scholarly journals Cancer risk across mammals

Nature ◽  
2021 ◽  
Author(s):  
Orsolya Vincze ◽  
Fernando Colchero ◽  
Jean-Francois Lemaître ◽  
Dalia A. Conde ◽  
Samuel Pavard ◽  
...  
Keyword(s):  
Body Size ◽  
Cancer Risk ◽  
Cancer Mortality ◽  
Adult Life ◽  
Life History Evolution ◽  
The Body ◽  
Cancer Resistance ◽  
Apparent Lack ◽  
Using Data ◽  
Related Mortality

AbstractCancer is a ubiquitous disease of metazoans, predicted to disproportionately affect larger, long-lived organisms owing to their greater number of cell divisions, and thus increased probability of somatic mutations1,2. While elevated cancer risk with larger body size and/or longevity has been documented within species3–5, Peto’s paradox indicates the apparent lack of such an association among taxa6. Yet, unequivocal empirical evidence for Peto’s paradox is lacking, stemming from the difficulty of estimating cancer risk in non-model species. Here we build and analyse a database on cancer-related mortality using data on adult zoo mammals (110,148 individuals, 191 species) and map age-controlled cancer mortality to the mammalian tree of life. We demonstrate the universality and high frequency of oncogenic phenomena in mammals and reveal substantial differences in cancer mortality across major mammalian orders. We show that the phylogenetic distribution of cancer mortality is associated with diet, with carnivorous mammals (especially mammal-consuming ones) facing the highest cancer-related mortality. Moreover, we provide unequivocal evidence for the body size and longevity components of Peto’s paradox by showing that cancer mortality risk is largely independent of both body mass and adult life expectancy across species. These results highlight the key role of life-history evolution in shaping cancer resistance and provide major advancements in the quest for natural anticancer defences.

scholarly journals Pervasive duplication of tumor suppressors in Afrotherians during the evolution of large bodies and reduced cancer risk

2020 ◽  
Author(s):  
Juan Manuel Vazquez ◽  
Vincent J. Lynch
Keyword(s):  
Body Size ◽  
Tumor Suppressor ◽  
Gene Duplication ◽  
Cancer Risk ◽  
Tumor Suppressors ◽  
Tumor Suppressor Genes ◽  
Cell Biology ◽  
Cancer Resistance ◽  
Anti Cancer ◽  
Protection Mechanisms

AbstractThe risk of developing cancer is correlated with body size and lifespan within species. Between species, however, there is no correlation between cancer and either body size or lifespan, indicating that large, long-lived species have evolved enhanced cancer protection mechanisms. Elephants and their relatives (Proboscideans) are a particularly interesting lineage for the exploration of mechanisms underlying the evolution of augmented cancer resistance because they evolved large bodies recently within a clade of smaller bodied species (Afrotherians). Here, we explore the contribution of gene duplication to body size and cancer risk in Afrotherians. Unexpectedly, we found that tumor suppresxssor duplication was pervasive in Afrotherian genomes, rather than restricted to Proboscideans. Proboscideans, however, have duplicates in unique pathways that may underlie some aspects of their remarkable anti-cancer cell biology. These data suggest that duplication of tumor suppressor genes facilitated the evolution of increased body size by compensating for decreasing intrinsic cancer risk.

Automatic Tool for Prediction of Type of Cancer Risk and Recommendations

2018 ◽  
pp. 447-454
Author(s):  
Pallavi Mirajkar ◽  
G. Prasanna Lakshmi
Keyword(s):  
Cancer Risk ◽  
Medical Practitioner ◽  
Prediction Performance ◽  
The Body ◽  
Prediction Tool ◽  
Cancer Disease ◽  
High Concern ◽  
Technical Possibility ◽  
Automatic Tool ◽  
Using Data

Cancer can begin in any part of the body and can spread to other parts also. It is uncontrollable and it has many types. In the proposed thesis research paper, a tool for prediction of type of cancer risk with five different cancer diagnosis and recommendations is presented. For recognizing cancer disease number of tests ought to be required from the patient. But using data mining techniques these test can be diminished. Indeed, an accurate prediction of cancer is very difficult task for medical practitioner and it is also high concern to the patients so that better treatment can be given and it will also increase the survival time of the patients. Our findings suggested that suitable prediction tool can effectively reduce the several tests for diagnosing cancer and prediction accuracy thereby increasing the technical possibility of early detection of cancer. The main features of the tool comprise a balance between the number of necessary inputs and prediction performance, being portable, and it empowers the automatic development of the cancer risk prediction tool in cancer disease.

scholarly journals Pervasive duplication of tumor suppressors in Afrotherians during the evolution of large bodies and reduced cancer risk

eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Juan M Vazquez ◽  
Vincent J Lynch
Keyword(s):  
Body Size ◽  
Tumor Suppressor ◽  
Gene Duplication ◽  
Cancer Risk ◽  
Tumor Suppressors ◽  
Tumor Suppressor Genes ◽  
Cell Biology ◽  
Cancer Resistance ◽  
Anti Cancer ◽  
Protection Mechanisms

