Xiao L, Liu YD, Zhang X, Zhang SC, Lyu JH. Body mass index predicts low muscle mass in esophageal squamous cell carcinoma patients undergoing chemoradiotherapy. World J Clin Oncol 2026; 17(4): 116601 [DOI: 10.5306/wjco.v17.i4.116601]
Corresponding Author of This Article
Jia-Hua Lyu, PhD, Associate Chief Physician, Senior Researcher, Department of Radiation, Sichuan Clinical Research Center for Cancer, Sichuan Cancer Hospital & Institute, Sichuan Cancer Center, School of Medicine, University of Electronic Science and Technology of China, No. 55 Section 4, Renmin South Road, Chengdu 610041, Sichuan Province, China. winlttljh@163.com
Research Domain of This Article
Nutrition & Dietetics
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Retrospective Cohort Study
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Apr 24, 2026 (publication date) through Apr 22, 2026
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World Journal of Clinical Oncology
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2218-4333
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Xiao L, Liu YD, Zhang X, Zhang SC, Lyu JH. Body mass index predicts low muscle mass in esophageal squamous cell carcinoma patients undergoing chemoradiotherapy. World J Clin Oncol 2026; 17(4): 116601 [DOI: 10.5306/wjco.v17.i4.116601]
Ling Xiao, Yu-Di Liu, Xue Zhang, Shi-Chuan Zhang, Jia-Hua Lyu, Department of Radiation, Sichuan Clinical Research Center for Cancer, Sichuan Cancer Hospital & Institute, Sichuan Cancer Center, School of Medicine, University of Electronic Science and Technology of China, Chengdu 610041, Sichuan Province, China
Co-corresponding authors: Shi-Chuan Zhang and Jia-Hua Lyu.
Author contributions: Xiao L was responsible for conceptualization, project administration, resources, and supervision; Xiao L and Liu YD managed data curation and visualization; they contributed equally to this article and are the co-first authors; Zhang X oversaw software; Xiao L, Liu YD, and Zhang SC were responsible for methodology; Lyu JH handled funding acquisition; Xiao L, Liu YD, Zhang X, Zhang SC, and Lyu JH contributed to investigation, validation, writing original draft, and writing review and editing; Zhang SC and Lyu JH contributed equally to this article, and they are the co-corresponding authors of this manuscript; all authors thoroughly reviewed and endorsed the final manuscript.
Institutional review board statement: This study was approved by the Medical Ethics Committee of Sichuan Cancer Hospital, approval No. SCCHEC2015010.
Informed consent statement: The informed consent was waived by the Institutional Review Board.
Conflict-of-interest statement: The authors report no relevant conflicts of interest for this article.
STROBE statement: The authors have read the STROBE Statement-checklist of items, and the manuscript was prepared and revised according to the STROBE Statement-checklist of items.
Data sharing statement: The original contributions presented in the study are included in the article. Further inquiries can be directed to the corresponding author.
Corresponding author: Jia-Hua Lyu, PhD, Associate Chief Physician, Senior Researcher, Department of Radiation, Sichuan Clinical Research Center for Cancer, Sichuan Cancer Hospital & Institute, Sichuan Cancer Center, School of Medicine, University of Electronic Science and Technology of China, No. 55 Section 4, Renmin South Road, Chengdu 610041, Sichuan Province, China. winlttljh@163.com
Received: November 18, 2025 Revised: December 12, 2025 Accepted: January 21, 2026 Published online: April 24, 2026 Processing time: 157 Days and 14.5 Hours
Abstract
BACKGROUND
Radiotherapy-induced toxicity and low muscle mass (LMM) significantly compromise treatment efficacy and survival in patients with esophageal squamous cell carcinoma (ESCC). Although body mass index (BMI) is a simple nutritional screening tool, its utility in predicting LMM in patients with ESCC remains unclear.
AIM
To investigate the association between baseline BMI and LMM prevalence and to evaluate the impact of LMM on survival outcomes in ESCC patients undergoing chemoradiotherapy.
