# Obesity and Metabolic Syndrome in Childhood Leukemia and in Long-Term Survivors: Causes and Personalized Treatments

**Authors:** Francisco José Corominas-Herrero, Diana Navas-Carrillo, Juan Antonio Ortega-García, Isabel Martínez-Romera, Esteban Orenes-Piñero

PMC · DOI: 10.3390/cancers17213446 · Cancers · 2025-10-27

## TL;DR

Childhood leukemia survivors are increasingly facing obesity and metabolic issues due to treatments and genetics, but personalized approaches may help prevent these problems.

## Contribution

This review identifies treatment-related and genetic factors contributing to obesity in leukemia survivors and highlights personalized medicine as a novel intervention strategy.

## Key findings

- Cranial radiotherapy, corticosteroids, and younger age at diagnosis are linked to weight gain and metabolic issues.
- Genetic polymorphisms in FTO, MC4R, and LEPR may increase obesity risk in survivors.
- Poor dietary habits and high-fat diets contribute to obesity and metabolic syndrome in survivors.

## Abstract

Acute lymphoblastic leukemia (ALL) is the most common pediatric cancer, accounting for about 34% of all cases. Survival rates have significantly improved to around 85% due to advances in chemotherapy, radiotherapy, and supportive care. However, new challenges have emerged, particularly the rising prevalence of obesity and metabolic syndrome among survivors. This review examines the link between leukemia treatment, obesity, and metabolic risk. Key factors such as cranial radiotherapy, corticosteroid use, and younger age at diagnosis are associated with increased weight gain and long-term metabolic issues. Genetic factors like FTO, MC4R, and LEPR polymorphisms may also contribute. Survivors often have poor dietary habits, including low micronutrient intake and high-fat, calorie-dense diets. Obesity and metabolic syndrome are linked to higher cardiovascular morbidity and reduced quality of life. Personalized medicine approaches that integrate genomics, metabolomics, and lifestyle data show promise for targeted prevention and intervention strategies.

Acute lymphoblastic leukemia (ALL) remains the most frequent pediatric malignancy, accounting for approximately 34% of all pediatric cancers, with remarkable improvements in survival (approximately 85%) due to advances in chemotherapy, radiotherapy, and supportive care. However, as survival rates have increased, new challenges have emerged—particularly the growing prevalence of obesity and metabolic syndrome among survivors. This review compiles evidence from the past decade on the relationship between leukemia treatment, obesity, and metabolic risk. The findings indicate that cranial radiotherapy, corticosteroid use, and younger age at diagnosis are key risk factors for excessive weight gain and long-term metabolic disturbances. Genetic factors such as FTO, MC4R, and LEPR polymorphisms may further influence susceptibility to obesity. Nutritional analyses highlight poor diet quality, insufficient micronutrient intake, and high-fat, energy-dense dietary patterns in survivors. Beyond endocrine dysfunction, obesity and metabolic syndrome are associated with elevated cardiovascular morbidity and reduced quality of life. Personalized medicine approaches—integrating genomics, metabolomics, and lifestyle data—hold promise for targeted prevention and intervention strategies. Early detection, continuous metabolic monitoring, and health education remain essential components in the long-term management of childhood leukemia survivors. In this review, we analyzed the dietary patterns of children and long-term leukemia survivors explaining why higher rates of obesity and comorbidities appear during or after treatments, and discussed interventions to prevent these conditions.

## Linked entities

- **Genes:** FTO (FTO alpha-ketoglutarate dependent dioxygenase) [NCBI Gene 79068], MC4R (melanocortin 4 receptor) [NCBI Gene 4160], LEPR (leptin receptor) [NCBI Gene 3953]
- **Diseases:** obesity (MONDO:0011122), metabolic syndrome (MONDO:0000816), acute lymphoblastic leukemia (MONDO:0004967)

## Full-text entities

- **Genes:** FTO (FTO alpha-ketoglutarate dependent dioxygenase) [NCBI Gene 79068] {aka ALKBH9, BMIQ14, GDFD, IFEX9}, MC4R (melanocortin 4 receptor) [NCBI Gene 4160] {aka BMIQ20}, LEPR (leptin receptor) [NCBI Gene 3953] {aka CD295, LEP-R, LEPRD, OB-R, OBR, huB219}
- **Diseases:** weight gain (MESH:D015430), Leukemia (MESH:D007938), Obesity (MESH:D009765), ALL (MESH:D054198), cancers (MESH:D009369), endocrine dysfunction (MESH:D004700), Metabolic Syndrome (MESH:D024821)

## Full text

_Full body text omitted from this summary view._ Fetch the complete paper as Markdown: https://tomesphere.com/paper/PMC12607413/full.md

## Figures

1 figure with captions in the complete paper: https://tomesphere.com/paper/PMC12607413/full.md

## References

67 references — full list in the complete paper: https://tomesphere.com/paper/PMC12607413/full.md

---
Source: https://tomesphere.com/paper/PMC12607413