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Cancer rates vary between people, between cultures, and between tissue types, driven by clinically relevant distinctions in the risk factors that lead to different cancer types. Despite the importance of cancer location in human health, little is known about tissue-specific cancers in non-human animals. We can gain significant insight into

Cancer rates vary between people, between cultures, and between tissue types, driven by clinically relevant distinctions in the risk factors that lead to different cancer types. Despite the importance of cancer location in human health, little is known about tissue-specific cancers in non-human animals. We can gain significant insight into how evolutionary history has shaped mechanisms of cancer suppression by examining how life history traits impact cancer susceptibility across species. Here, we perform multi-level analysis to test how species-level life history strategies are associated with differences in neoplasia prevalence, and apply this to mammary neoplasia within mammals. We propose that the same patterns of cancer prevalence that have been reported across species will be maintained at the tissue-specific level. We used a combination of factor analysis and phylogenetic regression on 13 life history traits across 90 mammalian species to determine the correlation between a life history trait and how it relates to mammary neoplasia prevalence. The factor analysis presented ways to calculate quantifiable underlying factors that contribute to covariance of entangled life history variables. A greater risk of mammary neoplasia was found to be correlated most significantly with shorter gestation length. With this analysis, a framework is provided for how different life history modalities can influence cancer vulnerability. Additionally, statistical methods developed for this project present a framework for future comparative oncology studies and have the potential for many diverse applications.

ContributorsFox, Morgan Shane (Author) / Maley, Carlo C. (Thesis director) / Boddy, Amy (Committee member) / Compton, Zachary (Committee member) / School of Mathematical and Statistical Sciences (Contributor) / School of Molecular Sciences (Contributor) / School of Life Sciences (Contributor) / Barrett, The Honors College (Contributor)
Created2021-05
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This dissertation investigates the condition of skeletal muscle insulin resistance using bioinformatics and computational biology approaches. Drawing from several studies and numerous data sources, I have attempted to uncover molecular mechanisms at multiple levels. From the detailed atomistic simulations of a single protein, to datamining approaches applied at the systems

This dissertation investigates the condition of skeletal muscle insulin resistance using bioinformatics and computational biology approaches. Drawing from several studies and numerous data sources, I have attempted to uncover molecular mechanisms at multiple levels. From the detailed atomistic simulations of a single protein, to datamining approaches applied at the systems biology level, I provide new targets to explore for the research community. Furthermore I present a new online web resource that unifies various bioinformatics databases to enable discovery of relevant features in 3D protein structures.
ContributorsMielke, Clinton (Author) / Mandarino, Lawrence (Committee member) / LaBaer, Joshua (Committee member) / Magee, D. Mitchell (Committee member) / Dinu, Valentin (Committee member) / Willis, Wayne (Committee member) / Arizona State University (Publisher)
Created2013
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While exercising mammalian muscle increasingly relies on carbohydrates for fuel as aerobic exercise intensity rises above the moderate range, flying birds are extraordinary endurance athletes and fuel flight, a moderate-high intensity exercise, almost exclusively with lipid. In addition, Aves have long lifespans compared to weight-matched mammals. As skeletal muscle mitochondria