METHODS
In this retrospective cohort study, 360 consecutive patients with ESCC treated with chemoradiotherapy at Sichuan Cancer Hospital from 2012 to 2023 were enrolled. LMM was assessed using skeletal muscle index derived from L3-level computed tomography images based on validated sex-specific cutoff values. Multivariable logistic regression was performed to analyze the association between BMI and LMM. A Cox proportional hazards model was used to assess the association between LMM and overall survival (OS) after adjusting for key confounders, including age, sex, clinical stage, and treatment regimen.
RESULTS
The prevalence of LMM was 23.0% in the patient cohort. Multivariable analysis showed that each 1-unit increase in BMI was associated with a 38.7% reduction in the odds of LMM (odds ratio: 0.613; 95% confidence interval: 0.531-0.707; P < 0.001). Patients with LMM had significantly shorter median OS than those without LMM (17.0 months vs 28.7 months; P < 0.001). The subgroup with combined low BMI and LMM had the poorest prognosis (median OS: 17.0 months). Baseline BMI was an independent predictor of LMM in patients with ESCC undergoing chemoradiotherapy and was significantly correlated with survival.
CONCLUSION
A combined evaluation of BMI and LMM enables the early identification of high-risk individuals, underscoring the importance of routine pretreatment assessment and timely nutritional and functional interventions to improve clinical outcomes.
Core Tip: Baseline body mass index (BMI) is a strong, independent predictor of low muscle mass (LMM) in patients with esophageal squamous cell carcinoma undergoing chemoradiotherapy. Higher BMI is associated with a significantly lower risk of LMM and improved survival. The combination of low BMI and LMM serves as a simple and effective composite marker for identifying high-risk patients with the poorest prognosis, highlighting the need for early nutritional and functional interventions to improve clinical outcomes.
Citation: Xiao L, Liu YD, Zhang X, Zhang SC, Lyu JH. Body mass index predicts low muscle mass in esophageal squamous cell carcinoma patients undergoing chemoradiotherapy. World J Clin Oncol 2026; 17(4): 116601
Esophageal cancer is a significant global health burden, ranking as the 11th most common malignancy and the 7th leading cause of cancer-related mortality worldwide[1]. East Asia, particularly China, bears the predominant disease burden[1]. In China, esophageal cancer accounts for over 40% of global incidence and mortality, with esophageal squamous cell carcinoma (ESCC) being the predominant pathological type[1,2]. The disease exhibits remarkable geographical clustering and a strong sex disparity (male-to-female ratio ≈ 3:1). Established risk factors include tobacco use, alcohol consumption, hot beverage intake, and consumption of preserved foods[1,2]. Due to its insidious early symptoms, approximately 70% of patients are diagnosed at advanced stages[3-5]. For patients with inoperable disease or those who decline surgery, definitive concurrent chemoradiotherapy is the standard of care[3-5]. However, treatment-related toxicities severely limit patient tolerance, presenting a critical barrier to therapeutic efficacy and survival.
Esophageal cancer is associated with one of the highest malnutrition rates among all cancers, largely due to inadequate nutritional intake caused by progressive dysphagia[6]. This nutritional impairment increases the risk of secondary low muscle mass (LMM). The resulting loss of skeletal muscle mass not only diminishes tolerance to chemoradiotherapy and increases the risk of severe adverse reactions but also directly contributes to functional decline, reduced quality of life, and elevated mortality, ultimately limiting treatment success[7,8].
Current gold-standard methods for muscle mass assessment include computed tomography (CT), dual-energy X-ray absorptiometry, and magnetic resonance imaging[9]. Among these, CT has emerged as a practical clinical tool because of its quantitative precision and compatibility with routine tumor response assessments[9]. Body mass index (BMI) is an accessible nutritional screening indicator. BMI significantly influences treatment tolerance, toxicity risk, and long-term survival, making it valuable for clinical decision-making in cancer management and prognosis prediction[10-12]. Nevertheless, the effectiveness of BMI in LMM screening and outcome prediction among patients undergoing chemoradiotherapy remains uncertain. Therefore, this study aims to address two key questions. First, what is the association between baseline BMI and CT-defined LMM in patients with ESCC undergoing chemoradiotherapy? Second, how does CT-defined LMM impact long-term survival? This retrospective cohort study examines the relationship between baseline BMI and LMM in these patients and evaluates the mediating role of BMI in the “LMM-survival” pathway. The goal is to provide an evidence-based rationale for early identification and targeted interventions.
