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Cancer is a disease that occurs in many and perhaps all multicellular organisms. Current research is looking at how different life history characteristics among species could influence cancer rates. Because somatic maintenance is an important component of a species' life history, we hypothesize the same ecological forces shaping the life

Cancer is a disease that occurs in many and perhaps all multicellular organisms. Current research is looking at how different life history characteristics among species could influence cancer rates. Because somatic maintenance is an important component of a species' life history, we hypothesize the same ecological forces shaping the life history of a species should also determine its cancer susceptibility. By looking at varying life histories, potential evolutionary trends could be used to explain differing cancer rates. Life history theory could be an important framework for understanding cancer vulnerabilities with different trade-offs between life history traits and cancer defenses. Birds have diverse life history strategies that could explain differences in cancer suppression. Peto's paradox is the observation that cancer rates do not typically increase with body size and longevity despite an increased number of cell divisions over the animal's lifetime that ought to be carcinogenic. Here we show how Peto’s paradox is negatively correlated for cancer within the clade, Aves. That is, larger, long-lived birds get more cancer than smaller, short-lived birds (p=0.0001; r2= 0.024). Sexual dimorphism in both plumage color and size differ among Aves species. We hypothesized that this could lead to a difference in cancer rates due to the amount of time and energy sexual dimorphism takes away from somatic maintenance. We tested for an association between a variety of life history traits and cancer, including reproductive potential, growth rate, incubation, mating systems, and sexual dimorphism in both color and size. We found male birds get less cancer than female birds (9.8% vs. 11.1%, p=0.0058).
ContributorsDolan, Jordyn Nicole (Author) / Maley, Carlo (Thesis director) / Harris, Valerie (Committee member) / Boddy, Amy (Committee member) / School of Molecular Sciences (Contributor) / Department of Psychology (Contributor) / Barrett, The Honors College (Contributor)
Created2019-05
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Mr. Green has stage 4 prostate cancer which has spread to the bones and liver and has become resistant to radiation and standard chemotherapy treatment. After 3 rounds of chemotherapy, his primary oncologist recommends that he participate in a clinical trial. He went to Dr. Red at the Saguaro Clinic

Mr. Green has stage 4 prostate cancer which has spread to the bones and liver and has become resistant to radiation and standard chemotherapy treatment. After 3 rounds of chemotherapy, his primary oncologist recommends that he participate in a clinical trial. He went to Dr. Red at the Saguaro Clinic after reading on the internet about a new Phase 1 clinical trial that the clinic is hosting, which is designed to target a specific receptor called AB-111 that may be present in malignant prostate, cervical, ovarian, and breast cells. After signing consent and completing the blood screens in the morning at the clinic, Mr. Green is told his liver enzymes are too high and the ranges specified in the protocol prohibit him from enrolling. Mr. Green is noticeably affected and distressed at this news, and Dr. Red recommends end-of-life care. Behind the scenes, this event is noted on official medical documents and trial study rosters as a "screen fail." This narrative, while fictional, is realistic because similar events occur in cancer clinical trial sites on a regular basis. I look at the inner "world" and mental journey of possible clinical trial candidates as they seek out information about clinical trials and gain understanding of their function \u2014 specifically in the context of Phase 1 cancer clinical trials. To whom is the language of the term "screen failure" useful? How does excluding individuals from clinical trials protect their health and does the integrity of the trial data supersede the person's curative goals? What is the message that cancer patients (potential research subjects) receive regarding clinical trials from sources outside their oncologists?
ContributorsMcKane, Alexandra (Author) / Maienschein, Jane (Thesis director) / Ellison, Karin (Committee member) / Foy, Joseph (Committee member) / Barrett, The Honors College (Contributor)
Created2013-12
Description
The interaction between England and Scotland is complicated and continually changing. Scottish writer Sir Walter Scott examines this long-standing relationship through his various writings. Scott conveys a presence that is both acutely aware of the damages enacted upon Scotland by various English political efforts, and sensitive to the delicate relationshi

The interaction between England and Scotland is complicated and continually changing. Scottish writer Sir Walter Scott examines this long-standing relationship through his various writings. Scott conveys a presence that is both acutely aware of the damages enacted upon Scotland by various English political efforts, and sensitive to the delicate relationship that the two regions had begun to form during his lifetime. Through a critical analysis of Scott's novel, Rob Roy, one can see the various strategies Scott used to balance the need to address prior controversies within the relationship, and the petition to move beyond the prior conflict and develop a mutual understanding of each culture. Through this, Scott is able to regenerate a sense of Scottish nationalism for his people, and encourage improved relations within the British Isles.
ContributorsChotena, Chelsea (Author) / Facinelli, Diane (Thesis director) / Foy, Joseph (Committee member) / White, Julianne (Committee member) / Barrett, The Honors College (Contributor)
Created2013-05
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Cancer rates in our nearest relatives are largely unknown. Comparison of human cancer rates with other primates should help us to understand the nature of our susceptibilities to cancer. Data from deceased primates was gathered from 3 institutions, the Duke Lemur Center, San Diego Zoo, and Jungle Friends primate sanctuary.

