Glutamine is the most abundant amino acid in human serum, and it can provide carbon and nitrogen for biosynthesis, which is crucial for proliferating cells. Moreover, it is widely known that glutamine metabolism is reprogrammed in cancer cells. Many cancer cells undergo metabolic reprogramming targeting glutamine, increasing its uptake to meet their rapid proliferation demands. An increasing amount of study is being done on the particular glutamine metabolic pathways in cancer cells. Further investigation into the function of glutamine in immune cells is warranted given the critical role these cells play in the fight against cancer. Immune cells use glutamine for a variety of biological purposes, including the growth, differentiation, and destruction of cancer cells. With the encouraging results of cancer immunotherapy in recent years, more investigation into the impact of glutamine metabolism on immune cell function in the cancer microenvironment could lead to the discovery of new targets and therapeutic approaches. Oral supplementation with glutamine also enhances the immune capabilities of cancer patients, improves the sensitivity to chemotherapy and radiotherapy, and improves prognosis. The unique metabolism of glutamine in cancer cells, its function in various immune cells, the impact of inhibitors of glutamine metabolism, and the therapeutic use of glutamine supplements are all covered in detail in this article.

Inflammasomes are essential regulators of innate immunity, inflammation, and cellular apoptosis, and they have surfaced as significant modulators of cancer progression and regulation. Inflammasomes are macromolecular complexes assembled in response to damage-associated molecular patterns (DAMPs) and pathogen-associated molecular patterns (PAMPs). They induce inflammation via the oligomerization and activation of caspases. These cysteine proteases cleave the pro-inflammatory cytokines IL-1β and IL-18 into their physiologically active mature versions. Recent discoveries reveal that inflammasomes are implicated not only in infections but also in malignancies, suggesting a significant connection between inflammation and tumor development. This article emphasizes that inflammasomes cause pyroptosis in a variety of immune cells, such as dendritic cells, macrophages, T cells, and fibroblasts, in addition to tumor cells. The induction of CD8+ T cells allows inflammasomes to commence an immunological response against the tumor, successfully inhibiting its growth and progression. The inflammasome comprises four main types: NLRP1, NLRP3, NLRC4, and AIM2. Nevertheless, the inflammasomes are activated by infection, injury, or stimulation of host cells, thus triggering the inflammatory response. The essential roles of the NLRP1, NLRP3, NLRC4, and AIM2 inflammasomes are emphasized in both tumors and immune cells. Furthermore, the article provides an overview of inhibitors targeting various tumor inflammasome pathways currently in clinical trials. Here, in this review, we underscore the role of the inflammatory response in cancer progression and highlight the significance of inflammasomes in regulating immune cells within the tumor microenvironment. Targeting these inflammasomes offers novel strategies for cancers.

Patients withEGFR-sensitizing mutations in non-small cell lung cancer (NSCLC) predominantly receive first-line tyrosine kinase inhibitors (TKIs). Subsequent TKI resistance manifests through heterogeneous clinicopathological features, including distinct resistance subtypes (primary vs. acquired),PD-L1expression levels, and molecular profiles from re-biopsies. While immunotherapy represents a potential subsequent option, the predictive biomarkers guiding optimal patient selection remain undefined. This multicenter retrospective study analyzed 1,396 EGFR-mutant NSCLC patients from five Chinese institutions, with 312 meeting stringent inclusion criteria. Comprehensive treatment data encompassing EGFR-TKIs, platinum-based chemotherapy, anti-angiogenic agents, and immune checkpoint inhibitors (ICIs) were collected. Cox proportional hazards regression identified progression-free survival (PFS)-associated variables, enabling resistance subtyping. Comparative effectiveness analyses across therapeutic modalities were performed. Multivariable Cox regression identified two independent predictors of immunotherapy PFS:EGFRmutation subtypes (exon21 L858R vs. exon19del; HR 0.84, 95 % CI [0.70-0.99], P = 0.042) and TKI resistance classification (acquired vs. primary: HR 2.28, 95 % CI [1.52-3.43], P = 0.001). Patients with primary TKI resistance showed improved outcomes with ICIs (median PFS 8.5 vs. 4.0 months; HR 0.46,95 % CI [0.29-0.76], P = 0.002), particularly in L858R-mutant subgroups. In contrast, acquired resistance cohorts-especially those with exon19del mutations-derived limited clinical benefit (HR 1.09, 95 % CI [0.84-1.42];P = 0.510). These findings suggest that resistance subtype and mutation profile may aid immunotherapy selection in EGFR-mutant NSCLC, requiring validation through prospective studies. This multicenter analysis demonstrates that immunotherapy outcomes in EGFR-mutant NSCLC after TKI failure are influenced by both resistance subtypes (primary vs. acquired) and specific EGFR mutation profiles (L858R vs. exon19del). Patients with primary resistance and L858R mutations derive clinically meaningful benefit from ICIs, while those with acquired resistance, particularly exon19del variants, showed limited efficacy. These findings support further investigation of resistance-phenotype-guided therapeutic algorithms in prospective trials to optimize treatment sequencing strategies.