MATERIALS AND METHODS
Study design and population
This single-center retrospective cohort study enrolled 360 consecutive patients with ESCC who underwent chemoradiotherapy at Sichuan Cancer Hospital between 2012 and 2023. Inclusion criteria were as follows: (1) Histopathologically confirmed ESCC; (2) Treatment with radiotherapy (dose ≥ 40 Gy) combined with chemotherapy; (3) Availability of complete baseline laboratory data (e.g., complete blood count, serum biochemistry) within 1 week before treatment; and (4) Availability of abdominal or thoracic CT images obtained within 4 weeks before treatment for skeletal muscle assessment. Exclusion criteria were as follows: (1) Distant metastasis (M1) or other primary malignant tumors; (2) Incomplete clinical data; and (3) Failure to complete the planned chemoradiotherapy regimen.
Variable definition and data collection
The primary exposure, BMI, was calculated as pretreatment weight (kg) divided by height squared (m2). BMI was analyzed both as a continuous variable and a categorical variable (low BMI: < 18.5 kg/m2; normal BMI: 18.5-24.0 kg/m2; high BMI: ≥ 24.0 kg/m2). Skeletal muscle area (SMA) was measured from CT images at the third lumbar vertebra (L3) level using SliceOmatic software (v5.0). Skeletal muscle index (SMI) was calculated as skeletal muscle area/height2 (cm2/m2). LMM was defined as having an SMI below Asian population–specific cutoff values (male: < 40.8 cm2/m2; female: < 34.9 cm2/m2). Overall survival (OS) was evaluated. Covariates included demographic characteristics (age, sex); clinicopathological factors (tumor-node-metastasis stage according to American Joint Committee on Cancer 7th edition, tumor location); treatment parameters (radiotherapy dose, chemotherapy regimen); and baseline metabolic markers (blood glucose, lipid profile).
Statistical analysis
Statistical analyses were performed using R version 4.3.1. Continuous variables were expressed as mean ± SD or median (interquartile range), and categorical variables as n (%). Group comparisons were conducted using t-tests, Mann-Whitney U tests, χ2 tests, or Fisher’s exact tests, as appropriate. Optimal cutoff values for continuous covariates were determined using an optimally stratified log-rank test. Restricted cubic splines (RCSs) were used to model potential nonlinear relationships between BMI and LMM; a P value for nonlinearity < 0.05 was considered significant. Survival curves were generated using the Kaplan-Meier method and compared using log-rank tests. The impact of LMM on OS was assessed using Cox proportional hazards models adjusted for relevant covariates, with results reported as hazard ratios (HRs) and 95% confidence intervals (CIs). All tests were two-sided, with P < 0.05 considered statistically significant.
RESULTS
Baseline patient characteristics
This study included 360 patients with ESCC undergoing chemoradiotherapy. Patients were stratified into three BMI categories: Low BMI (< 18.5 kg/m2; n = 36), normal BMI (18.5-24.0 kg/m2; n = 239), and high BMI (≥ 24.0 kg/m2; n = 85). The cohort was predominantly male (79.7%), with a median age of 65 years [interquartile range (IQR): 58.75-70]. Intergroup comparisons revealed significant differences in median survival time (P = 0.019), with median survivals of 14.5 months (IQR: 7.7-34.8), 22.0 months (IQR: 12.2-37.95), and 26.0 months (IQR: 15.0-41.57) for the low, normal, and high BMI groups, respectively. The groups differed significantly in smoking history (P = 0.006) and tumor-related characteristics: T stage (P = 0.006), N stage (P = 0.016), and clinical stage (P = 0.001). In particular, a higher proportion of patients in the low BMI group presented with advanced disease: 63.9% (23/36) were T4, 80.6% (29/36) were N2-3 stage, and 100% (36/36) had stage III-IV disease. However, the groups did not differ significantly in survival state, sex, age, Karnofsky performance score (KPS), alcohol history, tumor location, or receipt of chemotherapy between the BMI groups (all P > 0.05; Table 1).
