Aging and Cancers

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Tumor Microenvironment".

Deadline for manuscript submissions: 30 June 2025 | Viewed by 12267

Special Issue Editors


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Guest Editor
Department of Biomedical Sciences, University of Cagliari, 09124 Cagliari, Italy
Interests: the role of tissue microenvironment in the development and progression of cancer; importance aging; tissue pattern formation; cell competition; cell senescence

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Guest Editor
Weill Cornell Medicine, Belfer Research Building, 413 E 69th St, New York, NY 10021, USA
Interests: aging; stem cells; tissue homeostasis; cancer; organelle biology

Special Issue Information

Dear Colleagues,

Aging and cancer both result from complex biological processes whose intricacies continue to challenge and stimulate generations of researchers in their respective fields. From this perspective, one would deem any attempt to combine the two topics as inappropriate and counterproductive in improving our unravelling capacity. Yet, studies over the past several decades have repeatedly suggested that aging and cancer are mechanistically related, other than being temporally associated. This line of thinking is gaining more and more momentum based on recent findings documenting the widespread changes occurring in the aged tissue landscapes, some of which bear direct relevance to the emergence of neoplastic diseases. In fact, the age-associated alterations in tissue/organismal context stand as a major factor fueling cancer development in the elderly population.

Within this framework, this Special Issue will highlight both biological and molecular pathways (including genetic and epigenetic) that can help explain the link between aging and cancer.

Dr. Fabio Marongiu
Dr. Saloni Sinha
Guest Editor

Manuscript Submission Information

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Keywords

  • aging
  • cancer development
  • cell competition
  • tissue maintenance and decline
  • cell senescence
  • immune surveillance
  • clonal evolution
  • tissue pattern

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Published Papers (5 papers)

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Research

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13 pages, 2094 KiB  
Article
Downregulation of Aging-Associated Gene SUCLG1 Marks the Aggressiveness of Liver Disease
by Desislava K. Tsoneva, Alessandro Napoli, Mariya Teneva, Tommaso Mazza and Manlio Vinciguerra
Cancers 2025, 17(3), 339; https://doi.org/10.3390/cancers17030339 - 21 Jan 2025
Viewed by 1372
Abstract
Introduction: The most common liver disease is nonalcoholic fatty liver disease, characterized by an intrahepatic accumulation of lipids that most often accompanies obesity. Fatty liver can evolve, in the presence of oxidative stress and inflammation, into disabling and deadly liver diseases such as [...] Read more.
Introduction: The most common liver disease is nonalcoholic fatty liver disease, characterized by an intrahepatic accumulation of lipids that most often accompanies obesity. Fatty liver can evolve, in the presence of oxidative stress and inflammation, into disabling and deadly liver diseases such as cirrhosis, hepatocellular carcinoma (HCC), and cholangiocarcinoma (CC). Old age seems to favor HCC and CC, in agreement with the inflammaging theory, according to which aging accrues inflammation. Cancer, in general, is an age-related disease, as incidence and mortality for most types of cancer increase with age. However, how molecular drivers in tumors differ or are mutated more frequently among patients of different ages remains scarcely investigated. A recent integrative analysis of the age-associated multi-omic landscape across cancers and healthy tissues demonstrated that age-related gene expression changes are linked to numerous biological processes. HCC and CC have among the lowest five-year survival estimates due to their aggressive progression. Materials and methods: In this study, we extracted top gene candidates from the above-mentioned pan-analyses (i.e., B2M, C1qA, SUCLG1) and tested by qPCR their expression and their correlation with disease progression in 48 tissue samples covering liver disease stages (fatty liver, hepatitis, cirrhosis, HCC and CC) and normal tissues. Results: Here, we report a significant downregulation in the expression of the age-associated gene SUCLG1 during the progression of liver disease toward HCC and CC, which also associates with poor patient survival. Conclusion: SUCGL1, a mitochondrial enzyme gene that catalyzes the conversion of succinyl CoA to succinate, might be therapeutically targeted for the development and progression of age-associated liver cancers with low survival rates. Full article
(This article belongs to the Special Issue Aging and Cancers)
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Review

