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OPPORTUNITIES AND CHALLENGES FOR TARGETING CANCER METABOLISM. 靶向癌症代谢的机遇与挑战。
Transactions of the American Clinical and Climatological Association Pub Date : 2025-01-01
Chi V Dang
{"title":"OPPORTUNITIES AND CHALLENGES FOR TARGETING CANCER METABOLISM.","authors":"Chi V Dang","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Otto Warburg sparked the field of cancer metabolism in the 1920s through his observations that human and animal cancer tissues converted significant amounts of glucose to lactate with an elusive underlying mechanism. The discovery of oncogenes led to the notion that neoplasia results from deregulated cell division control with metabolism at the margin, standing by to support cell growth. Studies over the past several decades have linked oncogenes to the direct regulation of metabolism, such as the myelocytomatosis (MYC) oncogene, driving glycolysis and other central metabolic pathways, necessary for cell growth and proliferation. Deregulated oncogenic drive of metabolism renders tumor cells addicted to glucose and other nutrients, such that nutrient deprivation can trigger cancer cell death. The revelation of this addiction stimulated pharmaceutical companies to target metabolism for cancer therapy, but due to several failed clinical studies, this exuberance fizzled commercially. However, the transformative impact of cancer immunotherapy ushered in an interest in understanding the hostile metabolic tumor microenvironment that limits the function of anti-tumor T cells and clinical responses to immunotherapy. This interest drives the convergence of immunometabolism and cancer cell metabolism research to provide a richer understanding of tumor metabolic vulnerability. Herein, I discuss the historical and current context of opportunities and challenges to targeting cancer metabolism.</p>","PeriodicalId":23186,"journal":{"name":"Transactions of the American Clinical and Climatological Association","volume":"135 ","pages":"196-205"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12323494/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144795565","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
A QUARTER CENTURY OF CALCIUM-PERMEABLE ION CHANNEL, TRPV4: PERSPECTIVES ON EXPRESSION AND FUNCTION IN ENDOTHELIAL CELLS-TIME TO TRANSLATE. 四分之一世纪的钙渗透离子通道trpv4：内皮细胞表达和功能的观点-时间翻译。
Transactions of the American Clinical and Climatological Association Pub Date : 2025-01-01
Wolfgang Liedtke
{"title":"A QUARTER CENTURY OF CALCIUM-PERMEABLE ION CHANNEL, TRPV4: PERSPECTIVES ON EXPRESSION AND FUNCTION IN ENDOTHELIAL CELLS-TIME TO TRANSLATE.","authors":"Wolfgang Liedtke","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Calcium-permeable transient receptor potential cation channel subfamily V member 4 (TRPV4) channels, first described in 2000, are activated by osmotic, mechanical, thermal, actinic, and chemical cues; play multiple roles in multiple physiologic processes, organ systems, and diseases; and are expressed in diverse cell lineages, with channel function-expression regulated by metabolic and endocrine state, inflammation, mechanical microenvironment, and other forms of cellular stress. Here, I will focus on TRPV4's role in endothelia, citing three examples that can guide translational efforts and development of TPRV4-focused therapeutics. (i) Peroxynitrite-dependent impairment of endothelial TRPV4 drives obesity-related hypertension. (ii) Blood-brain barrier in MS: TRPV4 drives endothelial inflammation and pro-inflammatory interaction between endothelia and microglia in active lesions. (iii) Gain-of-function spinal cord endothelial TRPV4 causes spinal muscular atrophy via developmental barrier impairment, leakage, and subsequent motoneuron injury. Thus, different pathophysiologic mechanisms need to be met with different strategies when selectively targeting endothelial TRPV4, namely restoration of impaired function (i), versus inhibition of excessive function (ii)-(iii).</p>","PeriodicalId":23186,"journal":{"name":"Transactions of the American Clinical and Climatological Association","volume":"135 ","pages":"240-259"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12323486/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144795586","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
LEADING A TRANSDISCIPLINARY TEAM MODEL ACROSS A COMPREHENSIVE CAMPUS. 在综合性校园中领导跨学科团队模式。
Transactions of the American Clinical and Climatological Association Pub Date : 2025-01-01
Robert S Dipaola
