Rationale: Primary pulmonary inflammatory myofibroblastic tumor (IMT) with distant metastasis is extremely rare. Moreover, metastasis of pulmonary IMT to bone marrow has never been reported in previous studies. Therapeutic approaches for anaplastic lymphoma kinase (ALK)-negative pulmonary IMT with metastasis are limited. Yet there is no report on the treatment of advanced IMT cases with anti-angiogenesis drugs.Patient concerns: We described a patient with a complaint of fatigue, with the chest computed tomography (CT) scan revealing 2 masses in bilateral lung.Diagnoses: The CT-guided lung biopsy examined 1 lesion in the right lung, and the post-operative pathological diagnosis of ALK-negative pulmonary IMT was recommended. However, the lung lesions were found significantly enlarged during the subsequent visit 8 months later, along with multiple metastases to the bone and abdominal cavity. A bone marrow biopsy revealed bone marrow infiltration by spindle cells.Interventions: The patient began to take Celecoxib due to the rapid progression of IMT, however, resulting in the aggravated gastric ulcer. He stopped taking the medicine 1 month later, with no remarkable change in the lesions by CT. Apatinib was administrated instead of Celecoxib.Outcomes: After the 5-month treatment of Apatinib, the mass in the abdominal cavity significantly shrank and the lung lesions slightly decreased in size. With the 9-month administration of Apatinib, the lung lesions and the abdominal mass kept stable, compared with the situation in the 5-month follow-up.Lessons: Although pulmonary IMT shows the potential of metastasis, its metastasizing to bone marrow is a highly unusual event. Apatinib is effective for pulmonary IMT, and should be taken into consideration for the treatment of inoperable pulmonary IMT patients who lack ALK rearrangement.

Background: Ferroptosis, a regulated form of cell death, has emerged as a critical modulator of melanoma's tumor progression and immune evasion. However, its integration with the tumor immune microenvironment (TME) and clinical prognostication remains underexplored. This study aims to construct a multi-omics framework combining ferroptosis-related signatures, immune infiltration patterns, and machine-learning approaches to stratify melanoma patients and guide therapeutic decision-making.Methods: We developed a multi-omics framework integrating bulk transcriptomics (TCGA/GEO), single-cell RNA sequencing, and machine learning to decode melanoma's ferroptosis-immune axis. Ferroptosis-immune subtypes were identified through consensus clustering and immune profiling, while prognostic models were constructed via LASSO/stepwise Cox regression and machine learning optimization.Results: Three ferroptosis-immune subtypes exhibiting distinct survival outcomes and immune phenotypes were identified. A 40-gene prognostic signature (externally validated) effectively stratified patient survival risk and predicted chemotherapy sensitivity. Single-cell analysis revealed elevated ferroptosis activity within an immunosuppressive microenvironment, specifically implicating POSTN–ITGB5 signaling in fibroblast-immune cell crosstalk. A clinically applicable nomogram integrating risk scores and clinical factors demonstrated robust predictive accuracy (AUC 0.829–0.845). Machine learning refined a 4-gene prognostic signature (CLN6, GMPR, AP1S2, ITGA6), with functional validation confirming the role of CLN6 in proliferation and migration.Conclusion: This study establishes a prognostic framework and therapeutic roadmap for precision immuno-oncology in melanoma, bridging multi-omics discovery with clinical translation.

Background: Epidermal growth factor receptor (EGFR)-mutant nonsmall cell lung cancer (NSCLC) patients are less likely to be programmed death-ligand 1 (PD-L1)-positive compared with wild-type EGFR mutant tumors. Given the rarity of actionable driver genes in squamous cell lung cancer (SQCC), the frequency of SQCC patients simultaneously carrying EGFR driver gene mutation and having PD-L1 over-expression is extremely low. Studies on the effectiveness and safety of EGFR-TKIs or immune-checkpoint inhibitors (ICIs) in this subset of patients are lacking. Patient concerns: The patient suffered from coughing and chest pain for 1 month. A chest CT revealed a mass with a cavity in the right lung, enlarged mediastinal lymph nodes, diffuse pleural thickening in the right pleura, and pleural effusion of the right chest. Diagnosis: A pleural biopsy was performed using a video-assisted thoracoscope. The pathological examination revealed a poorly differentiated squamous cell carcinoma of lung. Further genetic testing identified exon 19 deletion mutation in EGFR with abundance of 0.27%. Meanwhile, immunohistochemical PD-L1 analysis showed a TPS of 90%. Interventions: The patient was initially resistant to EGFR-TKIs but exhibited a rapid and marked response to pembrolizumab. Outcomes: After 5 cycles of pembrolizumab monotherapy, the patient developed Grade 3 immune-related dermatitis, and ICI therapy was suspended. Conclusions: ICI monotherapy could be an effective therapy in SQCC patients with low-abundance of EGFR mutations and PD-L1 over-expression. However, close attention should be paid to immune-related adverse events.

Lactylation, a post-translational modification derived from elevated lactate levels, has gained attention as a potential regulator of melanoma’s tumor metabolism and immune responses. Here, we combined single-cell RNA sequencing and bulk transcriptome profiling of cutaneous melanoma samples to establish a lactation-centric prognostic model. Our analyses revealed melanocytes as the most acetylation-enriched cell population and identified a six-gene lactylation signature that stratified patients into high- and low-risk groups with distinct survival outcomes. Mechanistically, high-risk tumors demonstrated significant immunosuppressive features characterized by M2 macrophage accumulation and depleted CD8+ T-cell activity, corresponding to reduced sensitivity to certain chemotherapeutic drugs. Pathway enrichment studies implicated DNA repair, Hedgehog, and JAK-STAT signaling in driving the aggressive phenotype of high-acetylation tumors. Additionally, pseudotime trajectory analyses highlighted developmental shifts in gene expression related to lactylation during melanocyte differentiation. The signature demonstrated robust predictive accuracy in training, testing, and external validation cohorts. Functional validation confirmed the critical role of RAN in promoting proliferation and migration in vitro. These findings unveil lactylation as a critical epigenetic factor influencing melanoma progression and immune evasion, offering a novel prognostic framework and potential therapeutic targets for precision medicine.