Full Project 1: LSR Alters Metabolic Signaling to Drive Aggressive Breast Cancer Behaviors
完整项目 1:LSR 改变代谢信号以驱动侵袭性乳腺癌行为
基本信息
- 批准号:10247134
- 负责人:
- 金额:$ 3.11万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:2010
- 资助国家:美国
- 起止时间:2010-09-28 至 2022-08-31
- 项目状态:已结题
- 来源:
- 关键词:AddressAffectAfrican AmericanAggressive behaviorAnabolismBehaviorBindingBioenergeticsBiologicalBiological AssayBiological FactorsBreastBreast Cancer CellCancerousCaucasiansCell divisionCell physiologyCellsCharacteristicsCholesterolChronicClinicalCollaborationsCytoplasmic TailDataData SetDiagnosisDietDiseaseDistant MetastasisEndocytosisEnergy-Generating ResourcesEnvironmentEtiologyEventFatty acid glycerol estersGene ChipsGene ExpressionGenesGenetic TranscriptionGlycogenGoalsGuanosine Triphosphate PhosphohydrolasesHepaticHigh Fat DietHospitalsIn VitroIncidenceLeadLeptinLesionLinkLipidsLipolysisLipoprotein ReceptorLipoproteinsMalignant - descriptorMalignant NeoplasmsMammary Gland ParenchymaMammary NeoplasmsMeasuresMediatingMembraneMembrane LipidsMetabolicMetabolic syndromeMetabolismMolecularMusNeoplasm MetastasisNuclearObesityObservational StudyOutcomePathway AnalysisPathway interactionsPatient-Focused OutcomesPatientsPhenotypePhosphoproteinsPredispositionPrevalencePropertyProteinsProteomicsPublishingRaceRecurrenceRegulationResearchResistanceResourcesRoleSignal PathwaySignal TransductionSignaling MoleculeSiteStatistical ModelsTestingTight JunctionsTumor SubtypeVariantWomanWorkXenograft procedureanticancer researchcancer health disparitycancer stem cellcancer subtypescell behavioreffective therapyepidemiology studyethnic diversityexperimental studyglucose uptakehealth disparityimprovedin vivoinsightlipid metabolismlipid transportmalignant breast neoplasmmetabolomicsmortalitynew therapeutic targetnovelnovel strategiesobesogenicoverexpressionracial disparityreceptor expressionreceptor functionresponserhorho GTP-Binding Proteinsstemstem-like celltherapeutic developmenttumortumor behaviortumor microenvironmenttumor progressiontumorigenesistumorigenicuptake
项目摘要
Project Summary/Abstract
African American (AA) women have higher breast cancer mortality rates compared to other races. A greater
prevalence of basal-like breast cancers in AA women explain some disparities, as these tumors are
clinically the most aggressive, characterized by cancer stem No effective therapies exist and
cell features.
survival is poor. Escalating this disparity is the disease promoting effects of obesity, which is significantly
higher in AA. The majority of studies on breast cancer disparities examine tumor characteristics, but the
etiologic factors that lead to this disparity remain undefined. Our primary objective is to identify the
mechanisms involved in promoting aggressive breast cancer in AAs, as a consequence of stromal effects at
the site of the cancerous lesion. A key molecular pathway has been identified which integrates these
clinical, microenvironmental and biological factors to affect tumor behavior. Aim 1 takes a novel approach,
combining our published proteomic and gene expression datasets detailing race and tumor-subtype specific
stromal interactions with our recently published data on the identified pathway promoting cancer stem cell-
like, aggressive behaviors. Aims 2 and 3 extend these data to experimental studies to elucidate mechanistic
details. To accomplish these tasks, our team established research partnerships that provides access to
resources including the Normal Breast Study: a unique epidemiologic study from ethnically diverse patients
at UNC Hospitals. There are several important biological implications of this work. The observation that AA
breast tissue is enriched with distinct proteins, the prevalence of obesity in AA, and the predisposition to
develop basal-like tumors strongly suggests a biological link between race, metabolism and cancer subtype.
The role of differentially regulated metabolic-sensitive proteins in the tumor microenvironment will provide
novel insights into the biological basis of racial disparities. The long-term goal of our collaboration is to
understand tumor-microenvironment interactions and their influence on breast cancer disparities. Our
distinctive approach will expose unique characteristics of the breast tissue microenvironment and will
integrate advances in the field of tumor microenvironment with health disparities research.
Relevance
This proposal addresses breast cancer disparities by studying a key pathway that drive the aggressiveness
of breast cancers. By combining observational studies on differences in this pathway by race, BMI, and
breast cancer subtype with experimental studies to understand the role of this pathway in cellular
phenotypes, this project will provide important and novel insight into the biological basis of racial disparities.
