# Investigating cancer-associated cachexia in genetic subtypes of lung cancer

> **NIH NIH F30** · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · 2024 · $48,504

## Abstract

PROJECT SUMMARY
Cancer-associated cachexia (CAC) is characterized by the involuntary loss of skeletal muscle and adipose
tissue mass. This multifactorial syndrome is driven by the combination of reduced food intake and altered
systemic metabolism. Approximately half of all cancer patients present with complications associated with
cachexia, leading to increased mortality, functional impairment, and reduced quality of life. Effective therapies
to treat cancer-associated cachexia are currently lacking, with treatment focused on nutritional support and
symptom mitigation. Resolution of cachexia is optimally achieved through treatment of the underlying disease.
Targeting the metabolic alterations that drive cachexia to identify novel drug targets remains an area of active
inquiry.
Treatment of cachexia has remained elusive due to disease heterogeneity. Emerging evidence has suggested
there are multiple subtypes of this complex disease, which may explain the lack of consensus in the criteria
used to describe cancer-associated cachexia. Additionally, these definitions are further muddied in the context
of obesity, which can confound diagnoses of cachexia based upon body-mass index and hide loss of skeletal
muscle mass. While recent work has described the catabolic changes in metabolic organs such as skeletal
muscle, adipose tissue, and liver that occur with cachexia, as well as identified inflammatory mediators that
can drive these processes, further studies are needed to more comprehensively identify systemic physiological
changes that occur in CAC. This innovative proposal will address major gaps in our understanding of CAC:
 1) Do common cancer mutations modulate the development of CAC?
 2) How do dietary interventions impact the course of CAC?
Prior studies have been limited by lack of tractable, in vivo models of CAC that develop in an autochthonous
setting. Using genetically engineered mouse models, we identify a novel model of CAC that is driven by tumor
genetics and dietary intervention. Based upon characteristics of this model, we will identify novel potential drug
targets specific to subsets of cancer-associated cachexia.

## Key facts

- **NIH application ID:** 10903345
- **Project number:** 1F30CA284910-01A1
- **Recipient organization:** NEW YORK UNIVERSITY SCHOOL OF MEDICINE
- **Principal Investigator:** Michael Cross
- **Activity code:** F30 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2024
- **Award amount:** $48,504
- **Award type:** 1
- **Project period:** 2024-05-13 → 2028-05-12

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10903345

## Citation

> US National Institutes of Health, RePORTER application 10903345, Investigating cancer-associated cachexia in genetic subtypes of lung cancer (1F30CA284910-01A1). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/10903345. Licensed CC0.

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