP group (n = 91), 13 (14.3%) had T-LGL. Baseline patient characteristics for patients with immune thrombocytopenia (ITP) with and without abnormal T-LGL are shown in Table I. Flow cytometry phenotyping for the 13 patients with ITP and T-LGL is shown in Table II. Of the 13 patients, 11 had excess T-LGL (>0.3 x109/L) and two had positive TCR clonality only. Median T-LGL cell count per patient was 0.5 x109/L (IQR 0.4–1.3) and none had >2.0 x109/L cells. All 10 patients who were tested had evidence of a clonal TCR gene rearrangement. In the nonimmune thrombocytopenia group (n = 29), three (10.3%) had T-LGL. The median T-LGL cell count for the control group was 1.0 x109/L (IQR 0.3–1.6). One patient was tested for TCR gene rearrangement and the result showed a clonal population. There was no significant difference in the proportion of patients with ITP and/or non-immune thrombocytopenic patients with T-LGL (p = .23). All patients with ITP and T-LGL belong to group of 78 ITP patients who had flow cytometry done after 2018. Only one patient with non-immune thrombocytopenia and T-LGL had the flow cytometry done before 2018.
Flagellum and toxin phase variation impacts intestinal colonization and disease development in a mouse model of Clostridioides difficile infection
Published in Gut Microbes, 2022
Dominika Trzilova, Mercedes A. H. Warren, Nicole C. Gadda, Caitlin L. Williams, Rita Tamayo
Many bacterial species employ phase variation to generate phenotypic heterogeneity within a clonal population. Bacteria frequently encounter selective pressures in their environment, and phenotypic heterogeneity helps ensure survival by creating subpopulations that are differentially equipped to overcome these pressures.1 Phase variation typically affects the production of surface factors that directly interface with the bacterium’s environment, such as flagella, pili, and exopolysaccharides. Both mucosal pathogens and commensal species employ phase variation to balance the fitness advantages conferred by these structures with the costs of producing them; in a host environment, the ability to phase vary can promote immune evasion and persistence in the host.2 Phase variation can be achieved by multiple epigenetic and genetic mechanisms, including DNA modification by methylation, slipped-strand mispairing, homologous recombination, and site-specific recombination.1,3
Utilizing the prognostic impact of minimal residual disease in treatment decisions for pediatric acute lymphoblastic leukemia
Published in Expert Review of Hematology, 2021
Francesco Ceppi, Frida Rizzati, Antonella Colombini, Valentino Conter, Giovanni Cazzaniga
During early differentiation of either B and T cell, somatic rearrangement of the Immunoglobulin (IG) and T-cell Receptor (TR) gene loci occurs by joining the germline variable (V), diversity (D), and joining (J) gene segments [31]. Each lymphocyte receives a unique set of V-(D-)J segments, which encode the variable domains of IG or TR molecules. The distinctiveness of each rearrangement is further based on random nucleotide insertion and deletion at the junction sites of V, D, and J gene segments, resulting in ‘fingerprint-like’ sequences in the junctional regions of IG and TR genes. Each lymphocyte’s unique signature is established by this combined sequence. Since leukemia is clonal in origin, each malignant lymphoid disease represents the growth of a clonal population with a distinct IG/TR signature [32].