Table 1 Participant baseline characteristics stratified by body mass index categories, n (%).
Univariate and multivariate logistic regression analyses were conducted to examine the cross-sectional relationship between baseline BMI and the risk of LMM. As a continuous variable, BMI was significantly and inversely associated with LMM risk in the unadjusted model [model 1: Odds ratio (OR) = 0.620; 95%CI: 0.543-0.709; P < 0.001], in the model adjusted for demographic and clinicopathological factors (model 2: OR = 0.611, 95%CI: 0.531-0.703, P < 0.001), and in the fully adjusted model (model 3). Model 3 adjusted for age, sex, KPS, smoking and alcohol history, tumor location, radiotherapy dose, chemotherapy regimen, T stage, N stage, and baseline levels of glucose, total cholesterol, and triglycerides. In this fully adjusted model, each 1-unit increase in BMI was associated with a 38.7% reduction in the odds of LMM (OR = 0.613; 95%CI: 0.531-0.707; P < 0.001; Table 2). When analyzing BMI as a categorical variable, both the normal BMI group (18.5-24.0 kg/m2; OR = 0.159; 95%CI: 0.078-0.379; P < 0.001) and the high BMI group (≥ 24.0 kg/m2; OR = 0.032; 95%CI: 0.010-0.107; P < 0.001) exhibited a significantly lower risk of LMM compared with to the low BMI group (< 18.5 kg/m2) in the fully adjusted model (model 3). Furthermore, there was a significant dose-response trend, with the risk of LMM decreasing as BMI increased (P < 0.001).
Table 2 Association between body mass index and low muscle mass.
Dose-response relationship of BMI and LMM with mortality
RCS analysis revealed a significant inverse association between BMI and both LMM risk and all-cause mortality (P for overall association < 0.002 for both outcomes). The analysis identified a common inflection point at BMI = 21.5 kg/m2. Below this threshold, lower BMI was associated with a sharp increase in the risk of LMM (OR = 7.75; 95%CI: 3.86-15.57) and all-cause mortality (HR = 1.38; 95%CI: 1.04-1.84). Above this threshold, the association was protective, with higher BMI associated with reduced risk of LMM (OR = 0.13; 95%CI: 0.06-0.26) and mortality (HR = 0.72; 95%CI: 0.55-0.96). No evidence of U- or J-shaped nonlinear associations was detected (P = 0.494 for LMM; P = 0.441 for mortality). These results delineate a critical risk threshold at BMI = 21.5 kg/m² and suggest a statistical association of a higher BMI beyond this point within the studied range (Figure 1).
Figure 1 Associations of body mass index with low muscle mass and all-cause mortality.
Restricted cubic spline analyses depict the relationship between body mass index (BMI) (kg/m2) and the odds ratio for low muscle mass and the hazard ratio for all-cause mortality. The solid lines represent the adjusted association, and the shaded areas indicate the 95% confidence intervals. The vertical dashed line marks the common inflection point at body mass index = 21.5 kg/m2. The overall P value and the P value for nonlinearity are presented in each panel. A: Association between BMI and the risk of low muscle mass (odds ratio); B: Association between BMI and the risk of all-cause mortality (hazard ratio). CI: Confidence interval; BMI: Body mass index; OR: Odds ratio; HR: Hazard ratio.
Survival analysis by BMI and muscle mass status
Kaplan-Meier survival analysis underscores the critical role of muscle mass in survival prognosis (Figure 2). Results indicated no significant survival differences across BMI categories among patients with normal muscle mass (low BMI + normal muscle mass vs high BMI + normal muscle mass: P = 0.124; normal BMI + normal muscle mass vs high BMI + normal muscle mass: P = 0.316). However, regardless of BMI category, the survival probability was significantly reduced in patients with concurrent LMM: Examples included high BMI + LMM (vs high BMI + normal muscle mass, P = 0.031), low BMI + LMM (vs high BMI + normal muscle mass, P = 0.044), and normal BMI + LMM (vs high BMI + normal muscle mass, P = 0.002). Further analysis within the normal BMI subgroup showed that patients with LMM had significantly poorer survival than those with normal muscle mass in the same BMI category (P = 0.013, Figure 2).