The risk of developing cancer is correlated with body size and lifespan within species. Between species, however, there is no correlation between cancer and either body size or lifespan, indicating that large, long-lived species have evolved enhanced cancer protection mechanisms. Elephants and their relatives (Proboscideans) are a particularly interesting lineage for the exploration of mechanisms underlying the evolution of augmented cancer resistance because they evolved large bodies recently within a clade of smaller bodied species (Afrotherians). Here, we explore the contribution of gene duplication to body size and cancer risk in Afrotherians. Unexpectedly, we found that tumor suppressor duplication was pervasive in Afrotherian genomes, rather than restricted to Proboscideans. Proboscideans, however, have duplicates in unique pathways that may underlie some aspects of their remarkable anti-cancer cell biology. These data suggest that duplication of tumor suppressor genes facilitated the evolution of increased body size by compensating for decreasing intrinsic cancer risk.

scholarly journals Sex-Biased Winter Distribution and Timing of Migration of Hermit Thrushes (Catharus Guttatus) in Eastern North America

The Auk ◽  
2003 ◽  
Vol 120 (3) ◽  
pp. 836-847
Author(s):  
Philip C. Stouffer ◽  
Gens M. Dwyer
Keyword(s):  
Body Size ◽  
The Body ◽  
Eastern United States ◽  
Climate Data ◽  
Winter Distribution ◽  
Early Arrival ◽  
Catharus Guttatus ◽  
Breeding Grounds ◽  
Timing Of Migration ◽  
Using Data

Abstract We analyzed distribution of Hermit Thrushes (Catharus guttatus faxoni) wintering in the eastern United States and northeastern Mexico using data from 2,077 specimens collected in winter or during migration. Hermit Thrushes collected in winter showed a sex-biased latitudinal distribution, with the female mean 1.2° south of the male mean. Three general, nonmutually exclusive hypotheses have been proposed to account for that pattern in other species: (1) dominance of males over females, which forces females to lower latitudes; (2) larger body size of males, which permits males to overwinter in colder areas; and (3) earlier arrival by males on breeding grounds, which selects for males to winter closer to the breeding grounds. The dominance hypothesis requires that females be subordinate, an assumption that is not supported by previous research with wintering Hermit Thrushes. We also found no difference in sex ratio among habitats, despite strong differences in habitat quality. The body-size hypothesis requires that the larger sex be able to withstand colder temperatures. Male Hermit Thrushes are larger, but neither multiyear climate data nor weather in the specific month and year when birds were collected showed males to face significantly colder temperatures on the wintering grounds. Our data are most consistent with the arrival-time hypothesis. Males collected during spring migration migrated ∼20 days before females. When males began migrating in March, they experienced colder weather than sedentary females. By wintering farther north and migrating earlier, males expedite their return to their breeding grounds, although the small difference in winter distribution between the sexes is marginal compared to the effect of males’ much earlier departure. Presumably, any cost to males of wintering or migrating under more demanding conditions is balanced by the advantage of early arrival on the breeding grounds.

The Body Size of Headstarted and Wild Juvenile European Pond Turtles (Emys orbicularis)

2017 ◽  
Vol 25 (2) ◽  
pp. 161
Author(s):  
Sławomir Mitrus ◽  
Bartłomiej Najbar ◽  
Adam Kotowicz ◽  
Anna Najbar
Keyword(s):  
Body Size ◽  
The Body ◽  
Emys Orbicularis

Breast Cancer Resistance Protein: A Potential Therapeutic Target for Cancer

2020 ◽  
Vol 21 ◽  
Author(s):  
Sonali Mehendale-Munj
Keyword(s):  
Breast Cancer ◽  
Breast Cancer Resistance Protein ◽  
Protein A ◽  
The Body ◽  
Cancer Therapies ◽  
Cancer Resistance ◽  
Lung Cancers ◽  
Resistance Protein ◽  
Atp Regulation ◽  
Treatment Procedures

: Breast Cancer Resistance Protein (BCRP) is an efflux transporter responsible for causing multidrug re-sistance(MDR). It is known to expel many potent antineoplastic drugs, owing to its efflux function. Efflux of chemothera-peutics because of BCRP develops resistance to manydrugs, leading to failure in cancer treatment. BCRP plays an important role in physiology by protecting the organism from xenobiotics and other toxins. It is a half-transporter affiliated to theATP-binding cassette (ABC) superfamily of transporters, encoded by the gene ABCG2 and functions in response to adenosine triphosphate (ATP). Regulation of BCRP expression is critically controlled at molecular levels which help in maintaining the balance of xenobiotics and nutrients inside the body. Expression of BCRP can be found in brain, liver, lung cancers and acute myeloid leukemia (AML). Moreover, it is also expressed at high levels in stem cells and many cell lines. This frequent expression of BCRP has an impact on the treatment procedures and if not scrutinized may lead to failure of many cancer therapies.

scholarly journals First record of Pachycrocuta brevirostris (Gervais, 1850) from Ukraine on the background of the European occurrence of the species

