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      Is Open Access

      Is Myelodysplasia a Consequence of Normal Aging?

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          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Purpose of Review

          To review available data on the relationship of MDS and aging and to address the question if biological changes of (premature) aging are a prerequisite for the development of MDS.

          Recent Findings

          Whereas the association of MDS with advanced age and some common biologic features of aging and MDS are well established, additional evidence for both, especially on the role of stem cells, the stem cell niche, and inflammation, has been recently described.

          Summary

          Biologically, many but not all drivers of aging also play a role in the development and propagation of MDS and vice versa. As a consequence, aging contributes to the development of MDS which can be seen as an interplay of clonal disease and normal and premature aging. The impact of aging may be different in specific MDS subtypes and risk groups.

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          Most cited references82

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          Hallmarks of Cancer: The Next Generation

          Douglas Hanahan, Robert A. Weinberg (2011)
          The hallmarks of cancer comprise six biological capabilities acquired during the multistep development of human tumors. The hallmarks constitute an organizing principle for rationalizing the complexities of neoplastic disease. They include sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, and activating invasion and metastasis. Underlying these hallmarks are genome instability, which generates the genetic diversity that expedites their acquisition, and inflammation, which fosters multiple hallmark functions. Conceptual progress in the last decade has added two emerging hallmarks of potential generality to this list-reprogramming of energy metabolism and evading immune destruction. In addition to cancer cells, tumors exhibit another dimension of complexity: they contain a repertoire of recruited, ostensibly normal cells that contribute to the acquisition of hallmark traits by creating the "tumor microenvironment." Recognition of the widespread applicability of these concepts will increasingly affect the development of new means to treat human cancer. Copyright © 2011 Elsevier Inc. All rights reserved.
          Article 0 comments Cited 11509 times – based on 0 reviews     Review now
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            The Hallmarks of Aging

            Carlos López-Otín, Maria Blasco, Linda Partridge … (2014)
            Aging is characterized by a progressive loss of physiological integrity, leading to impaired function and increased vulnerability to death. This deterioration is the primary risk factor for major human pathologies, including cancer, diabetes, cardiovascular disorders, and neurodegenerative diseases. Aging research has experienced an unprecedented advance over recent years, particularly with the discovery that the rate of aging is controlled, at least to some extent, by genetic pathways and biochemical processes conserved in evolution. This Review enumerates nine tentative hallmarks that represent common denominators of aging in different organisms, with special emphasis on mammalian aging. These hallmarks are: genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, deregulated nutrient sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, and altered intercellular communication. A major challenge is to dissect the interconnectedness between the candidate hallmarks and their relative contributions to aging, with the final goal of identifying pharmaceutical targets to improve human health during aging, with minimal side effects. Copyright © 2013 Elsevier Inc. All rights reserved.
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              Frailty in Older Adults: Evidence for a Phenotype

              L P Fried, C Tangen, J Walston … (2001)
              Article 0 comments Cited 2850 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Michael Pfeilstöcker:
                ORCID: http://orcid.org/0000-0002-1730-6554
                michael.pfeilstoecker@oegk.at
                Journal
                Journal ID (nlm-ta): Curr Oncol Rep
                Journal ID (iso-abbrev): Curr Oncol Rep
                Title: Current Oncology Reports
                Publisher: Springer US (New York )
                ISSN (Print): 1523-3790
                ISSN (Electronic): 1534-6269
                Publication date (Electronic): 4 November 2021
                Publication date PMC-release: 4 November 2021
                Publication date (Print): 2021
                Volume: 23
                Issue: 12
                Electronic Location Identifier: 142
                Affiliations
                [1 ]GRID grid.459707.8, ISNI 0000 0004 0522 7001, Department of Internal Medicine IV, , Klinikum Wels-Grieskirchen, ; Wels, Austria
                [2 ]GRID grid.21604.31, ISNI 0000 0004 0523 5263, Paracelsus Medical University, ; Salzburg, Austria
                [3 ]GRID grid.5361.1, ISNI 0000 0000 8853 2677, Department of Internal Medicine V, Hematology and Oncology, Comprehensive Cancer Center Innsbruck (CCCI), , Medical University of Innsbruck, ; Innsbruck, Austria
                [4 ]GRID grid.413662.4, ISNI 0000 0000 8987 0344, 3rd Medical Department, , Hanusch Hospital, ; H.Collinstr 30, 1140 Vienna, Austria
                Author information
                http://orcid.org/0000-0001-8182-990X
                http://orcid.org/0000-0002-8993-9561
                http://orcid.org/0000-0002-1730-6554
                Article
                Publisher ID: 1136
                DOI: 10.1007/s11912-021-01136-5
                PMC ID: 8568861
                PubMed ID: 34735656
                SO-VID: fd70af40-6007-4e36-b8a5-4a4c4a21ac46
                Copyright © © The Author(s) 2021
                License:

                Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

                History
                Date accepted : 27 July 2021
                Categories
                Subject: Geriatric Oncology (L Balducci, Section Editor)
                Custom metadata
                issue-copyright-statement © Springer Science+Business Media, LLC, part of Springer Nature 2021

                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: myelodysplastic syndromes,aging,chip,elderly,clonality,myeloid neoplasia
                Data availability:
                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: myelodysplastic syndromes, aging, chip, elderly, clonality, myeloid neoplasia

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