This study aims to compare the survival discrimination of the Tumor-Node-Metastasis (TNM) eighth and ninth editions for patients with localized and locally advanced (LLA) anal squamous cell carcinoma (ASCC) treated non-surgically and to evaluate the prognostic impact of T classification and lymph node (LN) status with data from the Surveillance, Epidemiology, and End Results database. We retrospectively included 6,876 patients in the comparison. We observed the inversion of survival outcomes for stages IIB and IIIA diseases in the TNM eighth edition [median overall survival (OS): 112 months for stage IIB vs. not reached for stage IIIA]. By contrast, it demonstrated improvement in the TNM ninth edition (median OS: not reached for IIB disease vs. 120 months for IIIA disease, P<0.001). In the correlation analysis, we observed an increased correlation between T classification and TNM staging systems (r value increased from 0.78 to 0.93) and a decreased correlation for the LN status (r value decreased from 0.83 to 0.59). For OS, variable importance analysis demonstrated more weight of importance for the T classification than the LN status (0.0871 vs. 0.0048). Additionally, decision curve analysis and time-dependent receiver operating characteristic analysis confirmed the prognostic accuracy of T classification rather than the LN status. In conclusion, TNM ninth edition is a better prognostic indicator than the eighth edition for patients with LLA ASCC treated non-surgically. T classification plays a more important prognostic role than the LN status and warrants further validation.

Background: Colon cancer is one of the most common diagnosed malignancies. Although the use of surgery, chemotherapy, radiotherapy, targeted therapy, immunotherapy and other comprehensive treatment, distant metastasis is still one of the main causes for dying of colon cancer. The common metastatic site of colon cancer is liver, lung and bone. In this article, we report a rare case of breast metastasis of signet ring cell carcinoma from the colon. Case Presentation: A 44-year-old woman was diagnosed with colon cancer and received a radical surgery of colon cancer in 2019. Combined with postoperative pathological and CT images, a diagnosis of cT3N2M0 mucinous adenocarcinoma of colon (according to AJCC cancer staging manual, Version 8) was established. Adjuvant chemotherapy (XELOX: oxaliplatin 130 mg/m² on day 1 plus capecitabine 1000 mg/m² twice daily on days 1 to 14 every 3 weeks for 18 weeks) was performed followed by surgical resection. 14 months later, the patient received mastectomy for breast mass, which was diagnosed pathologically as metastasis of signet ring cell carcinoma from the colon. XELOX chemotherapy regimen (oxaliplatin 130 mg/m² on day 1 plus capecitabine 1000 mg/m² twice daily on days 1 to 14 every 3 weeks for 24 weeks) combined with bevacizumab (7.5mg/kg on day 1) were used after the mastectomy. The patient was stable disease according to her last examination (RECIST criteria).Conclusion: It is rare to report a patient diagnosed with colon cancer which metastasis to breast. We hope to increase treatment experience for patients with this rare metastasis.