2021 ◽  
Author(s):  
Adrian Marciszak ◽  
Yuriy Semenov ◽  
Piotr Portnicki ◽  
Tamara Derkach
Keyword(s):  
Body Size ◽  
First Record ◽  
The Body ◽  
Crocuta Crocuta ◽  
Early Pleistocene ◽  
Eastern Asia ◽  
South Eastern

AbstractCranial material ofPachycrocuta brevirostrisfrom the late Early Pleistocene site of Nogaisk is the first record of this species in Ukraine. This large hyena was a representative of the Tamanian faunal complex and a single specialised scavenger in these faunas. The revisited European records list ofP.brevirostrisdocumented the presence of this species in 101 sites, dated in the range of 3.5–0.4 Ma. This species first disappeared in Africa, survived in Europe until ca. 0.8–0.7 Ma, and its last, relict occurrence was known from south-eastern Asia. The main reason of extinction ofP.brevirostrisprobably was the competition withCrocuta crocuta. The cave hyena was smaller, but its teeth were proportionally larger to the body size, better adapted to crushing bones and slicing meat, and could also hunt united in larger groups.

scholarly journals Appetite disinhibition rather than hunger explains genetic effects on adult BMI trajectory

2021 ◽  
Author(s):  
Eric J. Brunner ◽  
Koutatsu Maruyama ◽  
Martin Shipley ◽  
Noriko Cable ◽  
Hiroyasu Iso ◽  
...  
Keyword(s):  
Weight Gain ◽  
Genetic Susceptibility ◽  
Eating Behaviors ◽  
Mixed Model ◽  
Adult Life ◽  
Cohort Effect ◽  
The Body ◽  
European Ancestry ◽  
Nucleotide Polymorphisms ◽  
Bmi Trajectories

Abstract Background/objectives The mediating role of eating behaviors in genetic susceptibility to weight gain during mid-adult life is not fully understood. This longitudinal study aims to help us understand contributions of genetic susceptibility and appetite to weight gain. Subjects/methods We followed the body-mass index (BMI) trajectories of 2464 adults from 45 to 65 years of age by measuring weight and height on four occasions at 5-year intervals. Genetic risk of obesity (gene risk score: GRS) was ascertained, comprising 92 BMI-associated single-nucleotide polymorphisms and split at a median (=high and low risk). At the baseline, the Eating Inventory was used to assess appetite-related traits of ‘disinhibition’, indicative of opportunistic eating or overeating and ‘hunger’ which is susceptibility to/ability to cope with the sensation of hunger. Roles of the GRS and two appetite-related scores for BMI trajectories were examined using a mixed model adjusted for the cohort effect and sex. Results Disinhibition was associated with higher BMI (β = 2.96; 95% CI: 2.66–3.25 kg/m2), and accounted for 34% of the genetically-linked BMI difference at age 45. Hunger was also associated with higher BMI (β = 1.20; 0.82–1.59 kg/m2) during mid-life and slightly steeper weight gain, but did not attenuate the effect of disinhibition. Conclusions Appetite disinhibition is most likely to be a defining characteristic of genetic susceptibility to obesity. High levels of appetite disinhibition, rather than hunger, may underlie genetic vulnerability to obesogenic environments in two-thirds of the population of European ancestry.

Telomere Length and Arsenic: Improving Animal Models of Toxicity by Choosing Mice With Shorter Telomeres

2021 ◽  
Vol 40 (3) ◽  
pp. 211-217
Author(s):  
Brayden Whitlock
Keyword(s):  
Animal Models ◽  
Telomere Length ◽  
Mouse Models ◽  
Arsenic Exposure ◽  
Tumor Formation ◽  
The Body ◽  
Cancer Resistance ◽  
Selective Pressures ◽  
Toxicity Monitoring ◽  
In Captivity

Arsenic is both a chemotherapeutic drug and an environmental toxicant that affects hundreds of millions of people each year. Arsenic exposure in drinking water has been called the worst poisoning in human history. How arsenic is handled in the body is frequently studied using rodent models to investigate how arsenic both causes and treats disease. These models, used in a variety of arsenic-related testing, from tumor formation to drug toxicity monitoring, have virtually always been developed from animals with telomeres that are unnaturally long, likely because of accidental artificial selective pressures. Mice that have been bred in captivity in laboratory conditions, often for over 100 years, are the standard in creating animal models for this research. Using these mice introduces challenges to any work that can be affected by the length of telomeres and the related capacities for tissue repair and cancer resistance. However, arsenic research is particularly susceptible to the misuse of such animal models due to the multiple and various interactions between arsenic and telomeres. Researchers in the field commonly find mouse models and humans behaving very differently upon exposure to acute and chronic arsenic, including drug therapies which seem safe in mice but are toxic in humans. Here, some complexities and apparent contradictions of the arsenic carcinogenicity and toxicity research are reconciled by an explanatory model that involves telomere length explained by the evolutionary pressures in laboratory mice. A low-risk hypothesis is proposed which has the power to determine whether researchers can easily develop more powerful and accurate mouse models by simply avoiding mouse lineages that are very old and have strangely long telomeres. Swapping in newer mouse lineages for the older, long-telomere mice may vastly improve our ability to research arsenic toxicity with virtually no increase in cost or difficulty of research.

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