While exercising mammalian muscle increasingly relies on carbohydrates for fuel as aerobic exercise intensity rises above the moderate range, flying birds are extraordinary endurance athletes and fuel flight, a moderate-high intensity exercise, almost exclusively with lipid. In addition, Aves have long lifespans compared to weight-matched mammals. As skeletal muscle mitochondria account for the majority of oxygen consumption during aerobic exercise, the primary goal was to investigate differences in isolated muscle mitochondria between these species and to examine to what extent factors intrinsic to mitochondria may account for the behavior observed in the intact tissue and whole organism. First, maximal enzyme activities were assessed in sparrow and rat mitochondria. Citrate synthase and aspartate aminotransferase activity were higher in sparrow compared to rat mitochondria, while glutamate dehydrogenase activity was lower. Sparrow mitochondrial NAD-linked isocitrate dehydrogenase activity was dependent on phosphate, unlike the mammalian enzyme. Next, the rate of oxygen consumption (JO), electron transport chain (ETC) activity, and reactive oxygen species (ROS) production were assessed in intact mitochondria. Maximal rates of fat oxidation were lower than for carbohydrate in rat but not sparrow mitochondria. ETC activity was higher in sparrows, but no differences were found in ROS production between species. Finally, fuel selection and control of respiration at three rates between rest and maximum were assessed. Mitochondrial fuel oxidation and selection mirrored that of the whole body; in rat mitochondria the reliance on carbohydrate increased as the rate of oxygen consumption increased, whereas fat dominated under all conditions in the sparrow. These data indicate fuel selection, at least in part, can be modulated at the level of the mitochondrial matrix when multiple substrates are present at saturating levels. As an increase in matrix oxidation-reduction potential has been linked to a suppression of fat oxidation and high ROS production, the high ETC activity relative to dehydrogenase activity in avian compared to mammalian mitochondria may result in lower matrix oxidation-reduction potential, allowing fatty acid oxidation to proceed while also resulting in low ROS production in vivo.
ContributorsKuzmiak, Sarah (Author) / Willis, Wayne T (Thesis advisor) / Mandarino, Lawrence (Committee member) / Sweazea, Karen (Committee member) / Harrison, Jon (Committee member) / Gadau, Juergen (Committee member) / Arizona State University (Publisher)
Created2012
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Cancer is a disease of multicellularity, with deep evolutionary origins. As such, the forces of both evolution and natural selection operate on multiple scales to govern tumor dynamics. As multicellular organisms increase in complexity, cellular-level fitness must be controlled in order to maintain organismal-level fitness. Mutations that might provide a

Cancer is a disease of multicellularity, with deep evolutionary origins. As such, the forces of both evolution and natural selection operate on multiple scales to govern tumor dynamics. As multicellular organisms increase in complexity, cellular-level fitness must be controlled in order to maintain organismal-level fitness. Mutations that might provide a benefit at the cellular level by allowing for rapid proliferation are subject to the same forces that function on the organismal level, wherein cancer suppression is a benefit – especially as organisms increase their body size and lifespan. In order to maintain these large cellular bodies and long lifespans, organisms must increase their means of cancer suppression, and it is likely that these two phenomena co-evolved together. On a smaller scale, the cooperative dynamics of circulating tumor cell (CTC) clusters engage in cooperation to form networks of connected single cells that provide protection, stability, and cooperative sharing of resources to enhance their survival as they detach from a primary tumor and metastasize at secondary sites. This work seeks to explore the phenomenon of multi-level selection in neoplastic disease by examining A) the mechanisms of cancer suppression at multiple scales, B) the ecological resilience and stability of cooperating cellular clusters and C) a large-scale dataset on cancer prevalence across mammals, sauropsids (birds and reptiles), and amphibians, illuminating the evolutionary life history characteristics that explain the tradeoffs between cancer suppression and overall organism fitness. By taking an ecological and evolutionary approach to understanding cancer, novel strategies of cancer treatment may be discovered alongside fundamental discoveries about the fundamental forces of selection that govern evolutionary dynamics from the cellular to the organismal scale.
ContributorsHarris, Valerie (Author) / Maley, Carlo C. (Thesis advisor) / Aktipis, Athena (Committee member) / Boddy, Amy M. (Committee member) / Compton, Carolyn (Committee member) / Arizona State University (Publisher)
Created2022
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This dissertation describes a series of four studies on cognitive aging, working memory, and cognitive flexibility in dogs (Canis lupus familiaris) and their wild relatives. In Chapters 2 and 3, I designed assessments for age-related cognitive deficits in pet dogs which can be deployed rapidly using inexpensive and accessible materials.

