The three dimensions of somatic evolution: Integrating the role of genetic damage, life‐history traits, and aging in carcinogenesis

Rozhok, Andrii I.; DeGregori, James

doi:10.1111/eva.12947

Cited by 9 publications

(6 citation statements)

References 80 publications

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“…The joint fluid CXCR4 expression levels of the control group were 3.05±1.11 and 2.13±0.63, and the joint fluid CXCL12 expression levels were 5.14±1.12 and 4.54±1.25. The present results suggested that CXCR4 and CXCL12 expression levels in the serum and articular fluid of the study group were significantly higher compared with the control group (P<0.05; Tables II and III [5][6][7][8].…”

Section: Resultsmentioning

confidence: 69%

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Expression levels of CXCR4 and CXCL12 in patients with rheumatoid arthritis and its correlation with disease activity

et al. 2020

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The present study aimed to investigate the expression levels of C-X-C motif chemokine receptor 4 (CXCR4) and CXC ligand 12 (CXCL12) in patients with rheumatoid arthritis (RA) and the correlation with disease activity. In total, 60 patients with RA were selected as the study group, comprising of 28 patients in active-stage and 32 patients in remission-stage. In addition, 60 patients with osteoarthritis were selected as the control group. Western blotting and ELISA were used to detect the expression of CXCR4 and CXCL12, respectively. The Spearman's correlation test was used to analyze correlations between CXCR4 and CXCL12, and erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), disease activity score 28 (DAS28) scores and rheumatoid factor (RF). The present results suggested that CXCR4 and CXCL12 expression levels in the serum and joint synovial fluid of the study group were significantly higher compared with the control group (P<0.05). Moreover, CXCR4 and CXCL12 expression levels in the RA-active group were higher compared with the remission (P<0.05) and control groups (P<0.01). The Pearson test results suggested that the expression levels of CXCR4 and CXCL12 in the serum and joint synovial fluid of patients with RA had a positive correlation with the ESR, CRP, RF and DAS28 scores (P<0.05). CXCL12 and CXCR4 were highly expressed in the serum and joint synovial fluid of patients with RA, and these expression levels were positively correlated with ESR, CRP, RF and DAS28 scores. Therefore, these clinical parameters may be used as indicators to evaluate the disease activity of patients with RA.

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Section: Resultsmentioning

confidence: 69%

“…The pathogenesis of RA is complex, involving many types of cells, including macrophages, T and B cells, fibroblasts, chondrocytes and dendritic cells (4). Despite study into the role of many genes and mechanisms underlying the development of RA, there is still no clear predisposing factor (5)(6)(7).…”

Section: Introductionmentioning

confidence: 99%

Expression levels of CXCR4 and CXCL12 in patients with rheumatoid arthritis and its correlation with disease activity

et al. 2020

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“…The evolution of a species is a long-term process that shapes their neoplastic profiles [172]. Evidence showed that oncogenic tumors date back approximately 2 million years ago [95].…”