{"title":"LEADING A TRANSDISCIPLINARY TEAM MODEL ACROSS A COMPREHENSIVE CAMPUS.","authors":"Robert S Dipaola","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>As the state's land-grant research institution, we implemented a transdisciplinary research strategy in the College of Medicine (COM) forming multiple research teams selected with criteria for success and progress. To assess for key factors, we reviewed the literature and data from studies conducted at the University of Kentucky (UK) that included a quantitative study with a mixed-methods approach to assess team dynamics, collaboration, and research outcomes, as well as a qualitative study (1,2). Team interactions were positively associated with scholarly products. We also experienced an approximate doubling of the COM National Institutes of Health (NIH) funding over four years. Based on these data and experiences, we developed a process for future team building. In summary, we describe a team-based model with consideration of evidential criteria for structure, monitoring, and success metrics, and we developed a process that could be used by leadership to develop transdisciplinary teams across the university for research, education, or service.</p>","PeriodicalId":23186,"journal":{"name":"Transactions of the American Clinical and Climatological Association","volume":"135 ","pages":"333-344"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12323462/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144795606","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
AVIAN INFLUENZA VIRUS: THE NEXT PANDEMIC? 禽流感病毒：下一次大流行？
Transactions of the American Clinical and Climatological Association Pub Date : 2025-01-01
Patricia L Winokur
{"title":"AVIAN INFLUENZA VIRUS: THE NEXT PANDEMIC?","authors":"Patricia L Winokur","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Novel avian influenza viruses continue to circulate in animal species around the world and show a propensity to reassort and acquire virulence factors, which raises the concern that these viruses may adapt to humans. Pandemic preparedness has relied heavily on vaccine stockpiles. However, avian influenza strains genetically drift over time, and stockpiled vaccines often fail to elicit protective immunity for these genetic variants. Various strategies can help overcome immune imprinting and immunological hyporeactivity as well as broaden the immune response to variant viruses. Adjuvants remain a key strategy for improving the immunological response to avian influenza antigens. Today, three vaccines are approved in the United States for H5N1 influenza viruses though continued focus on surveillance and pandemic preparedness is essential to prepare for the possibility of human-to-human spread of this highly pathogenic influenza virus.</p>","PeriodicalId":23186,"journal":{"name":"Transactions of the American Clinical and Climatological Association","volume":"135 ","pages":"87-98"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12323483/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144795590","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
INTEGRIN FUNCTION IN LEUKOCYTE-MEDIATED INFLAMMATION-ACTINOPATHIES IN IMMUNE DISEASES. 整合素在免疫疾病中白细胞介导炎症-放线素病变中的作用。
Transactions of the American Clinical and Climatological Association Pub Date : 2025-01-01
Clifford A Lowell
{"title":"INTEGRIN FUNCTION IN LEUKOCYTE-MEDIATED INFLAMMATION-ACTINOPATHIES IN IMMUNE DISEASES.","authors":"Clifford A Lowell","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Integrins play a critical role in leukocyte recruitment and activation within inflamed tissues. These heterodimeric cell-surface receptors recognize ligands on vascular endothelium or extracellular matrix to initiate intracellular signals leading to leukocyte adhesion, migration, and activation. The best-described role for integrins is in the leukocyte adhesion cascade, which is the process by which leukocytes exit the blood vasculature and enter the tissues in response to infection or injury. During the adhesion cascade, integrin signaling is required for changes in leukocyte cytoskeletal structure required for firm adhesion to endothelial cells, followed by intravascular crawling and transmigration from the bloodstream into the tissues. During this process, integrin signaling augments leukocytes' inflammatory and antimicrobial functions. Mutations in the genes encoding integrins or their downstream signaling molecules result in immunodeficiency and altered tissue repair following injury. Many of these mutations occur in proteins involved in the reorganization of the actin cytoskeleton and have become known as actinopathies, the classic example being Wiskott-Aldrich syndrome. We describe a new actinopathy-type mutation in the integrin signaling molecule SKAP2, which is associated with autoimmunity and type 1 diabetes.</p>","PeriodicalId":23186,"journal":{"name":"Transactions of the American Clinical and Climatological Association","volume":"135 ","pages":"74-86"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12323475/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144795604","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
OFFICERS AND COUNCIL FALL 2025. 官员和理事会将于2025年秋天。