This dissertation describes a series of four studies on cognitive aging, working memory, and cognitive flexibility in dogs (Canis lupus familiaris) and their wild relatives. In Chapters 2 and 3, I designed assessments for age-related cognitive deficits in pet dogs which can be deployed rapidly using inexpensive and accessible materials. These novel tests can be easily implemented by owners, veterinarians, and clinicians and therefore, may improve care for elderly dogs by aiding in the diagnosis of dementia. In addition, these widely deployable tests may facilitate the use of dementia in pet dogs as a naturally occurring model of Alzheimer’s Disease in humans.In Chapters 4 and 5, I modified one of these tests to demonstrate for the first time that coyotes (Canis latrans) and wolves (Canis lupus lupus) develop age-related deficits in cognitive flexibility. This was an important first step towards differentiating between the genetic and environmental components of dementia in dogs and in turn, humans. Unexpectedly, I also detected cognitive deficits in young, adult dogs and wolves but not coyotes. These finding add to a recent shift in understanding cognitive development in dogs which may improve cognitive aging tests as well as training, care, and use of working and pet dogs. These findings also suggest that the ecology of coyotes may select for flexibility earlier in development. In Chapter 5, I piloted the use of the same cognitive flexibility test for red and gray foxes so that future studies may test for lifespan changes in the cognition of small-bodied captive canids. More broadly, this paradigm may accommodate physical and behavioral differences between diverse pet and captive animals. In Chapters 4 and 5, I examined which ecological traits drive the evolution of behavioral flexibility and in turn, species resilience. I found that wolves displayed less flexibility than dogs and coyotes suggesting that species which do not rely heavily on unstable resources may be ill-equipped to cope with human habitat modification. Ultimately, this comparative work may help conservation practitioners to identify and protect species that cannot cope with rapid and unnatural environmental change.
ContributorsVan Bourg, Joshua (Author) / Wynne, Clive D (Thesis advisor) / Aktipis, C. Athena (Committee member) / Gilby, Ian C (Committee member) / Young, Julie K (Committee member) / Arizona State University (Publisher)
Created2022
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Evolutionary theory provides a rich framework for understanding cancer dynamics across scales of biological organization. The field of cancer evolution has largely been divided into two domains, comparative oncology - the study of cancer across the tree of life, and tumor evolution. This work provides a theoretical framework to unify

Evolutionary theory provides a rich framework for understanding cancer dynamics across scales of biological organization. The field of cancer evolution has largely been divided into two domains, comparative oncology - the study of cancer across the tree of life, and tumor evolution. This work provides a theoretical framework to unify these subfields with the intent that an understanding of the evolutionary dynamics driving cancer risk at one scale can inform the understanding of the dynamics on another scale. The evolution of multicellular life and the unique vulnerabilities in the cellular mechanisms that underpin it explain the ubiquity of cancer prevalence across the tree of life. The breakdown in cellular cooperation and communication that were required for multicellular life define the hallmarks of cancer. As divergent life histories drove speciation events, it similarly drove divergences in fundamental cancer risk across species. An understanding of the impact that species’ life history theory has on the underlying network of multicellular cooperation and somatic evolution allows for robust predictions on cross-species cancer risk. A large-scale veterinary cancer database is utilized to validate many of the predictions on cancer risk made from life history evolution. Changing scales to the cellular level, it lays predictions on the fate of somatic mutations and the fitness benefits they confer to neoplastic cells compared to their healthy counterparts. The cancer hallmarks, far more than just a way to unify the many seemingly unique pathologies defined as cancer, is a powerful toolset to understand how specific mutations may change the fitness of somatic cells throughout carcinogenesis and tumor progression. Alongside highlighting the significant advances in evolutionary approaches to cancer across scales, this work provides a lucid confirmation that an understanding of both scales provides the most complete portrait of evolutionary cancer dynamics.
ContributorsCompton, Zachary Taylor (Author) / Maley, Carlo C. (Thesis advisor) / Aktipis, Athena (Committee member) / Buetow, Kenneth (Committee member) / Nedelcu, Aurora (Committee member) / Compton, Carolyn (Committee member) / Arizona State University (Publisher)
Created2023
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Description
Type 1 diabetes (T1D) is a chronic autoimmune disease characterized by progressive autoimmune destruction of insulin-producing pancreatic β-cells. Genetic, immunological and environmental factors contribute to T1D development. The focus of this dissertation is to track the humoral immune response in T1D by profiling autoantibodies (AAbs) and anti-viral antibodies using an

Type 1 diabetes (T1D) is a chronic autoimmune disease characterized by progressive autoimmune destruction of insulin-producing pancreatic β-cells. Genetic, immunological and environmental factors contribute to T1D development. The focus of this dissertation is to track the humoral immune response in T1D by profiling autoantibodies (AAbs) and anti-viral antibodies using an innovative protein array platform called Nucleic Acid Programmable Protein Array (NAPPA).

