Leukocytic Phenotypes Associated with BPH Progression
与 BPH 进展相关的白细胞表型
基本信息
- 批准号:9789816
- 负责人:
- 金额:$ 30.59万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:2018
- 资助国家:美国
- 起止时间:2018-09-20 至 2021-06-30
- 项目状态:已结题
- 来源:
- 关键词:Autoimmune ProcessBasic ScienceBenignBenign Prostatic HypertrophyBioinformaticsCellsCharacteristicsChargeClinicalCollaborationsCommunitiesComorbidityCountryCritiquesDataDemographic AgingDiseaseEducationEnvironmentGoalsHealth Care CostsImmuneIncidenceInflammatoryInterventionLeukocytesLinkMalignant - descriptorMedicalMorbidity - disease rateNational Institute of Diabetes and Digestive and Kidney DiseasesOperative Surgical ProceduresPathway interactionsPatientsPhenotypePhysiciansPopulationProstateProstaticResearchResearch Project GrantsResistanceResourcesScientistSignal PathwaySignal TransductionSymptomsTNF geneUnited StatesUrologic DiseasesUrologyWorkextracellularinnovationlower urinary tract symptomsmacrophagemembermennew technologynew therapeutic targetnext generationolder patientpatient populationprogramsresponsesingle-cell RNA sequencingtherapy developmenturologic
项目摘要
OVERALL: SUMMARY
The goals of this Center for Benign Urological Diseases are: 1) to create and maintain an environment that
supports important and innovative research in the field of benign urology by focusing on a Scientific Research
Project examining “Leukocyte phenotypes associated with BPH progression,” 2) to educate and inform young
scientists and physicians about BPH, and 3) to develop new interactive projects and collaborations involving
other groups in the benign urology research community. The program brings together expertise in basic
science, bioinformatics, and clinical urology to apply new technologies in the field of benign urologic research.
The research team includes members from the benign and malignant urology fields as well as from non-
urologic cancers. Benign prostatic hyperplasia (BPH) and associated lower urinary tract symptoms (LUTS) are
highly prevalent and will become increasingly more frequent with an aging demographic. Approximately one-
third of BPH patients are resistant to current medical therapy, and a further third of initial responders (around
10% of the total patient population) subsequently develop therapy resistance after an initial positive response.
So, for around 40% of the patient population there is no effective medical therapy, leaving surgery as the sole
treatment option. Approximately 120,000 surgeries are performed annually in the United States to treat men
who are resistant to the available medical interventions. Many of these are elderly patients often with
significant co-morbidities who are often not ideal surgical candidates. BPH is closely associated with pro-
inflammatory co-morbidities. However, the characteristics and pathways linking immune/inflammatory changes
to BPH progression are unclear. We show in preliminary data that TNFα antagonists can reduce the incidence
of BPH in patients with autoimmune inflammatory conditions suggesting that a more complete understanding
of the leukocyte signaling network in the prostate could elucidate new therapeutic targets. This proposal will
utilize single-cell (sc)RNA-seq to fully characterize the leukocyte population in patients with small prostates and
low IPSS scores vs. those with large prostates, high symptom scores, and progression to surgery specifically
for a BPH indication. This will provide a comprehensive picture of the cells that are present and will allow for
the application of bioinformatics approaches to define the extracellular signaling pathways that are activated in
these inflammatory cells as disease progresses. The Administrative Core coordinates all Center activities,
maintains financial and administrative oversight, manages the Educational Enrichment Program charged with
the education of the next generation of scientists, and informs scientists and clinicians of our work. The
Administrative Core also coordinates with the NIDDK and the other IR-BU Centers and integrates our
approaches with the wider benign urologic research community.
总体:总结
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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Simon W Hayward其他文献
MP35-02 <strong>BENIGN PROSTATIC HYPERPLASIA AND AUTOIMMUNE INFLAMMATORY DISEASES COINCIDENCE AND CONSEQUENCES</strong>
- DOI:
10.1016/j.juro.2016.02.1594 - 发表时间:
2016-04-01 - 期刊:
- 影响因子:
- 作者:
Jaclyn Pruitt;Jacqueline Petkewicz;Brittany Lapin;Omar E Franco;Brian T. Helfand;Charles B. Brendler;Chi-Hsiung Wang;Simon W Hayward - 通讯作者:
Simon W Hayward
MP62-14 ACTIVATION OF ABERRANT ANDROGEN RECEPTOR SIGNALING IN CARCINOMA ASSOCIATED FIBROBLASTS INDUCES PROSTATE CANCER PROGRESSION
- DOI:
10.1016/j.juro.2016.02.922 - 发表时间:
2016-04-01 - 期刊:
- 影响因子:
- 作者:
Omar E Franco;Rodrigo Javier;Susan E Crawford;Gustavo E Ayala;Simon W Hayward - 通讯作者:
Simon W Hayward
Simon W Hayward的其他文献
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{{ truncateString('Simon W Hayward', 18)}}的其他基金
AP-1 Factors in the Pathogenesis and Progression of Benign Prostatic Hyperplasia
AP-1在良性前列腺增生发病机制和进展中的影响因素
- 批准号:
8782874 - 财政年份:2014
- 资助金额:
$ 30.59万 - 项目类别:
AP-1 Factors in the Pathogenesis and Progression of Benign Prostatic Hyperplasia
AP-1在良性前列腺增生发病机制和进展中的影响因素
- 批准号:
9136661 - 财政年份:2014
- 资助金额:
$ 30.59万 - 项目类别:
AP-1 Factors in the Pathogenesis and Progression of Benign Prostatic Hyperplasia
AP-1在良性前列腺增生发病机制和进展中的影响因素
- 批准号:
8891421 - 财政年份:2014
- 资助金额:
$ 30.59万 - 项目类别:
AP-1 Factors in the Pathogenesis and Progression of Benign Prostatic Hyperplasia
AP-1在良性前列腺增生发病机制和进展中的影响因素
- 批准号:
9316616 - 财政年份:2014
- 资助金额:
$ 30.59万 - 项目类别:
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