Transactions of the American Clinical and Climatological Association Pub Date : 2025-01-01
{"title":"OFFICERS AND COUNCIL FALL 2025.","authors":"","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":23186,"journal":{"name":"Transactions of the American Clinical and Climatological Association","volume":"135 ","pages":"iii"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12323491/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144795563","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
INSIGHTS INTO ACUTE KIDNEY INJURY AND TRANSITION TO CHRONIC KIDNEY DISEASE BY SINGLE-CELL TECHNOLOGIES. 单细胞技术对急性肾损伤和向慢性肾脏疾病过渡的见解。
Transactions of the American Clinical and Climatological Association Pub Date : 2025-01-01
Benjamin D Humphreys
{"title":"INSIGHTS INTO ACUTE KIDNEY INJURY AND TRANSITION TO CHRONIC KIDNEY DISEASE BY SINGLE-CELL TECHNOLOGIES.","authors":"Benjamin D Humphreys","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Outcomes after acute kidney injury (AKI) cover a wide spectrum ranging from full recovery to incomplete repair leading to transition to chronic kidney disease (CKD). This \"AKI to CKD transition\" is incompletely understood at a cellular level and there is a pressing need to identify the basic mechanisms of successful recovery from AKI and to develop therapeutic interventions to prevent the AKI to CKD transition. In recent years, single-cell transcriptomic and epigenomic technologies have substantially improved our understanding of cell types and states in homeostasis and after injury. In this paper, I will review our recent work applying single-cell technologies to better understand AKI and its transition to CKD, focusing on a proximal tubule cell state that we have termed \"failed repair.\" Failed repair proximal tubule cells are characterized by pro-inflammatory and pro-fibrotic gene expression patterns and may drive the AKI to CKD transition.</p>","PeriodicalId":23186,"journal":{"name":"Transactions of the American Clinical and Climatological Association","volume":"135 ","pages":"383-392"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12323478/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144795602","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
THE OBESITY PARADOX IN HEART FAILURE: TIME TO MOVE FORWARD. 心力衰竭的肥胖悖论：是时候向前看了。
Transactions of the American Clinical and Climatological Association Pub Date : 2025-01-01
Anita Deswal
{"title":"THE OBESITY PARADOX IN HEART FAILURE: TIME TO MOVE FORWARD.","authors":"Anita Deswal","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Obesity is a risk factor for incident heart failure (HF), linked to, but also independent of, coexisting comorbidities. The association of obesity is stronger for HF with preserved versus reduced ejection fraction. Further, obesity is associated with a higher risk of HF hospitalization in patients with HF. However, multiple studies in patients with prevalent HF have suggested that higher body mass index (BMI) is associated with lower mortality-the \"obesity survival paradox.\" This paradox was also observed with preexisting obesity prior to the development of HF. These observations had complicated the case for the routine recommendation of weight loss in patients with obesity and HF. However, recent trials with anti-obesity medications are leading to a better understanding of the benefits of weight loss in HF and thus support a reevaluation of the obesity survival paradox in HF.</p>","PeriodicalId":23186,"journal":{"name":"Transactions of the American Clinical and Climatological Association","volume":"135 ","pages":"43-51"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12323472/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144795624","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
THE BERT AND PEGGY DUPONT LECTURE. 伯特和佩吉·杜邦的讲座。
Transactions of the American Clinical and Climatological Association Pub Date : 2025-01-01
{"title":"THE BERT AND PEGGY DUPONT LECTURE.","authors":"","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":23186,"journal":{"name":"Transactions of the American Clinical and Climatological Association","volume":"135 ","pages":"306-308"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12323469/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144795577","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
The Jeremiah Metzger Lecture. 耶利米·梅茨格的演讲。
Transactions of the American Clinical and Climatological Association Pub Date : 2025-01-01
{"title":"The Jeremiah Metzger Lecture.","authors":"","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":23186,"journal":{"name":"Transactions of the American Clinical and Climatological Association","volume":"135 ","pages":"177-180"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12323449/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144795583","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
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