AAbs provide value in identifying individuals at risk, stratifying patients with different clinical courses, improving our understanding of autoimmune destructions, identifying antigens for cellular immune response and providing candidates for prevention trials in T1D. A two-stage serological AAb screening against 6,000 human proteins was performed. A dual specificity tyrosine-phosphorylation-regulated kinase 2 (DYRK2) was validated with 36% sensitivity at 98% specificity by an orthogonal immunoassay. This is the first systematic screening for novel AAbs against large number of human proteins by protein arrays in T1D. A more comprehensive search for novel AAbs was performed using a knowledge-based approach by ELISA and a screening-based approach against 10,000 human proteins by NAPPA. Six AAbs were identified and validated with sensitivities ranged from 16% to 27% at 95% specificity. These two studies enriched the T1D “autoantigenome” and provided insights into T1D pathophysiology in an unprecedented breadth and width.

The rapid rise of T1D incidence suggests the potential involvement of environmental factors including viral infections. Sero-reactivity to 646 viral antigens was assessed in new-onset T1D patients. Antibody positive rate of EBV was significantly higher in cases than controls that suggested a potential role of EBV in T1D development. A high density-NAPPA platform was demonstrated with high reproducibility and sensitivity in profiling anti-viral antibodies.

This dissertation shows the power of a protein-array based immunoproteomics approach to characterize humoral immunoprofile against human and viral proteomes. The identification of novel T1D-specific AAbs and T1D-associated viruses will help to connect the nodes in T1D etiology and provide better understanding of T1D pathophysiology.
ContributorsBian, Xiaofang (Author) / LaBaer, Joshua (Thesis advisor) / Mandarino, Lawrence (Committee member) / Chang, Yung (Committee member) / Arizona State University (Publisher)
Created2015
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ABSTRACT

Domestic dogs have assisted humans for millennia. However, the extent to which these helpful behaviors are prosocially motivated remains unclear. To assess the propensity of pet dogs to spontaneously and actively rescue distressed humans, this study tested whether sixty pet dogs would release their seemingly trapped owners from a large

ABSTRACT

Domestic dogs have assisted humans for millennia. However, the extent to which these helpful behaviors are prosocially motivated remains unclear. To assess the propensity of pet dogs to spontaneously and actively rescue distressed humans, this study tested whether sixty pet dogs would release their seemingly trapped owners from a large box. To examine the causal mechanisms that shaped this behavior, the readiness of each dog to open the box was tested in three conditions: 1) the owner sat in the box and called for help (“Distress” test), 2) an experimenter placed high-value food rewards in the box (“Food” test), and 3) the owner sat in the box and calmly read aloud (“Reading” test).

Dogs were as likely to release their distressed owner as to retrieve treats from inside the box, indicating that rescuing an owner may be a highly rewarding action for dogs. After accounting for ability, dogs released the owner more often when the owner called for help than when the owner read aloud calmly. In addition, opening latencies decreased with test number in the Distress test but not the Reading test. Thus, rescuing the owner could not be attributed solely to social facilitation, stimulus enhancement, or social contact-seeking behavior.

