Human epidermal growth factor receptor‑2 (HER2) negative advanced gastric cancer (GC) has a high global incidence and mortality rate with limited options for second‑line treatment. Monotherapy is not effective and the combination of chemotherapy and immunotherapy has not yet been included in the guidelines. The present study aimed to explore a new treatment approach by conducting a single‑center, retrospective, observational real‑world study. A total of 21 patients with advanced HER2‑negative GC, who had progressed after receiving standard first‑line regimens [tegafur, gimeracil and oteracil potassium capsules (S‑1) or capecitabine plus oxaliplatin], were selected. The application of programmed cell death‑1 (PD‑1) inhibitor combined with taxanes was selected as the second‑line treatment. The primary outcomes measured were progression‑free survival (PFS), pathological complete response, objective response rate (ORR), disease control rate (DCR) and adverse reactions in the present patient cohort. The median (m)PFS in the overall population was 7.1 months, with a 95% confidence interval (CI) of 6.0‑8.2 months and the median overall survival (mOS) was 11.3 months, with a 95% CI of 4.5‑18.2 months. The ORR was 9.5% and the DCR was 90.5%. Univariate and multivariate analyses indicated that Ki67 <70% and tumor marker‑positive status [one or two increases among carcinoembryogenic antigen (CEA), cancer antigen (CA) 199 and CA125] were independent prognostic factors for PFS and overall survival (OS) in second‑line treatment. Significant statistical differences were noted in PFS (mPFS=5.3 months, 95% CI: 3.1‑7.5 months vs. mPFS=9.1 months, 95% CI: 6.2‑12.0 months; P=0.002) and OS (mOS=8.8 months, 95% CI: 7.0‑10.7 months vs. mOS=17.2 months, 95% CI: 16.0‑18.5 months; P=0.013) between the Ki67‑high group (Ki67 ≥70%) and the Ki67‑low group (Ki67 <70%). Significant statistical differences were noted in OS between tumor marker‑negative status (CEA, CA199 and CA125 within normal range) and tumor marker‑positive status (one or two increases among CEA, CA199 and CA125; mOS=17.2 months, 95% CI: 16.0‑18.4 months vs. mOS=8.8 months, 95% CI: 5.3‑12.4 months; P=0.018); however, no significant differences were noted in PFS between these two groups. The present study retrospectively analyzed the new second‑line approach of PD‑1 inhibitor combined with taxanes for HER2 negative GC which effectively improved patient PFS and OS compared with single‑agent chemotherapy. The expression levels of Ki67 and the tumor marker‑negative status possess potential clinical value in monitoring prognosis and guiding future individualized use of chemotherapy combined with immunotherapy.

Gallbladder cancer (GBC) is a highly aggressive tumor associated with risk factors, such as chronic infection, gallstones, and exposure to harmful chemicals. Our study explores the role of polycyclic aromatic hydrocarbons (PAHs) and long noncoding RNA HEGBC in GBC progression. We found that PAHs activate the aryl hydrocarbon receptor (AhR), which enhances HEGBC expression and promotes GBC cell proliferation, invasion, and metastasis both in vitro and in vivo. Mechanistically, AhR binds to the HEGBC promoter, establishing a positive feedback loop that further activates AhR transcription. Moreover, CYP1A1 was identified as a key downstream effector of PAHs-AhR/HEGBC-mediated proliferation, migration, and invasion of GBC cells in vitro and in vivo. These findings provide the integrative view of a molecular mechanism loop for regulating the malignant progression of GBC centered by PAHs/AhR/HEGBC, which represents a promising strategy for the treatment of GBC.

The role of SLC35A2 in breast cancer remains poorly understood, with limited available information on its significance. This study aimed to investigate the expression of SLC35A2 and clinicopathological variables in breast cancer patients. Immunohistochemical analysis of SLC35A2 protein was conductedon 40 adjacent non-neoplastic tissues and 320 breast cancer tissues. The study also assesed the association between SLC35A2 expression and breast cancer clinicopathological features of breast cancer, as well as its impact on overall survival. In comparison to adjacent non-neoplastic tissues, a significantly higher expression of SLC35A2 was observed in breast cancer tissues (P = 0.020), and this expression was found to be independently correlated with HER2 positivity (P = 0.001). Survival analysis indicated that patients with low SLC35A2 expression had a more favorable prognosis in HER2-positive subtype breast cancer (P = 0.017). These results suggest that SLC35A2 is overexpressed in breast cancer tissues compared to adjacent non-neoplastic tissues and may serve as a potential prognostic marker for HER2-positive subtype breast cancer. Furthermore, breast cancer patients with the HER2 positive subtype who exhibited decreased levels of SLC35A2 expression demonstrated improved long-term prognostic outcomes.