Figure 2 Survival analysis by combined body mass index and muscle mass status.
Patients were stratified by body mass index (BMI) (low: < 18.5 kg/m2; normal: 18.5-24 kg/m2; high: ≥ 24 kg/m2) and muscle mass status [normal muscle mass or low muscle mass (LMM)]. Panels A-E use high BMI and normal muscle mass as the reference group (blue curves). A: High BMI and LMM; B: Low BMI and normal muscle mass; C: Low BMI and LMM; D: Normal BMI and normal muscle mass; E: Normal BMI and LMM; F: Uses normal BMI and normal muscle mass as the reference group (blue curve). BMI: Body mass index.
Multivariate analysis identified BMI as an independent predictor of survival in participants with LMM. In the fully adjusted model (model 3), which controlled for age, sex, KPS, smoking and alcohol history, tumor location, radiotherapy dose, chemotherapy regimen, T stage, N stage, and baseline levels of glucose, total cholesterol, and triglyceride, each unit increase in BMI (as a continuous variable) was associated with a 5.9% reduction in the hazard of all-cause mortality (HR = 0.941, 95%CI: 0.892-0.993, P = 0.025). When analyzed by BMI category using the underweight group (< 18.5 kg/m2) as the reference, the group with high BMI (≥ 24.0 kg/m2) showed a significantly lower hazard of mortality in the fully adjusted model (HR = 0.574; 95%CI: 0.346-0.951; P = 0.047). However, the normal BMI group (18.5-24.0 kg/m2) did not show a statistically significant difference in mortality risk compared to the underweight reference group (HR = 0.783; 95%CI: 0.495-1.239; P = 0.296). A significant inverse dose-response trend was observed across BMI categories (P = 0.020; Table 3).
Table 3 Associations between body mass index and all-cause mortality in participants with sarcopenia.
This study investigated the relationships among baseline nutritional status, skeletal muscle mass, and clinical outcomes in patients with ESCC undergoing chemoradiotherapy. We observed an independent, linear dose-response relationship between BMI and LMM: For each 1-unit increase in BMI, the odds of LMM were reduced by 38.7% (OR = 0.613; 95%CI: 0.531-0.707; P < 0.001). This finding was established using multivariate logistic regression and RCS analyses. This monotonic decrease in LMM risk across the BMI range of 18-28 kg/m2 highlights that nutritional status is a key determinant of muscle maintenance. LMM was identified as a key mediating condition linking nutritional status to clinical outcomes. The combination of BMI and LMM status revealed a significant synergistic effect: “low BMI with LMM” was a robust composite marker for identifying patients with the poorest prognosis, whereas “high BMI without LMM” was associated with the most favorable prognosis. These findings provide strong rationale for precise risk stratification and early intervention during the critical treatment window in patients with ESCC.
Cancer patients exhibit a heightened risk of malnutrition, driven by elevated metabolic demands of the tumor and treatment-related adverse effects that compromise dietary intake. Among all malignant neoplasms, ESCC exhibits the highest prevalence of malnutrition[6,13], primarily attributable to tumor-induced obstruction that impairs deglutition and systemic metabolic dysregulation. Chronic malnutrition leads to progressive muscle loss, defined in this study as LMM, which is not merely an age-associated phenotype but an independent risk factor that compromises therapeutic efficacy, elevates treatment-related toxicity, diminishes health-related quality of life, and adversely impacts survival outcomes in cancer patients[8,14,15]. Therefore, for the ESCC population in whom malnutrition is highly endemic, the identification of facile tools for rapid nutritional assessment and LMM risk stratification is of substantial clinical significance to facilitate timely intervention.