项目总结/摘要
非裔美国人(AA)女性的乳腺癌死亡率高于其他种族。更大
AA女性中基底细胞样乳腺癌的患病率解释了一些差异,因为这些肿瘤
临床上最具侵略性,其特征是癌症干没有有效的治疗方法存在,
细胞特征
生存很差。使这种差异升级的是肥胖症的疾病促进作用,
在AA中更高。大多数关于乳腺癌差异的研究检查肿瘤特征,但
导致这种差异的病因学因素仍然不明确。我们的主要目标是确定
作为基质效应的结果,AAs中参与促进侵袭性乳腺癌的机制,
癌性病变的部位。已经确定了一个关键的分子途径,
临床、微环境和生物学因素影响肿瘤行为。Aim 1采用了一种新颖的方法,
结合我们发表的蛋白质组学和基因表达数据集,详细说明了种族和肿瘤亚型特异性
基质相互作用与我们最近发表的关于促进癌症干细胞的已鉴定途径的数据,
比如攻击性行为目的2和3将这些数据扩展到实验研究,以阐明
续费为了完成这些任务,我们的团队建立了研究伙伴关系,
资源包括正常乳腺研究:一项来自不同种族患者的独特流行病学研究
在医院里。这项工作有几个重要的生物学意义。观察到AA
乳腺组织富含不同的蛋白质,AA中肥胖的患病率,以及
发生基底细胞样肿瘤强烈表明种族、代谢和癌症亚型之间存在生物学联系。
差异调节的代谢敏感蛋白在肿瘤微环境中的作用将提供
对种族差异的生物学基础的新见解。我们合作的长期目标是
了解肿瘤微环境的相互作用及其对乳腺癌差异的影响。我们
独特的方法将暴露乳房组织微环境的独特特征,
将肿瘤微环境领域的进展与健康差异研究相结合。
相关性
这项提案通过研究一个关键途径来解决乳腺癌的差异,
乳腺癌通过结合观察性研究,研究了不同种族、BMI和
乳腺癌亚型与实验研究,以了解这一途径的作用,在细胞
表型,这个项目将提供重要的和新的见解种族差异的生物学基础。
项目成果
期刊论文数量(0)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
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Keith Burridge其他文献
Keith Burridge的其他文献
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{{ truncateString('Keith Burridge', 18)}}的其他基金
Endothelial Cell Uptake of Infected Erythrocytes in Cerebral Malaria
脑型疟疾中感染红细胞的内皮细胞摄取
- 批准号:
9112857 - 财政年份:2015
- 资助金额:
$ 3.11万 - 项目类别:
Endothelial Cell Uptake of Infected Erythrocytes in Cerebral Malaria
脑型疟疾中感染红细胞的内皮细胞摄取
- 批准号:
8969179 - 财政年份:2015
- 资助金额:
$ 3.11万 - 项目类别:
Rho-mediated Signaling in Lung Endothelial Cells Induced by Neutrophil Adhesion
中性粒细胞粘附诱导的肺内皮细胞中 Rho 介导的信号传导
- 批准号:
8321142 - 财政年份:2012
- 资助金额:
$ 3.11万 - 项目类别:
Rho-mediated Signaling in Lung Endothelial Cells Induced by Neutrophil Adhesion
中性粒细胞粘附诱导的肺内皮细胞中 Rho 介导的信号传导
- 批准号:
8473275 - 财政年份:2012
- 资助金额:
$ 3.11万 - 项目类别:
Rho-mediated Signaling in Lung Endothelial Cells Induced by Neutrophil Adhesion
中性粒细胞粘附诱导的肺内皮细胞中 Rho 介导的信号传导
- 批准号:
8651535 - 财政年份:2012
- 资助金额:
$ 3.11万 - 项目类别:
Full Project 1: LSR Alters Metabolic Signaling to Drive Aggressive Breast Cancer Behaviors
完整项目 1:LSR 改变代谢信号以驱动侵袭性乳腺癌行为
- 批准号:
9044449 - 财政年份:2010
- 资助金额:
$ 3.11万 - 项目类别:
CB2 Cannabinoid Receptor-mediated Regulation of Prostate Cancer Growth
CB2 大麻素受体介导的前列腺癌生长调节
- 批准号:
8068504 - 财政年份:2010
- 资助金额:
$ 3.11万 - 项目类别:
Cell Adhesion and the Regulation of Rho GTPases
细胞粘附和 Rho GTP 酶的调节
- 批准号:
7999960 - 财政年份:2009
- 资助金额:
$ 3.11万 - 项目类别:
CYTOSKELETAL REGULATION OF ENDOTHELIAL CELL JUNCTIONS
内皮细胞连接的细胞骨架调节
- 批准号:
7474511 - 财政年份:2007
- 资助金额:
$ 3.11万 - 项目类别:
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