Colorectal cancer has a poor prognosis and is prone to recurrence and metastasis. DPP7, a prolyl peptidase, is reported to regulate lymphocyte quiescence. However, the correlation of DPP7 with prognosis in CRC remains unclear. With publicly available cohorts, the Wilcoxon rank-sum test and logistic regression were employed to analyze the relationship between DPP7 expression and the clinicopathological features of CRC patients. Specific pathways of differentially expressed genes were determined through biofunctional analysis and gene set enrichment analysis (GSEA). qPCR and immunohistochemical staining were used to determine DPP7 expression levels in surgical specimens. The public dataset and analysis of the biospecimens of CRC patients revealed that DPP7, in the CRC samples, was expressed significantly higher than in non-tumor tissues. Moreover, increased DPP7 was significantly associated with a higher N stage, lymphatic invasion, and shorter overall survival. Functionally, DPP7 is involved in neuroactive ligand–receptor interaction and olfactory transduction signaling. We identified a series of targeted drugs and small-molecule drugs with responses to DPP7. To conclude, DPP7 is a valuable diagnostic and prognostic biomarker for CRC and considered as a new therapeutic target.

Recently, SMARCA4-deficient undifferentiated tumor (SMARCA4-UT) has emerged as a distinct subset of lung cancer. Previous studies have suggested that SMARCA4-UT is often associated with smoking-related mutations, such as KRAS and STK11, rather than EGFR or ALK alterations. Nevertheless, no specific precision therapy has been identified for SMARCA4-UT. Here, we report the first case of concomitant ALK rearrangement and SMARCA4 (BRG1) deficiency in a nonsmoking female with thoracic cancer. Alectinib was given as the first-line therapy, and the patient achieved a remarkable complete response. Our case highlights the significance of ALK rearrangement identification for the precise therapeutic potential of SMARCA4-UT.

Rationale: Intimal sarcoma of inferior vena cava (IVC) is a rare soft tissue sarcoma with no typical symptoms and specific imaging features in the early stage, and there is a lack of standardized treatment and methods. Patient concerns: A 54-year-old female patient presented to Fenghua District People’s Hospital with a post-active cough and hemoptysis and was subsequently referred to our hospital. Diagnoses: The patient was pathologically diagnosed as intimal sarcoma of IVC complicating multiple intrapulmonary metastases. Chest CT revealed left lung malignant tumor with multiple intrapulmonary metastases; while enhanced upper abdominal CT showed cancer embolus of IVC with extension to right atrium and bilateral renal veins. Besides, hematoxylin and eosin staining suggested intimal sarcoma of veins. Immunohistochemical staining showed positivity for PD-L1, Ki-67, CD31, Desmin and ERG. Interventions: The patient initially received GT chemotherapy (gemcitabine injection + docetaxel). Then, immunotherapy (tislelizumab) was added based on the results of genetic testing (TP53 gene mutation). Outcomes: The disease was stabilized after receiving the treatment. Lessons: Given the lack of characteristic clinical manifestations in patients with intimal sarcoma of IVC, imaging examination combined with immunohistochemical index were helpful for diagnosis of intimal sarcoma of IVC. Furthermore, the combination of tislelizumab and GT chemotherapy was feasible in such patients with positive PD-L1 expression and TP53 mutation.

Anaplastic lymphoma kinase ( ALK ) rearrangements are exceedingly rare in gastric cancer, and uncommon fusion types add to the difficulties of proper, precise treatment strategies. Although detected in non-small cell lung cancer (NSCLC), inflammatory myofibroblastic tumors (IMTs), and Spitz tumors, the DCTN1–ALK fusion has not previously been reported in gastric cancer. This report describes the first case of gastric adenocarcinoma harboring a DCTN1–ALK fusion that was successfully treated with the ALK-targeted agent alectinib after first- and second-line chemotherapy-based regimens had failed. Progression-free survival on alectinib was 11.5 months until KRAS amplification emerged on serial circulating tumor DNA analysis, leading to rapid systemic relapse. The other documented cases with DCTN1–ALK fusion treated with the first or second generation of ALK inhibitors indicated this rare fusion as an actionable driver gene mutation. This successful personalized anti-tumor strategy highlights the clinical utility of comprehensive genomic profiling and liquid biopsy in detecting and monitoring actionable ALK fusions in solid tumors.

Primary MET amplification is an infrequent tumorigenic driver gene alteration identified in pulmonary neoplasms. Data on the effectiveness of MET-tyrosine kinase inhibitor (TKI) therapy in de novo MET amplification are relatively scarce, and there remains a dearth of empirical evidence supporting the use of precision therapy as first-line treatment for advanced non-small cell lung cancer (NSCLC) with primary MET amplification. We present a case of advanced lung adenocarcinoma in an elderly patient with primary MET amplification. The patient had an initial ECOG Performance Status (PS) 2. DNA-NGS analysis of tissue samples revealed a MET gene copy number (GCN) of 8, indicating MET amplification, without other oncogenic mutations associated with available drugs being detected. This finding was validated by MET fluorescence in situ hybridization (FISH), which showed cluster amplification. Initial treatment with savolitinib resulted in a sustained partial response lasting more than sixteen months. Our results suggest that savolitinib is effective and safe for the treatment of elderly patients with de novo amplified MET metastatic NSCLC and may therefore be considered a potential treatment option worthy of prospective study confirmation.