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Cancer
Published in Gia Merlo, Kathy Berra, Lifestyle Nursing, 2023
Genetic and epigenetic changes can alter gene expression and, as they accumulate, enable cells to acquire functional abnormalities known as the hallmarks of cancer (Hanahan & Weinberg, 2011). Current models of cancer development identify eight hallmarks of cancer: Sustained proliferative signaling, evasion of growth suppressors, resistance to cell death/apoptosis, replicative immortality, dysregulated metabolism, immune system evasion, angiogenesis, and invasion and metastasis (World Cancer Research Fund/American Institute for Cancer Research, 2018). Models also incorporate two characteristics—genomic instability and tumor-promoting inflammation—that facilitate cancer’s development.
Diagnosis and Pathobiology
Published in Franklyn De Silva, Jane Alcorn, The Elusive Road Towards Effective Cancer Prevention and Treatment, 2023
Franklyn De Silva, Jane Alcorn
Human cancer is diverse, with an enormous number of individual disease entities [37, 281]. Under normal conditions of tissue development and repair, individual cells or population of cells go through expansion in response to various stimuli or factors that regulate the cell cycle and their ability to survive and migrate within conditional microenvironments [282]. In cancer, these responses are dysregulated and the multitude of genetic and epigenetic mechanisms that underlie all cancers [283] can be categorized into the hallmarks of cancer initially proposed by Hanahan and Weinberg in 2000 and again revised in 2011 [70, 184] (Figure 2.3). Limitless replicative potential, self-sufficiency in growth signals, evasion of apoptosis, insensitivity to growth suppressors, tissue invasion, avoidance of immune destruction, and deregulation of cellular energertics (i.e., hallmarks of cancer), as well as tumor-promoting inflammation and genome instability and mutations (i.e., enabling characteristics), outline the development, survival, and progression of a malignant tumor [184].
Food Interactions, Sirtuins, Genes, Homeostasis, and General Discussion
Published in Chuong Pham-Huy, Bruno Pham Huy, Food and Lifestyle in Health and Disease, 2022
Chuong Pham-Huy, Bruno Pham Huy
In recent years, the roles of sirtuins in cancer biology have gained the attention of many scientists worldwide. Growing evidence demonstrates that sirtuins regulate many processes that go awry in cancer cells, such as cellular metabolism, the regulation of chromatin structure, and the maintenance of genomic stability (95). Sirtuins have involved in diverse cellular processes including DNA repair, tumor suppressor p53, energy metabolism, and tumorigenesis. Notably, genomic instability and metabolic reprogramming are two hallmarks of cancer (96). However, the ability of sirtuins to promote or suppress tumorigenesis seems to depend on the specific tumor type, cellular context, and signaling pathway affected (70, 73, 87, 95–98). Sirtuins play fundamental roles in carcinogenesis and maintenance of the malignant phenotype, mainly participating in cancer cell viability, apoptosis, metastasis, and tumorigenesis. Although sirtuin family members have a high degree of homology, they may play different roles in various kinds of cancer (98).
Targeting myeloid cells with bispecific antibodies as novel immunotherapies of cancer
Published in Expert Opinion on Biological Therapy, 2022
Celine A.N. Sewnath, Leonie M. Behrens, Marjolein van Egmond
Cancer is one of the leading causes of death globally [1] and is a highly complex disease. Currently, eight hallmarks of cancer have been identified, including limitless proliferation, resistance to cell death, and the ability to evade destruction by the immune system [2]. Immune cells play an important role during different phases of cancer development. In early stages, immune cells have a function in immunosurveillance, resulting in eradication of tumor cells [3]. However, during development tumor cells gain characteristics that enable them to evade the immune system. For instance, upregulation of immune checkpoints or downregulation of MHC class I are often observed [4,5]. Furthermore, secretion of immunosuppressive cytokines and selective attraction of immunoregulatory cells, such as regulatory T cells and myeloid-derived suppressor cells, are frequently present [6–8]. Thus, as cancer progresses, an immunosuppressive tumor microenvironment (TME) is induced, preventing activation and recruitment of cytotoxic immune cells to kill tumor cells. Immunotherapy was developed to overcome immunosuppression as it aims to reeducate the immune system of patients, ultimately resulting in eradication of cancer cells [9].
Effectiveness of Ketogenic Diets on the Survival of Adult Oncological Patients
Published in Nutrition and Cancer, 2021
Worldwide, cancer is the second most prevalent disease after cardiovascular diseases (1). It is the second leading cause of death globally, accounting for 1 in 6 deaths in 2018 (2). Characteristic hallmarks of cancer have been described, which are transversally present and would explain the complexity of its biology. Within these seals, reprogramming of energy metabolism has been described, which would give cancer cells (CaCe) a special adaptive advantage (3). This feature was first described in 1920 by Otto Warburg, who observed that most CaCe, independent of the availability of oxygen and the functionality of their mitochondrias, capture and metabolize large amounts of glucose to convert it to lactate, instead of completely oxidizing it to carbon dioxide (4, 5). This phenomenon, known broadly as the Warburg Effect or aerobic glycolysis, represents an inefficient use of glucose, characterized by a lower generation of ATP compared to mitochondrial respiration per mole of glucose (4). This lower production of ATP is compensated by a greater glucose uptake through over-expression of GLUT 1 and 3 transporters (3, 6). This metabolic characteristic allows the study of tumors by positron emission tomography (PET) using a radiolabeled glucose analog (F-fluorodeoxyglucose; FDG) (4).
Reverse phase protein arrays in acute leukemia: investigative and methodological challenges
Published in Expert Review of Proteomics, 2021
Fieke W. Hoff, Terzah M. Horton, Steven M. Kornblau
We hypothesize that the genetic complexity of the leukemic cells, ultimately results in a constrained number of protein patterns pathway utilizations, needed for the cell to become leukemic (similar to the ‘Hallmarks of Cancer’) [58,59]. The ‘Hallmarks of Cancer’ are a conceptual framework of 6 (and later 10) biological capabilities acquired during the multistep development of human tumors. Though all malignancies share those same hallmarks of cancer, heterogeneities between patients complicate patients’ response to therapy and subject them to varied outcomes. If this idea is correct, then each combination of genetic events, regardless of their direct downstream consequence, must somehow meet each of the hallmarks. We hypothesize that those combinations of CONs together represent the quantitative hallmarks in acute leukemia, and can significantly accelerate the identification and development of new therapeutic targets.