Dogs displayed more stress behaviors in the Distress test than in the Reading test, and stress scores decreased with test number in the Reading test but not in the Distress test. This evidence of emotional contagion supports the hypothesis that rescuing the distressed owner was an empathetically-motivated prosocial behavior. Success in the Food task and previous (in-home) experience opening objects were both strong predictors of releasing the owner. Thus, prosocial behavior tests for dogs should control for physical ability and previous experience.
ContributorsVan Bourg, Joshua Lazar (Author) / Wynne, Clive D (Thesis advisor) / Gilby, Ian C (Committee member) / Aktipis, C. Athena (Committee member) / Arizona State University (Publisher)
Created2019
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Description

Microbes in the gastrointestinal tract are under selective pressure to manipulate host eating behavior to increase their fitness, sometimes at the expense of host fitness. Microbes may do this through two potential strategies: (i) generating cravings for foods that they specialize on or foods that suppress their competitors, or (ii)

Microbes in the gastrointestinal tract are under selective pressure to manipulate host eating behavior to increase their fitness, sometimes at the expense of host fitness. Microbes may do this through two potential strategies: (i) generating cravings for foods that they specialize on or foods that suppress their competitors, or (ii) inducing dysphoria until we eat foods that enhance their fitness. We review several potential mechanisms for microbial control over eating behavior including microbial influence on reward and satiety pathways, production of toxins that alter mood, changes to receptors including taste receptors, and hijacking of the vagus nerve, the neural axis between the gut and the brain. We also review the evidence for alternative explanations for cravings and unhealthy eating behavior. Because microbiota are easily manipulatable by prebiotics, probiotics, antibiotics, fecal transplants, and dietary changes, altering our microbiota offers a tractable approach to otherwise intractable problems of obesity and unhealthy eating.

ContributorsAlcock, Joe (Author) / Maley, Carlo C. (Author) / Aktipis, C. Athena (Author) / College of Liberal Arts and Sciences (Contributor)
Created2014-10-01
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Description

We sought to evaluate the reproducibility of a liquid chromatography-tandem mass spectrometry (LC-MS/MS)-based approach to measure the stable-isotope enrichment of in vivo-labeled muscle ATP synthase β subunit (β-F1-ATPase), a protein most directly involved in ATP production, and whose abundance is reduced under a variety of circumstances. Muscle was obtained from

We sought to evaluate the reproducibility of a liquid chromatography-tandem mass spectrometry (LC-MS/MS)-based approach to measure the stable-isotope enrichment of in vivo-labeled muscle ATP synthase β subunit (β-F1-ATPase), a protein most directly involved in ATP production, and whose abundance is reduced under a variety of circumstances. Muscle was obtained from a rat infused with stable-isotope-labeled leucine. The muscle was homogenized, β-F1-ATPase immunoprecipitated, and the protein was resolved using 1D-SDS PAGE. Following trypsin digestion of the isolated protein, the resultant peptide mixtures were subjected to analysis by HPLC-ESI-MS/MS, which resulted in the detection of multiple β-F1-ATPase peptides. There were three β-F1-ATPase unique peptides with a leucine residue in the amino acid sequence, and which were detected with high intensity relative to other peptides and assigned with >95% probability to β-F1-ATPase. These peptides were specifically targeted for fragmentation to access their stable-isotope enrichment based on MS/MS peak areas calculated from extracted ion chromatographs for selected labeled and unlabeled fragment ions. Results showed best linearity (R[superscript 2] = 0.99) in the detection of MS/MS peak areas for both labeled and unlabeled fragment ions, over a wide range of amounts of injected protein, specifically for the β-F1-ATPase[subscript 134-143] peptide. Measured stable-isotope enrichment was highly reproducible for the β-F1-ATPase[subscript 134-143] peptide (CV = 2.9%). Further, using mixtures of synthetic labeled and unlabeled peptides we determined that there is an excellent linear relationship (R[superscript 2] = 0.99) between measured and predicted enrichment for percent enrichments ranging between 0.009% and 8.185% for the β-F1-ATPase[subscript 134-143] peptide. The described approach provides a reliable approach to measure the stable-isotope enrichment of in-vivo-labeled muscle β-F1-ATPase based on the determination of the enrichment of the β-F1-ATPase[subscript 134-143] peptide.

ContributorsEverman, Sarah (Author) / Yi, Zhengping (Author) / Langlais, Paul (Author) / Mandarino, Lawrence (Author) / Luo, Moulun (Author) / Roberts, Christine (Author) / Katsanos, Christos (Author) / College of Health Solutions (Contributor)
Created2011-10-12