The lactate–lactylation axis in tumor radioresistance: metabolic, epigenetic, and immune mechanisms with emerging links to RNA regulation - Scorecard - MDSpire
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The lactate–lactylation axis in tumor radioresistance: metabolic, epigenetic, and immune mechanisms with emerging links to RNA regulation
Clinical Scorecard: The Role of the Lactate-Lactylation Pathway in Tumor Resistance to Radiation: Insights into Metabolic, Epigenetic, and Immune Mechanisms with New Connections to RNA Regulation
At a Glance
Category
Detail
Condition
Tumor Radioresistance
Key Mechanisms
Lactate metabolism and protein lactylation as regulators of tumor adaptation to irradiation.
Target Population
Patients with solid tumors undergoing radiotherapy.
Care Setting
Oncology and radiotherapy departments.
Key Highlights
Lactate is a key metabolite influencing tumor radioresistance.
Lactylation is an emerging epigenetic modification linked to chromatin regulation.
Metabolic rewiring in tumors aids in DNA damage repair and survival post-irradiation.
Immune suppression in the tumor microenvironment is associated with lactate accumulation.
Therapeutic strategies targeting lactate metabolism are under investigation.
Guideline-Based Recommendations
Diagnosis
Assess lactate levels in tumor microenvironment as a potential biomarker for radioresistance.
Management
Consider targeting lactate metabolism and lactylation in treatment plans for radioresistant tumors.
Monitoring & Follow-up
Monitor metabolic adaptations and lactate levels during radiotherapy.
Risks
Evaluate the risk of tumor recurrence due to radioresistance linked to lactate metabolism.
Patient & Prescribing Data
Patients with solid tumors receiving radiotherapy.
Inhibitors of MCT and LDH, and lactate-depleting therapies may enhance radiosensitivity.
Clinical Best Practices
Integrate metabolic profiling in the assessment of tumor response to radiotherapy.
Utilize combination therapies targeting metabolic pathways to improve treatment outcomes.