BMI is a nutritional screening modality commonly employed owing to its simplicity[16]. However, BMI fails to differentiate between adipose tissue and muscle mass, and its diagnostic accuracy is compromised in patients with edema or body composition perturbations (e.g., cancer cachexia). Contemporary evidence delineates a multifaceted association between BMI and cancer incidence/prognosis: While elevated BMI elevates the risk of esophageal adenocarcinoma, breast, renal, and colorectal cancers[17-19], it paradoxically correlates with favorable prognostic outcomes in gastric and lung cancers[20,21]. In ESCC, numerous investigations have posited that BMI serves as a valuable biomarker for treatment response, therapeutic tolerance, and long-term survival outcomes[10,22,23]. However, current evidence regarding the BMI-sarcopenia association in ESCC is predominantly derived from resectable, early-stage cohorts: Sugawara et al[24] demonstrated that in 75 predominantly early-stage (62% at stages 0-I/II) patients with ESCC undergoing esophagectomy, BMI was significantly correlated with SMI (r = 0.49, P < 0.001) and skeletal muscle mass (r = 0.57, P < 0.001), with the prevalence of sarcopenia reaching 28.6% in the low BMI subgroup (< 20 kg/m2). Similarly, Kim et al[11] validated that “patients with high BMI and no sarcopenia exhibited superior prognostic outcomes” in a cohort of 1141 predominantly early-stage (82.6% at stages 0-I/II) resectable patients with ESCC. Conversely, the present study enrolled unresectable, locally advanced patients with ESCC who received chemoradiotherapy as first-line treatment. These patients exhibit substantially higher tumor burden than resectable early-stage counterparts, and chemoradiotherapy is likely to induce nutritional insufficiency and accelerated muscle wasting, resulting in fundamental differences in body composition profiles compared with early-stage resectable patients. Notably, the prevalence of LMM in the low BMI subgroup (< 18.5 kg/m2) was as high as 66.67% in our cohort. Given the unmet clinical need for sarcopenia screening tools tailored to the chemoradiotherapy setting, this study focused on unresectable stages III-IV patients with ESCC receiving definitive chemoradiotherapy, with the aim of systematically evaluating the association between baseline BMI and CT-defined LMM, as well as their prognostic implications. Our baseline data revealed that patients with low BMI presented with more advanced tumor stage and inferior KPS. Additionally, higher BMI was associated with improved survival outcomes: Each 1-unit increment in BMI was associated with a 5.9% reduction in mortality risk, and patients in the high BMI subgroup (≥ 24.0 kg/m2) exhibited a significantly lower mortality risk relative to those in the low BMI subgroup (< 18.5 kg/m2). While baseline data revealed that higher BMI was associated with improved survival, subgroup analysis indicated that patients with normal BMI and LMM had significantly worse survival outcomes compared with those with normal BMI and normal muscle mass. These results highlight that muscle mass rather than BMI is the core driver of survival prognosis and call attention to the often-overlooked occult high-risk subgroup of normal BMI plus LMM.
The prognostic significance of LMM in cancer stems from its high prevalence and profound pathophysiological consequences. Its association with reduced OS has been validated across multiple malignancies, including ESCC, head and neck, lung, and gastrointestinal cancers[23,25]. This impact stems from the central role skeletal muscle plays in protein storage and metabolic regulation. LMM triggers a cascade of functional, metabolic, and immunological effects; it reduces tolerance to treatment-related toxicities[26]; metabolically, it promotes intramuscular lipid infiltration and insulin resistance[27]; and immunologically, it may impair antitumor immunity through reduced myokine secretion [e.g., interleukin (IL)-6, IL-8, IL-15][28-30].
This study has several limitations. First, its retrospective design prevents the establishment of causality and may introduce residual confounding. Second, the exclusion of patients who failed to complete the planned chemoradiotherapy regimen may have omitted those with LMM or malnutrition who discontinued treatment due to intolerance or toxicity, leading to a cohort biased toward “survivors” with better treatment tolerance. Third, we assessed muscle mass only at baseline, which prevented an analysis of dynamic changes during treatment. Fourth, the single-center design may limit its generalizability, necessitating validation in multicenter and multiethnic cohorts. Finally, this study focused solely on the mass component of LMM. Future work should integrate measures of muscle strength (handgrip) and function (gait speed) for a more comprehensive diagnosis.
CONCLUSION
In summary, this study shows that baseline BMI is a strong independent predictor of LMM in ESCC patients receiving chemoradiotherapy, with a significant linear dose-response relationship between these variables. The combination of low BMI and LMM could be a simple, clinically useful composite marker to identify a high-risk subgroup with a poor prognosis.
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