MedTrace Logo

Prognostic Value of Neurometabolic Networks in CRC (PVNM-CRC)

NCT06930586 · Status: RECRUITING · Type: OBSERVATIONAL · Enrollment: 213

Last updated 2025-04-30

No results posted yet for this study

Summary

Colorectal cancer (CRC), with annually increasing incidence and mortality worldwide, has become the second leading cause of cancer-related death. The development of CRC often follows the canonical normal-adenoma-carcinoma (N-A-C) sequence driven by progressive accumulation of molecular genetic events, highlighting the importance of early detection and removal of precancerous lesions. However, some patients who have had adenomas removed still have a high risk of developing new adenomas or CRC, especially for those with chronic or systemic disease, indicating that a compositive regulatory network is involved in the tumorigenesis of CRC. Additionally, despite advances in therapeutic strategies having improved the prognosis of CRC patients, tumor metastasis continues to be the predominant cause of mortality. These suggest the need to transcend limitations focusing solely on intertumoral microenvironment or single-timepoint event but adopt a more systemic perspective to elucidate the mechanisms underlying the whole sequence of CRC development and progression.

The gastrointestinal (GI) tract comprises a complex ecosystem with extensive interactions between normal or neoplastic epithelial cells with immune, neuronal, and other cell types, as well as microorganisms and metabolites within the gut lumen. Specifically, the intricate relationship between the GI tract and the central nervous system (CNS), collectively known as the brain-gut axis, plays a pivotal role in the pathogenesis of gastrointestinal disorders and neoplasm. For instance, chronic stress increased the risk of colon cancer via activating the COX-2/PEG2 system and promoted tumor cell dissemination by remodeling lymph vasculature. The bidirectional communications of the brain-gut axis are generally found to be mediated by neurotransmitters, inflammatory cytokines, metabolites, or gut microbiota. Nonetheless, the spotlight has shone primarily on the brain-gut crosstalk mechanisms in experimental cellular or animal models, with less attention paid to the structural and functional alterations on the brain networks at the patient level.

The evolution of functional neuroimaging modalities and neuroscience technologies has enabled accurate delineation of CNS activities. Specifically, nuclear medicine imaging technology using 2-18F fluoro-2-deoxy-D-glucose (18F-FDG) to adopt whole-body imaging information, is the optimal in vivo method for the investigation of regional human brain metabolism and associations with systemic disorders. We have previously identified the neuronal metabolic-ventricular dyssynchronization axis which might related to major arrhythmic events using myocardial perfusion imaging and the brain 18F-FDG positron emission tomography (PET). Given the potential dual interactions of the brain-gut axis, identification of specific brain regions associated with CRC development and progression might lead to a better understanding of the disease's neurobiological underpinnings and inform the development of targeted therapeutic strategies.

Hence, this study was structured to elucidate the role of neuro-metabolism and its potential mediator in regulating CRC tumorigenesis and metastasis. By delving into the neurometabolic-gut axis in CRC, the resulting mechanistic insights might be leveraged to identify diagnostic and prognostic biomarkers and to develop novel therapeutic interventions for CRC patients.

Conditions

Sponsors & Collaborators

  • The First Affiliated Hospital of Zhengzhou University

    lead OTHER

Eligibility

Min Age
18 Years
Sex
ALL
Healthy Volunteers
No

Timeline & Regulatory

Start
2024-03-01
Primary Completion
2026-12-31
Completion
2027-12-31

Countries

  • China

Study Locations

More Related Trials

Entities

Diseases

Read the full study record

This page highlights key information. For complete eligibility criteria, study locations, investigator contacts, and the full protocol, visit the original record on ClinicalTrials.gov.

View NCT06930586 on ClinicalTrials.gov