Background and aims: Muscle mass reduction (MMR) is one of the three etiologic criteria in the Global Leadership Initiative on Malnutrition (GLIM) framework. This study aimed to evaluate the value of MMR in GLIM criteria among ambulatory cancer patients. Methods: A single-center prospective cross-sectional study was conducted. All participants underwent calf circumference (CC) measurement and body composition measurement by bioelectrical impedance analysis (BIA). MMR was identified by CC, fat-free mass index (FFMI), appendicular skeletal muscle index (ASMI), or combinations of the above three indicators. Patients-generated Subjective Global Assessment (PG-SGA) was used as the comparator. Results: A total of 562 cancer patients receiving intravenous treatment were evaluated. Of the participants, 62.8% (355/562) were male. The median age of the patients was 59.0 years (range, 21–82 y). The median BMI was 22.8 kg/m² (range, 14.6–34.5 kg/m²). A total of 41.8% of patients were evaluated as malnutrition (PG-SGA ≥ 4), and 11.9% were diagnosed with severe malnutrition (PG-SGA ≥ 9). For the GLIM criteria, the prevalence of malnutrition was 26.9%, and severe malnutrition was 12.3%. For all criteria combinations of GLIM together versus PG-SGA, sensitivity was 60.4% (53.8–66.7), specificity was 97.9% (95.4–99.1), while the accordance between GLIM and PG-SGA was moderate (κ = 0.614). The performance of the GLIM worsened when MMR was excluded (κ = 0.515), with reduced sensitivity (50.2% (43.7–56.8)) and the same specificity (97.9% (95.4–99.1)). Including FFMI and ASMI by BIA can further improve the performance of GLIM than using CC alone (κ = 0.614 vs. κ = 0.565). Conclusions: It is important to include MMR in the GLIM framework. Using body composition measurement further improves the performance of the GLIM criteria than using anthropometric measurement alone.

Golgi glycoprotein 73 (GP73) is a type II Golgi transmembrane protein and a potential novel marker for the diagnosis of primary hepatocellular carcinoma (PHC). However, its reliability as a serum marker for the diagnosis of PHC following transcatheter arterial chemoembolization (TACE) remains unknown. The aim of the present study was to evaluate the diagnostic value of serum GP73 levels in patients with PHC, to determine its diagnostic accuracy in patients with PHC following TACE. Reverse transcription‑quantitative polymerase chain reaction analysis was used to measure GP73 expression in PHC and adjacent para‑carcinomatous liver tissue in 40 patients with PHC, and 15 normal liver samples from benign hepatic tumors. The associations between GP73 expression levels with clinicopathological characteristics of the patients were also analyzed. Serum GP73 levels were detected by ELISA in 68 patients with PHC following TACE and 29 healthy individuals. The levels of serum GP73 were tested 2 days prior to intervention, and 7 and 30 days following TACE. GP73 mRNA expression levels in PHC were significantly higher than in the corresponding para‑carcinomatous liver and normal liver samples. High expression levels of GP73 mRNA were associated with tumor size, vascular invasion and tumor differentiation, suggesting augmented tumor invasion and metastasis. The expression levels of serum GP73 were markedly higher in the patients with PHC compared with healthy individuals. Serum GP73 levels in the 68 patients with PHC were higher compared with the 29 normal controls [152.5 (76.4‑284.5) compared with 49.3 (12.6‑26.7) µg/l], and the difference was statistically significant (P<0.01). High levels of serum GP73 were associated with tumor differentiation. The levels of Barcelona clinic liver cancer stage A, B and C were 92.12 (38.9‑135.2), 122.9 (55.2-178.5), and 162.55 (110.8‑232.9) µg/l, respectively (P<0.05). The serum GP73 levels 7 days following TACE [99.2 (66.7‑150.8)] were significantly lower than prior to TACE, and the difference was statistically significant (P<0.05). In the group of 49 patients with serum α‑fetoprotein (AFP) levels 132 µg/l. Serum GP73 levels may serve as a potential independent diagnostic marker for PHC, and the combined evaluation of serum GP73 and AFP may increase the diagnostic efficiency of PHC. Significant overexpression of GP73 mRNA was associated with aggressive PHC. However, further research is required to confirm the potential of GP73 as a diagnostic marker.

Background: Sarcopenia has recently emerged as a new condition with increasing importance in lung cancer patients. The aim of this study was to investigate the influence of sarcopenia on tolerance and efficacy of afatinib.Methods: We retrospectively evaluated 35 patients with epidermal growth factor receptor (EGFR) mutant advanced non‐small cell lung cancer (NSCLC) treated with first‐line afatinib. Skeletal muscle area (SMA) was measured at the third lumbar vertebra using routine conducted computed tomography (CT) images for evaluation of disease burden. Sarcopenia was defined as skeletal muscle index (SMI = SMA/height²) ≤38.5 cm²/m² for women and ≤52.4 cm²/m² for men based on previous criteria. Fisher's exact tests, Kaplan–Meier method, and logistic regression modeling were used.Results: The median age at diagnosis was 65 years (range,39–84 years). A total of 24 (68.6%) patients were diagnosed with sarcopenia. The most frequent adverse events (AEs) related to afatinib were diarrhea (94.3%) followed by rash (77.1%) and paronychia (60%). Overall, 19 (54.3%) patients had dose reduction. Sarcopenic patients had a significantly higher rate of grade ≥ 2 diarrhea (75.0 vs. 27.3%, p = 0.011) and toxicity‐related dose reduction (75.0 vs. 9.1%, p = 0.001). Multivariate analysis also showed that sarcopenia (odds ratio [OR] 51.7, 95% confidence interval [CI]: 2.4–1081.3, p = 0.01) was an independent risk factor for dose reduction of afatinib. The median progression‐free survival (PFS) for afatinib was 12.0 months (95% CI: 10.6–13.4). Both dose reduction and sarcopenia did not affect therapeutic efficacy.Conclusions: Toxicity‐related dose reduction is common with initiation of afatinib 40 mg/day. Sarcopenic patients might begin treatment with a low dose of afatinib according to tolerance.