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Investigating Cancer-Associated Cachexia in Genetic Subtypes of Lung Cancer
Investigating Cancer-Associated Cachexia in Genetic Subtypes of Lung Cancer
상세정보
- 자료유형
- 학위논문 서양
- 최종처리일시
- 20260202104705
- ISBN
- 9798293886920
- DDC
- 616.99
- 저자명
- Cross, Michael.
- 서명/저자
- Investigating Cancer-Associated Cachexia in Genetic Subtypes of Lung Cancer
- 발행사항
- [Sl] : New York University, 2025
- 발행사항
- Ann Arbor : ProQuest Dissertations & Theses, 2025
- 형태사항
- 152 p
- 주기사항
- Source: Dissertations Abstracts International, Volume: 87-03, Section: B.
- 주기사항
- Advisor: Papagiannakopoulos, Thales.
- 학위논문주기
- Thesis (Ph.D.)--New York University, 2025.
- 초록/해제
- 요약Sickness behaviors are seen in cancer cachexia and affect up to half of lung cancer patients, yet why certain patients develop this devastating syndrome remains largely unknown. In this thesis, we demonstrate that among the most common cancer mutations, mutations in the tumor suppressor Lkb1 promote a dramatic reduction in food intake and the development of cachexia in pre-clinical models of lung cancer. In an attempt to improve caloric intake by placing tumor bearing animals on high-fat, energy dense diets, we paradoxically observed a dramatic exacerbation in anorexia and cachexia only in animals harboring Lkb1-mutant tumors. We demonstrate this diet-induced cachexia is mediated in part through local production of prostaglandin E2 and the depletion of omega-3 eicosanoids, rather than circulating factors. Furthermore, pharmacological inhibition of prostaglandin synthesis or dietary fueling of omega-3 eicosanoids improves sickness and cachexia. Importantly, we demonstrate that abrogation of lung sensory neuron signaling through vagotomy and chemogenetic inhibition improves cachexia-associated sickness. Additional work in this thesis attempts to characterize the classes of sensory neurons involved in sickness behaviors in cancers of the lung and characterizes how cachexia disrupts food intake behaviors. Together, the work outlined in this thesis establishes a role for localized rather than circulating signals in the development of cachexia and highlights a novel role for sensory neurons in sickness behaviors in cancer cachexia.
- 일반주제명
- Oncology
- 일반주제명
- Physiology
- 일반주제명
- Pathology
- 일반주제명
- Genetics
- 키워드
- Cachexia
- 키워드
- Sensory neurons
- 키워드
- Lung cancer
- 키워드
- Metabolism
- 기타저자
- New York University Basic Medical Science
- 기본자료저록
- Dissertations Abstracts International. 87-03B.
- 전자적 위치 및 접속
- 로그인 후 원문을 볼 수 있습니다.
MARC
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■006m o d
■007cr#unu||||||||
■020 ▼a9798293886920
■035 ▼a(MiAaPQ)AAI32116953
■040 ▼aMiAaPQ▼cMiAaPQ
■0820 ▼a616.99
■1001 ▼aCross, Michael.
■24510▼aInvestigating Cancer-Associated Cachexia in Genetic Subtypes of Lung Cancer
■260 ▼a[Sl]▼bNew York University▼c2025
■260 1▼aAnn Arbor▼bProQuest Dissertations & Theses▼c2025
■300 ▼a152 p
■500 ▼aSource: Dissertations Abstracts International, Volume: 87-03, Section: B.
■500 ▼aAdvisor: Papagiannakopoulos, Thales.
■5021 ▼aThesis (Ph.D.)--New York University, 2025.
■520 ▼aSickness behaviors are seen in cancer cachexia and affect up to half of lung cancer patients, yet why certain patients develop this devastating syndrome remains largely unknown. In this thesis, we demonstrate that among the most common cancer mutations, mutations in the tumor suppressor Lkb1 promote a dramatic reduction in food intake and the development of cachexia in pre-clinical models of lung cancer. In an attempt to improve caloric intake by placing tumor bearing animals on high-fat, energy dense diets, we paradoxically observed a dramatic exacerbation in anorexia and cachexia only in animals harboring Lkb1-mutant tumors. We demonstrate this diet-induced cachexia is mediated in part through local production of prostaglandin E2 and the depletion of omega-3 eicosanoids, rather than circulating factors. Furthermore, pharmacological inhibition of prostaglandin synthesis or dietary fueling of omega-3 eicosanoids improves sickness and cachexia. Importantly, we demonstrate that abrogation of lung sensory neuron signaling through vagotomy and chemogenetic inhibition improves cachexia-associated sickness. Additional work in this thesis attempts to characterize the classes of sensory neurons involved in sickness behaviors in cancers of the lung and characterizes how cachexia disrupts food intake behaviors. Together, the work outlined in this thesis establishes a role for localized rather than circulating signals in the development of cachexia and highlights a novel role for sensory neurons in sickness behaviors in cancer cachexia.
■590 ▼aSchool code: 0146.
■650 4▼aOncology
■650 4▼aPhysiology
■650 4▼aPathology
■650 4▼aGenetics
■653 ▼aCachexia
■653 ▼aSensory neurons
■653 ▼aLung cancer
■653 ▼aMetabolism
■690 ▼a0992
■690 ▼a0719
■690 ▼a0571
■690 ▼a0369
■71020▼aNew York University▼bBasic Medical Science.
■7730 ▼tDissertations Abstracts International▼g87-03B.
■790 ▼a0146
■791 ▼aPh.D.
■792 ▼a2025
■793 ▼aEnglish
■85640▼uhttp://www.riss.kr/pdu/ddodLink.do?id=T17358459▼nKERIS▼z이 자료의 원문은 한국교육학술정보원에서 제공합니다.
