CANCAN-RUTGERS

康康-罗格斯

• 批准号: 10621047
• 负责人: Eileen P. White
• 金额: $ 22.32万
• 依托单位: RBHS -CANCER INSTITUTE OF NEW JERSEY
• 依托单位国家: 美国
• 财政年份: 2022
• 资助国家: 美国
• 起止时间: 2022-06-22 至 2023-05-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/10621047
• 关键词: Adipose tissue; Affect; Anorexia; Atrophic; Body Weight decreased; Cachexia; Cancer Patient; Clinical; Human; Immune; Immunology; Institutes; International; Intrinsic factor; Malignant Neoplasms; Mediator of activation protein; Metabolic; Metabolic Diseases; Metabolic dysfunction; Neurosecretory Systems; Organ; Pathway interactions; Performance Status; Pre-Clinical Model; Quality of life; Science; Scientist; Skeletal Muscle; Tissues; Wasting Syndrome; Work; cancer cachexia; chemotherapy; clinical phenotype; effective therapy; improved; mortality; multidisciplinary; response; treatment response; tumor; tumor metabolism; virtual; wasting

Cancer cachexia (CC) is a systemic, metabolic wasting syndrome featuring body weight loss due to skeletal muscle and adipose tissue wasting. CC is suffered by ~80% of cancer patients that causes reduced performance status, intolerance to chemotherapy, and increased mortality. This debilitating condition is poorly understood and has no effective treatment. If CC therapy existed, it would improve treatment responses, increase quality of life, and prolong survival. With 50 years of study, the field has focused on defining pathways that promote atrophy in the end-organs most affected my cachexia. While this work has been fruitful, it has not led to identification of the upstream mediators of CC, nor has it generated effective therapies. There is an urgent need for high-quality discovery science and more detailed clinical phenotyping.We have created a virtual institute comprised of diverse, international, multidisciplinary scientists and clinicians with expertise in cancer, metabolism, neuroendocrine function, immunology, human metabolic diseases, preclinical models, and clinical phenotyping. We hypothesize that CC is driven by tumor-intrinsic factors that activate neurohormonal sickness pathways, which then induce anorexia, metabolic dysfunction, and tissue atrophy.

癌症恶病质（CC）是一种全身性代谢性消耗综合征，其特征是由于骨骼肌和脂肪组织消耗导致体重减轻。约80%的癌症患者患有CC，导致体能状态降低、对化疗不耐受和死亡率增加。这种使人衰弱的情况知之甚少，也没有有效的治疗方法。如果CC疗法存在，它将改善治疗反应，提高生活质量，延长生存期。经过50年的研究，该领域一直专注于确定促进最受恶病质影响的终末器官萎缩的途径。虽然这项工作已经取得了丰硕成果，但它并没有导致CC的上游介质的识别，也没有产生有效的治疗方法。我们创建了一个虚拟研究所，由来自不同国家的多学科科学家和临床医生组成，他们在癌症、代谢、神经内分泌功能、免疫学、人类代谢疾病、临床前模型和临床表型等领域拥有专业知识。我们假设CC是由肿瘤内在因素驱动的，这些因素激活神经激素疾病通路，然后诱导厌食症、代谢功能障碍和组织萎缩。