The occurrence of cancer in vertebrates: a mini review

Kitsoulis, Christos V.; Baxevanis, Athanasios D.; Abatzopoulos, Theodore J.

doi:10.1186/s40709-020-00119-0

Cited by 14 publications

(17 citation statements)

References 70 publications

(102 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Disruption of p53 protein function causes the occurrence of cancer cell features [ 12 ]. The presence of extra copies results in an effective DNA damage response through the hyperactive TP53 pathway ( Figure 3 a) [ 44 ].…”

Section: Cancer and Evolutionmentioning

confidence: 99%

See 1 more Smart Citation

Cancer, Retrogenes, and Evolution

Staszak

Makałowska

2021

Life

View full text Add to dashboard Cite

This review summarizes the knowledge about retrogenes in the context of cancer and evolution. The retroposition, in which the processed mRNA from parental genes undergoes reverse transcription and the resulting cDNA is integrated back into the genome, results in additional copies of existing genes. Despite the initial misconception, retroposition-derived copies can become functional, and due to their role in the molecular evolution of genomes, they have been named the “seeds of evolution”. It is convincing that retrogenes, as important elements involved in the evolution of species, also take part in the evolution of neoplastic tumors at the cell and species levels. The occurrence of specific “resistance mechanisms” to neoplastic transformation in some species has been noted. This phenomenon has been related to additional gene copies, including retrogenes. In addition, the role of retrogenes in the evolution of tumors has been described. Retrogene expression correlates with the occurrence of specific cancer subtypes, their stages, and their response to therapy. Phylogenetic insights into retrogenes show that most cancer-related retrocopies arose in the lineage of primates, and the number of identified cancer-related retrogenes demonstrates that these duplicates are quite important players in human carcinogenesis.

show abstract

Section: Cancer and Evolutionmentioning

confidence: 99%

“…Similar changes have been identified in hypoxia-tolerant human tumors [ 13 , 49 ]. Interestingly, despite many studies, no cases of malignant neoplasm have been found in this species [ 44 ].…”

Section: Cancer and Evolutionmentioning

confidence: 99%

Cancer, Retrogenes, and Evolution

Staszak

Makałowska

2021

Life

View full text Add to dashboard Cite

show abstract

“…Antioxidant capacity is elevated and DNA-damage is reduced (Conde-Pérezprina et al, 2012) in long-lived (Desmodus rotundus) compared to short-lived species (Myotis velifer) and in torpid compared to active individuals (Sturnia lilium; Wilhelm Filho et al, 2007). Consistent with low cancer incidence (Kitsoulis et al, 2020), DNA repair and signaling pathways are maintained throughout the lifespan (Huang et al, 2019) and two long-lived species (M. myotis, M. lucifugus) possess additional copies of the tumor suppressor FBX031 (Seim et al, 2013). The genomes and transcriptomes published by Seim et al together with further finished and ongoing genome sequencing projects of the approximately 1300 living bat species provide a solid basis for future comparative studies (Jebb et al, 2020).…”

Section: Bats (Chiroptera)mentioning

confidence: 96%

Alternative Animal Models of Aging Research

Holtze

Горшкова

Braude

et al. 2021

Front. Mol. Biosci.

View full text Add to dashboard Cite

Most research on mechanisms of aging is being conducted in a very limited number of classical model species, i.e., laboratory mouse (Mus musculus), rat (Rattus norvegicus domestica), the common fruit fly (Drosophila melanogaster) and roundworm (Caenorhabditis elegans). The obvious advantages of using these models are access to resources such as strains with known genetic properties, high-quality genomic and transcriptomic sequencing data, versatile experimental manipulation capabilities including well-established genome editing tools, as well as extensive experience in husbandry. However, this approach may introduce interpretation biases due to the specific characteristics of the investigated species, which may lead to inappropriate, or even false, generalization. For example, it is still unclear to what extent knowledge of aging mechanisms gained in short-lived model organisms is transferable to long-lived species such as humans. In addition, other specific adaptations favoring a long and healthy life from the immense evolutionary toolbox may be entirely missed. In this review, we summarize the specific characteristics of emerging animal models that have attracted the attention of gerontologists, we provide an overview of the available data and resources related to these models, and we summarize important insights gained from them in recent years. The models presented include short-lived ones such as killifish (Nothobranchius furzeri), long-lived ones such as primates (Callithrix jacchus, Cebus imitator, Macaca mulatta), bathyergid mole-rats (Heterocephalus glaber, Fukomys spp.), bats (Myotis spp.), birds, olms (Proteus anguinus), turtles, greenland sharks, bivalves (Arctica islandica), and potentially non-aging ones such as Hydra and Planaria.

show abstract

“…This model predicts that regeneration-competent species will show higher rates of cancers such as glioblastoma and neuroblastoma-like tumors. In addition, regenerative competence might be expected to decrease with age, as the probability of tumor formation increases (Kitsoulis et al, 2020).…”

Section: Hypothesis 3: Loss Of Regenerative Competence Is An Adaptati...mentioning

confidence: 99%

Why Has the Ability to Regenerate Following CNS Injury Been Repeatedly Lost Over the Course of Evolution?

Blackshaw

2022

Front. Neurosci.

View full text Add to dashboard Cite

While many vertebrates can regenerate both damaged neurons and severed axons in the central nervous system (CNS) following injury, others, including all birds and mammals, have lost this ability for reasons that are still unclear. The repeated evolutionary loss of regenerative competence seems counterintuitive, and any explanation must account for the fact that regenerative competence is lost in both cold-blooded and all warm-blooded clades, that both injury-induced neurogenesis and axonal regeneration tend to be lost in tandem, and that mammals have evolved dedicated gene regulatory networks to inhibit injury-induced glia-to-neuron reprogramming. Here, different hypotheses that have been proposed to account for evolutionary loss of regenerative competence are discussed in the light of new insights obtained into molecular mechanisms that control regeneration in the central nervous system. These include pleiotropic effects of continuous growth, enhanced thyroid hormone signaling, prevention of neoplasia, and improved memory consolidation. Recent evidence suggests that the most compelling hypothesis, however, may be selection for greater resistance to the spread of intra-CNS infections, which has led to both enhanced reactive gliosis and a loss of injury-induced neurogenesis and axonal regeneration. Means of testing these hypotheses, and additional data that are urgently needed to better understand the evolutionary pressures and mechanisms driving loss of regenerative competence, are also discussed.

show abstract

The occurrence of cancer in vertebrates: a mini review

Cited by 14 publications

References 70 publications

Cancer, Retrogenes, and Evolution

Cancer, Retrogenes, and Evolution

Alternative Animal Models of Aging Research

Why Has the Ability to Regenerate Following CNS Injury Been Repeatedly Lost Over the Course of Evolution?

Contact Info

Product

Resources

About