Section: Bc Is An Evolutionary Disordermentioning

confidence: 99%

Onco-Breastomics: An Eco-Evo-Devo Holistic Approach

Neagu,

Whitham,

Bruno

et al. 2024

IJMS

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Known as a diverse collection of neoplastic diseases, breast cancer (BC) can be hyperbolically characterized as a dynamic pseudo-organ, a living organism able to build a complex, open, hierarchically organized, self-sustainable, and self-renewable tumor system, a population, a species, a local community, a biocenosis, or an evolving dynamical ecosystem (i.e., immune or metabolic ecosystem) that emphasizes both developmental continuity and spatio-temporal change. Moreover, a cancer cell community, also known as an oncobiota, has been described as non-sexually reproducing species, as well as a migratory or invasive species that expresses intelligent behavior, or an endangered or parasite species that fights to survive, to optimize its features inside the host’s ecosystem, or that is able to exploit or to disrupt its host circadian cycle for improving the own proliferation and spreading. BC tumorigenesis has also been compared with the early embryo and placenta development that may suggest new strategies for research and therapy. Furthermore, BC has also been characterized as an environmental disease or as an ecological disorder. Many mechanisms of cancer progression have been explained by principles of ecology, developmental biology, and evolutionary paradigms. Many authors have discussed ecological, developmental, and evolutionary strategies for more successful anti-cancer therapies, or for understanding the ecological, developmental, and evolutionary bases of BC exploitable vulnerabilities. Herein, we used the integrated framework of three well known ecological theories: the Bronfenbrenner’s theory of human development, the Vannote’s River Continuum Concept (RCC), and the Ecological Evolutionary Developmental Biology (Eco-Evo-Devo) theory, to explain and understand several eco-evo-devo-based principles that govern BC progression. Multi-omics fields, taken together as onco-breastomics, offer better opportunities to integrate, analyze, and interpret large amounts of complex heterogeneous data, such as various and big-omics data obtained by multiple investigative modalities, for understanding the eco-evo-devo-based principles that drive BC progression and treatment. These integrative eco-evo-devo theories can help clinicians better diagnose and treat BC, for example, by using non-invasive biomarkers in liquid-biopsies that have emerged from integrated omics-based data that accurately reflect the biomolecular landscape of the primary tumor in order to avoid mutilating preventive surgery, like bilateral mastectomy. From the perspective of preventive, personalized, and participatory medicine, these hypotheses may help patients to think about this disease as a process governed by natural rules, to understand the possible causes of the disease, and to gain control on their own health.

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“…[54][55][56] Recently, Laconi and colleagues proposed that, "the tumor-suppressive potential of youth is more potent than previously realized, limiting cancers through half a century of human life even in the face of increased DNA mutations and highly perturbed tissue environments," 57 and much additional work suggests that organismal aging and the associated development of cellular senescence, proinflammation, and waning immunity appear to be major mechanisms that allow for the development of these permissive environments. [58][59][60][61][62][63][64] Pathologically significant mutations are propagated during the process of DNA replication, as nondividing cells will not pass on the cancer phenotype to progeny cells.…”

Section: Cellular Replication and The Creation Of Aged (Permissive) M...mentioning

confidence: 99%

Increased risk of cancer in dogs and humans: A consequence of recent extension of lifespan beyond evolutionarily determined limitations?

et al. 2022

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Cancer is among the most common causes of death for dogs (and cats) and humans in the developed world, even though it is uncommon in wildlife and other domestic animals. We provide a rationale for this observation based on recent advances in our understanding of the evolutionary basis of cancer. Over the course of evolutionary time, species have acquired and fine-tuned adaptive cancer-protective mechanisms that are intrinsically related to their energy demands, reproductive strategies, and expected lifespan. These cancer-protective mechanisms are general across species and/or specific to each species and their niche, and they do not seem to be limited in diversity. The evolutionarily acquired cancer-free longevity that defines a species' life history can explain why the relative cancer risk, rate, and incidence are largely similar across most species in the animal kingdom despite differences in body size and life expectancy. The molecular, cellular, and metabolic events that promote malignant transformation and cancerous growth can overcome these adaptive, species-specific protective mechanisms in a small proportion of individuals, while independently, some individuals in the population might achieve exceptional longevity. In dogs and humans, recent dramatic alterations in healthcare and social structures have allowed increasing numbers of individuals in both species to far exceed their species-adapted longevities (by two to four times) without allowing the time necessary for compensatory natural selection. In other words, the cancer-protectiveThis is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

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The three dimensions of somatic evolution: Integrating the role of genetic damage, life‐history traits, and aging in carcinogenesis

Cited by 9 publications

References 80 publications

Expression levels of CXCR4 and CXCL12 in patients with rheumatoid arthritis and its correlation with disease activity

Expression levels of CXCR4 and CXCL12 in patients with rheumatoid arthritis and its correlation with disease activity

Onco-Breastomics: An Eco-Evo-Devo Holistic Approach

Increased risk of cancer in dogs and humans: A consequence of recent extension of lifespan beyond evolutionarily determined limitations?

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