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55 pages, 2619 KiB  
Review
A Review of Telomere Attrition in Cancer and Aging: Current Molecular Insights and Future Therapeutic Approaches
by Mina Iskandar, Miguel Xiao Barbero, Muhamed Jaber, Roy Chen, Romulo Gomez-Guevara, Edwin Cruz and Sandy Westerheide
Cancers 2025, 17(2), 257; https://doi.org/10.3390/cancers17020257 - 14 Jan 2025
Viewed by 2813
Abstract
Background/Objectives: As cells divide, telomeres shorten through a phenomenon known as telomere attrition, which leads to unavoidable senescence of cells. Unprotected DNA exponentially increases the odds of mutations, which can evolve into premature aging disorders and tumorigenesis. There has been growing academic and [...] Read more.
Background/Objectives: As cells divide, telomeres shorten through a phenomenon known as telomere attrition, which leads to unavoidable senescence of cells. Unprotected DNA exponentially increases the odds of mutations, which can evolve into premature aging disorders and tumorigenesis. There has been growing academic and clinical interest in exploring this duality and developing optimal therapeutic strategies to combat telomere attrition in aging and cellular immortality in cancer. The purpose of this review is to provide an updated overview of telomere biology and therapeutic tactics to address aging and cancer. Methods: We used the Rayyan platform to review the PubMed database and examined the ClinicalTrial.gov registry to gain insight into clinical trials and their results. Results: Cancer cells activate telomerase or utilize alternative lengthening of telomeres to escape telomere shortening, leading to near immortality. Contrarily, normal cells experience telomeric erosion, contributing to premature aging disorders, such as Werner syndrome and Hutchinson–Gilford Progeria, and (2) aging-related diseases, such as neurodegenerative and cardiovascular diseases. Conclusions: The literature presents several promising therapeutic approaches to potentially balance telomere maintenance in aging and shortening in cancer. This review highlights gaps in knowledge and points to the potential of these optimal interventions in preclinical and clinical studies to inform future research in cancer and aging. Full article
(This article belongs to the Special Issue Aging and Cancers)
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13 pages, 996 KiB  
Review
Dietary Rhythms and MASLD-Related Hepatocellular Carcinoma
by Nadia Malakmahmoudi, Roberta Pisu, Ezio Laconi and Fabio Marongiu
Cancers 2024, 16(20), 3481; https://doi.org/10.3390/cancers16203481 - 14 Oct 2024
Viewed by 1321
Abstract
Dietary rhythms have emerged as a relevant variable in the equation relating nutrition and health. Both experimental and epidemiological studies point to potential beneficial effects of adequate fasting intervals between meals on the evolution of chronic diseases associated with aging. Metabolic dysfunction-associated steatotic [...] Read more.
Dietary rhythms have emerged as a relevant variable in the equation relating nutrition and health. Both experimental and epidemiological studies point to potential beneficial effects of adequate fasting intervals between meals on the evolution of chronic diseases associated with aging. Metabolic dysfunction-associated steatotic liver disease (MASLD) is eminently related to diet and unsurprisingly, diet-based approaches are a mainstay in countering its long-term clinical evolution, including the emergence of hepatocellular carcinoma (HCC). We briefly discuss current evidence linking fasting intervals, MASLD, and HCC and propose a working hypothesis to reconcile some of the apparently conflicting results. This hypothesis relates the beneficial effects of time-restricted eating schedules to the quantity and quality of food, and it is easily amenable to testing. Full article
(This article belongs to the Special Issue Aging and Cancers)
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Other

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9 pages, 570 KiB  
Perspective
A Novel Strategy to Model Age-Related Cancer for Elucidation of the Role of Th17 Inflammaging in Cancer Progression
by Qiuyang Zhang and S. Michal Jazwinski
Cancers 2022, 14(21), 5185; https://doi.org/10.3390/cancers14215185 - 22 Oct 2022
Cited by 3 | Viewed by 2043
Abstract
Cancer is a disease of aging, but most studies on cancer are in young but not aged animal models, and cancer clinical trials are rarely performed in older adults. Recognition of the connections between aging and cancer and improvement of treatment for elderly [...] Read more.
Cancer is a disease of aging, but most studies on cancer are in young but not aged animal models, and cancer clinical trials are rarely performed in older adults. Recognition of the connections between aging and cancer and improvement of treatment for elderly cancer patients has become one of the most critical medical issues with the global increase in the elderly population. Mouse models are essential experimental tools for understanding the molecular mechanisms of complex processes and related gene pathways of biological aging. However, few mouse models can be used to understand the role of aging in cancer development and the underlying mechanisms. One of the hallmarks of aging is chronic inflammation, often called inflammaging. This is our rationale for examining the role of aging-related inflammation in prostate cancer, a major aging malignancy. We have now developed a novel method to generate age-related cancer models in mice to better understand how age impacts cancer initiation and progression in the natural aging process. We discuss its application to elucidate some of the contributing mechanisms. Full article
(This article belongs to the Special Issue Aging and Cancers)
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12 pages, 671 KiB  
Perspective
Stem-Cell Theory of Cancer: Implications for Antiaging and Anticancer Strategies
by Shi-Ming Tu and Louis L. Pisters
Cancers 2022, 14(5), 1338; https://doi.org/10.3390/cancers14051338 - 4 Mar 2022
Cited by 3 | Viewed by 3567
Abstract
A stem-cell theory of cancer predicates that not only does the cell affect the niche, the niche also affects the cell. It implicates that even though genetic makeup may be supreme, cellular context is key. When we attempt to solve the mystery of [...] Read more.
A stem-cell theory of cancer predicates that not only does the cell affect the niche, the niche also affects the cell. It implicates that even though genetic makeup may be supreme, cellular context is key. When we attempt to solve the mystery of a long cancer-free life, perhaps we need to search no further than the genetics and epigenetics of the naked mole-rat. When we try to unlock the secrets in the longevity and quality of life, perhaps we need to look no further than the lifestyle and habits of the super centenarians. We speculate that people with Down’s syndrome and progeria age faster but have fewer cancers, because they are depleted of stem cells, and, as a consequence, have fewer opportunities for stem cell defects that could predispose them to the development of cancer. We contemplate whether these incredible experiments of nature may provide irrefutable evidence that cancer is a stem-cell disease—fewer aberrant stem cells, fewer cancers; no defective stem cells, no cancer. In this perspective, we investigate a stem-cell origin of aging and cancer. We elaborate an intriguing inverse relationship between longevity and malignancy in the naked mole-rat, in Down’s syndrome, and in progeria. We postulate that stem-cell pools and stemness factors may affect aging and dictate cancer. We propose that a healthy microbiome may protect and preserve stem cell reserves and provide meaningful antiaging effects and anticancer benefits. Full article
(This article belongs to the Special Issue Aging and Cancers)
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