bims-meluca Biomed News
on Metabolism of non-small cell lung carcinoma
Issue of 2026–04–19
three papers selected by
the Muñoz-Pinedo/Nadal (PReTT) lab, L’Institut d’Investigació Biomèdica de Bellvitge



  1. J Cachexia Sarcopenia Muscle. 2026 Apr;17(2): e70281
       BACKGROUND: Cancer cachexia, frequently observed in patients with non-small cell lung cancer, is associated with reduced immunotherapy efficacy and poor prognosis. Despite the Fearon criteria being widely used to define cachexia, its relevance in Asian populations remains uncertain. Recently, the Asian Working Group for Cachexia (AWGC) proposed novel diagnostic criteria adapted for Asian body compositions. However, it remains unclear whether the outcomes or predictive value for immunotherapy differ between the AWGC and Fearon definitions. In addition, the AWGC-specific cachexia subgroup, previously regarded as noncachexia under Fearon's definition, has not been fully characterized.
    METHODS: We retrospectively analysed 411 Japanese patients with advanced PD-L1-high non-small cell lung cancer who received first-line PD-1/PD-L1 monotherapy or chemoimmunotherapy. Survival outcomes and clinical and nutritional indices were compared using both the AWGC and Fearon criteria. The patients were subsequently classified into three groups: (1) noncachexia, (2) A-only cachexia (meeting only the AWGC criteria), and (3) A+F cachexia (meeting both criteria). The small subgroup meeting only Fearon's criteria (n = 13) was excluded from analysis.
    RESULTS: Per the AWGC definition, 168 patients (40.9%) were classified as having cachexia compared to 62 (15.1%) according to the Fearon definition. AWGC-defined cachexia was associated with shorter overall survival (OS) (18.2 vs. 48.5 months, adjusted HR 1.539, p = 0.003), while progression-free survival (PFS) under PD-1/PD-L1 inhibitor therapy or chemoimmunotherapy showed a nonsignificant trend (7.1 vs. 13.0 months, adjusted HR 1.253, p = 0.072). Fearon-defined cachexia similarly predicted worse OS (18.4 vs. 37.7 months, adjusted HR 1.743, p = 0.002) but not PFS (5.9 vs. 11.4 months, adjusted HR 1.326, p = 0.081). In the three-group comparisons, the A-only cachexia group (n = 119) showed intermediate characteristics: Compared with the noncachexia group, they had lower BMI, higher C-reactive protein and poorer nutritional indices (prognostic nutritional and geriatric nutritional risk indices); compared with the A+F cachexia group, they had higher BMI, lower C-reactive protein and better nutritional indices. The PFS in the A-only cachexia group was comparable with that in the noncachexia group; however, the OS was significantly shorter (21.8 vs. 48.5 months, p = 0.0002). Compared with the A+F cachexia group, the A-only cachexia group showed no significant differences but demonstrated a favourable trend toward better PFS (adjusted HR 0.72, p = 0.096) and OS (adjusted HR 0.66, p = 0.051).
    CONCLUSION: The AWGC and Fearon criteria demonstrated comparable prognostic values. The A-only cachexia subgroup, previously regarded as noncachexia, retained responsiveness to immunotherapy but exhibited significantly shorter survival, underscoring its clinical relevance as a previously unrecognized at-risk group.
    Keywords:  Asian working group for cachexia; cachexia; fearon criteria; immunotherapy; non‐small cell lung cancer
    DOI:  https://doi.org/10.1002/jcsm.70281
  2. J Proteome Res. 2026 Apr 16.
      Nonsmall-cell lung cancer (NSCLC) accounts for more than 80% of lung cancer cases. Epidermal growth factor receptor mutations (EGFRm) occur in 15 and 40% of NSCLC in Western and Asian populations, respectively. Current treatment for advanced NSCLC targets EGFRm with tyrosine kinase inhibitors (TKIs). Osimertinib is a third-generation EGFR-TKI now used as a first-line treatment in advanced/metastatic NSCLC; however, drug resistance frequently develops. Dysregulation of metabolism has been suggested to play a role in the development of drug resistance. Here, we investigated the role of lipid metabolism in the development of osimertinib resistance (OR) using pharmacologically-induced resistant cellular models. We used a multiomics approach, combining lipidomics with proteomics analyses. We found alterations in processes relating to metabolism, such as dysregulated sphingolipid metabolism. In particular, we identified that OR lines reduce free ceramides in favor of complex glycosphingolipids. Mechanistically, this metabolic shift avoids ceramide-mediated apoptosis via caspase-3 activation. Importantly, when we combined osimertinib with D-PDMP, an inhibitor of the key enzyme responsible for the conversion of ceramide to glucosylceramide, we increased the sensitivity to osimertinib. Overall, we have identified the glycosphingolipid metabolic pathway as a potential therapeutic target to reinstate sensitivity to osimertinib in NSCLC.
    Keywords:  ceramide; glucosylceramidase; glycosphingolipid; lipidomics; multiomics; nonsmall-cell lung cancer; sphingolipid, drug resistance
    DOI:  https://doi.org/10.1021/acs.jproteome.6c00216
  3. Front Pharmacol. 2026 ;17 1793151
       Background: Cisplatin is a primary treatment for non-small cell lung cancer (NSCLC), however, cisplatin resistance develops readily, leading to tumor progression. Mesenchymal stem cells (MSCs) distributed in the tumor microenvironment (TME), yet the effects and mechanisms of cisplatin on MSCs and their subsequent impact on TME remains unclear.
    Methods: The MSC-related prognostic signature was developed through Cox and LASSO regression analysis. Validation was performed by survival analysis, ROC analysis and nomogram construction. TME evaluation was carried out by GSEA and immune infiltration analysis. The effect of cisplatin on MSCs was investigated by polymerase chain reaction (PCR) array, qRT-PCR, ELISA and Western blot. The migration of RAW 264.7 macrophages was analyzed by transwell assays and the polarization was analyzed by flow cytometry.
    Results: High-risk of MSC-related prognostic signature (PDGFB, ANPEP, CD40) was significantly linked to poor prognosis in patients under cisplatin treatment for NSCLC and other cancers. Patients with high IL-6 expression demonstrated poor response to cisplatin therapy. MSCs were linked with an immunosuppressive TME characterized by macrophage infiltration, particularly M2 macrophages. Cisplatin upregulated IL-6 expression in MSCs via the MEK-ERK pathway. The ability of MSCs to promote RAW 264.7 macrophages recruitment and polarization was enhanced by cisplatin.
    Conclusion: We established MSC-related prognostic signature for cisplatin therapy in NSCLC. MSCs and IL-6 were associated with cisplatin resistance and macrophages infiltration. Thus, MSCs and IL-6 were potential targets for NSCLC therapeutic intervention.
    Keywords:  cisplatin; interleukin-6; macrophages; mesenchymal stem cells; tumor microenvironment
    DOI:  https://doi.org/10.3389/fphar.2026.1793151