Cancer rates in our nearest relatives are largely unknown. Comparison of human cancer rates with other primates should help us to understand the nature of our susceptibilities to cancer. Data from deceased primates was gathered from 3 institutions, the Duke Lemur Center, San Diego Zoo, and Jungle Friends primate sanctuary. This data contained over 400 unique individuals across 45 species with information on cancer incidence and mortality. Cancer incidence ranged from 0-71% and cancer mortality ranged from 0-67%. We used weighted phylogenetic regressions to test for an association between life history variables (specifically body mass and lifespan) and cancer incidence as well as mortality. Cancer incidence did not correlate with both body mass and lifespan (p>.05) however, cancer mortality did (p<.05). However, it is uncertain if the variables can be used as reliable predictors of cancer, because the data come from different organizations. This analysis presents cancer incidence rates and cancer mortality rates in species where it was previously unknown, and in some primate species, is surprisingly high. Microcebus murinus(grey mouse lemur) appear to be particularly vulnerable to cancer, mostly lymphomas. Further studies will be required to determine the causes of these vulnerabilities.
ContributorsWalker, William Charles (Author) / Maley, Carlo (Thesis director) / Boddy, Amy (Committee member) / School of Life Sciences (Contributor) / Barrett, The Honors College (Contributor)
Created2017-05
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Description
My mother died after a long battle with breast cancer in 2008. I was only nine when she was first diagnosed, and so much of my life has been shaped by her struggle for survival. She will always be the most amazing women I have ever known, and she taught

My mother died after a long battle with breast cancer in 2008. I was only nine when she was first diagnosed, and so much of my life has been shaped by her struggle for survival. She will always be the most amazing women I have ever known, and she taught me more about life, kindness, hope, and overcoming the odds than anyone else. I want to share my experience with you as a friend \u2014 not as a doctor, or a counselor, but as a friend. I want to tell you some of my stories with the emotions behind them. I will share how I learned t cope with whatever situation came our way and how I found unexpected ways to help my mom. I want you to find solace through our shared emotions even if they are at different times in our journeys. This is why in the following chapters, my stories are not chronological but categorized through the major emotions that drove my stories. I hope this book can help those who find themselves in similar situations to the one I found myself in when my mom picked me up from fourth grade with a bandana on her head instead of her normal, beautiful brown hair. This thesis is a creative exploration of emotions and finding hope in times of great loss.
ContributorsTornabene, Kathleen Elizabeth (Author) / Foy, Joseph (Thesis director) / Facinelli, Diane (Committee member) / Hyde, Suzanne (Committee member) / Barrett, The Honors College (Contributor)
Created2012-05
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Description

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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Age is the most significant risk factor for cancer development in humans. The somatic mutation theory postulates that the accumulation of genomic mutations over time results in cellular function degradation which plays an important role in understanding aging and cancer development. Specifically, degradation of the mechanisms that underlie somatic maintenance

Age is the most significant risk factor for cancer development in humans. The somatic mutation theory postulates that the accumulation of genomic mutations over time results in cellular function degradation which plays an important role in understanding aging and cancer development. Specifically, degradation of the mechanisms that underlie somatic maintenance can occur due to decreased immune cell function and genomic responses to DNA damage. Research has shown that this degradation can lead to the accumulation of mutations that can cause cancer in humans. Despite recent advances in our understanding of cancer in non-human species, how this risk factor translates across species is poorly characterized. Here, we analyze a veterinarian cancer dataset of 4,178 animals to investigate if age related cancer prevalence is similar in non-human animals. We intend for this work to be used as a primary step towards understanding the potential overlap and/or uniqueness between human and non-human cancer risk factors. This study can be used to better understand cancer development and how evolutionary processes have shaped somatic maintenance across species.

ContributorsAksoy, Selin (Author) / Maley, Carlo (Thesis director) / Boddy, Amy (Committee member) / Barrett, The Honors College (Contributor) / School of Life Sciences (Contributor) / Department of Psychology (Contributor)
Created2022-05
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Description

Cancers of the reproductive tissues make up a significant portion of the cancer burden and mortality experienced by humans. Humans experience several proximal causative carcinogens that explain a portion of cancer risk, but an evolutionary viewpoint can provide a unique lens into the ultimate causes of reproductive cancer vulnerabilities. A

Cancers of the reproductive tissues make up a significant portion of the cancer burden and mortality experienced by humans. Humans experience several proximal causative carcinogens that explain a portion of cancer risk, but an evolutionary viewpoint can provide a unique lens into the ultimate causes of reproductive cancer vulnerabilities. A life history framework allows us to make predictions on cancer prevalence based on a species’ tempo of reproduction. Moreover, certain variations in the susceptibility and prevalence of cancer may emerge due to evolutionary trade-offs between reproduction and somatic maintenance. For example, such trade-offs could involve the demand for rapid proliferation of cells in reproductive tissues that arises with reproductive events. In this study, I compiled reproductive cancer prevalence for 158 mammalian species and modeled the predictive power of 13 life history traits on the patterns of cancer prevalence we observed, such as Peto’s Paradox or slow-fast life history strategies. We predicted that fast-life history strategists will exhibit higher neoplasia prevalence risk due to reproductive trade-offs. Furthering this analytical framework can aid in predicting cancer rates and stratifying cancer risk across the tree of life.

ContributorsDarapu, Harshini (Author) / Maley, Carlo (Thesis director) / Boddy, Amy (Committee member) / Compton, Zachary (Committee member) / Barrett, The Honors College (Contributor) / School of Life Sciences (Contributor)
Created2022-05
Description

This paper examines the physics behind cancer treatment and more specifically radiation therapy. A phenomenon known as Compton scattering has played a substantial role in the treatment of breast cancer and improvement of lives of women around the world. Through Compton scattering, radiation therapy has been tremendously improved and has

This paper examines the physics behind cancer treatment and more specifically radiation therapy. A phenomenon known as Compton scattering has played a substantial role in the treatment of breast cancer and improvement of lives of women around the world. Through Compton scattering, radiation therapy has been tremendously improved and has allowed for the most accurate and effective treatment in breast cancer patients today.

ContributorsRombaoa, Matthew Bryce (Author) / Foy, Joseph (Thesis director) / Hines, Taylor (Committee member) / Barrett, The Honors College (Contributor) / School of Molecular Sciences (Contributor) / Department of Psychology (Contributor)
Created2023-05