Muscle circadian clock disruption as a cancer cachexia modifier
Active Project Grant Awarded Last action
- Award ID
- F32AR085458
- Recipient
-
University Of Florida UEI NNFQH1JAPEP3
- Awarding agency
-
National Insititue of Arthritis and Musculoskeletal and Skin Diseases
National Institutes of Health, Department of Health and Human Services
- Obligated
- $223,116
Award facts
- Assistance listing
- 93.846 Arthritis, Musculoskeletal and Skin Diseases Research
- Completion date 44% complete
- Place of performance
- Gainesville, FL 32611, USA
Award details come from USAspending.gov.
Description
- Abstract
- Cancer cachexia (CC) presents a profound challenge to cancer survival, affecting roughly 80% of cancer patients and contributing to a substantial proportion of cancer-related fatalities. Among its manifestations, skeletal muscle weakness and wasting stand as a pivotal concern, impacting both the quality of life and survival rates of afflicted individuals. The goal of this F32 application is to pursue research training in the newly emerging area of muscle circadian clock disruption in cancer the circadian clock mechanism in skeletal muscle regulates a rhythmic daily program of gene expression (i.e. clock output genes) contributing to muscle homeostasis, while muscle clock disarrangements are implicated in several models of muscle atrophy. My preliminary investigations unveiled transcriptomic shifts in core clock genes within skeletal muscle in various pre-clinical CC models, suggesting a potential role for the clock in cancer-induced muscle detriments. These observations are supported by compelling unpublished data from collaborative research between the esser and judge laboratories, showing disruptive alterations in the muscle circadian clock and clock output genes in pancreatic cancer-bearing mice. These combined findings provide the rationale for this F32 proposal. This proposal stands out for its scientific novelty, being the first to delineate the muscle clock profile and assess its impact as a modifier in the development and progression of CC. My overarching hypothesis is that the muscle clock serves as a CC modifier and loss of clock function will lead to accelerated and aggravate CC-induced muscle impairments. The outcomes of this proposal will 1) define the cachexia stage at which the muscle clock is disrupted, interrogate clock disruptions and its relationship with cachexia manifestations in a muscle type-specific fashion, and 2) provide an extensive assessment of both behavioral and muscle-specific changes in CC modulated by the muscle clock mechanism.
Transactions
| Action | Obligated | Date |
|---|---|---|
| Amendment | $76,300 | |
| Amendment | $0 | |
| Amendment | $73,408 | |
| Original award | $73,408 |
Quick answers
Who received award F32AR085458?
F32AR085458 was awarded to University Of Florida by National Insititue of Arthritis and Musculoskeletal and Skin Diseases (National Institutes of Health) on July 1, 2025.
How much is award F32AR085458 worth?
$223,116 has been obligated on F32AR085458.
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