Observational studies on the association between fish and poultry intake and the risk of total cancer mortality have been reported with mixed results. Thus, we aimed to assess this association by conducting a meta-analysis of prospective studies. We performed a literature search on PubMed database through February 1, 2017 to identify relative prospective studies. A random-effects model was used to calculate the summary estimates. We identified fourteen prospective studies involving 2,378,204 participants and 96,712 cancer mortality events. Comparing the highest category of consumption with lowest category, pooled relative risk (RR) of total cancer mortality was 0.99 (95% confidence interval [CI], 0.94–1.05) for fish (10 studies) and 0.96 (95% CI, 0.93–1.00) for poultry (8 studies), respectively. However, we failed to identify any dose–response association based on a limited number of eligible studies, with a pooled RR of 0.98 (95% CI, 0.92–1.05) and 0.97 (95% CI, 0.88–1.07) for each 100 g per day increment in fish and poultry consumption, respectively. In summary, this meta-analysis indicates that consumption of either fish or poultry is not substantially associated with lower risk of total cancer mortality. The observed weak inverse association for high poultry consumption needs to be verified in additional large prospective studies.

Background: The protein regulator of cytokinesis 1 (PRC1) is a prognostic marker characterized by low DNA methylation in lung cancer. This study aims to examine the function of PRC1 in non-small cell lung cancer (NSCLC) cells and investigates its regulatory mechanisms. Methods: PRC1 expression in NSCLC cells was assessed using qPCR and western blot analyses. Loss- and gain-of-function assays of PRC1 were performed in NSCLC cells to analyze its effect on cell cycle progression and growth. Genetic knockdown or pharmaceutical inhibition of cyclin Y (CCNY), tet methylcytosine dioxygenase 2 (TET2), and BTB domain and CNC homolog 1 (BACH1) was conducted to analyze their influence on PRC1 phosphorylation or transcription. Subcutaneous xenograft and orthotopic isograft tumor models were generated for in vivo verification. Tissue microarray (TMA) and bioinformatics analyses were employed to evaluate the clinical prognostic value of CCNY, TET2, and PRC1 in NSCLC. Results: PRC1 was highly expressed in NSCLC cells. Silencing either PRC1 or CCNY, which promotes PRC1 phosphorylation, substantially reduced cell growth in vitro, impaired spindle formation, promoted G2/M phase cell cycle arrest, increased multi-nucleated cells, and weakened tumorigenic activity of cells. Moreover, TET2 was found to induce DNA demethylation of PRC1 and activate its transcription by interacting with BACH1. Inhibition of TET2, BACH1, or the PLK1-PRC1 interaction weakened the tumorigenic potential of NSCLC cells in vivo. The TMA analysis revealed increased levels of CCNY, TET2, and phosphorylated PRC1 in tumor tissues. Bioinformatics analyses suggested that these molecules were correlated with unfavorable prognosis in NSCLC patients. Conclusion: This study demonstrates a critical oncogenic role of PRC1 in NSCLC. CCNY, which modulates PRC1 phosphorylation, and the TET2-BACH1 cascade, which modulates demethylation and transcription of PRC1, may serve as promising targets for NSCLC management.

Background: This study sought to explore the biological significance of genetic variation in RAS wild-type metastatic colorectal cancer (mCRC) in the real world, the difference in the efficacy of cetuximab in the treatment of mCRC with different genetic variants and identify clinical features and new predictors of efficacy. Methods: A retrospective analysis of the data of 60 patients with stage IV mCRC who received cetuximab at The First and Second Affiliated Hospital of Soochow University from 2016 to 2020 was conducted. The patients were divided into the following 3 groups according to the genetic test results: (I) group A (the all-RAS wild-type group); (II) group B (the all-RAS wild-type group with the tumor suppressor gene mutation); and (III) group C (the all-RAS wild-type group with the oncogenic driver gene mutation). A subgroup analysis was conducted to examine left CRC and local intervention, and the progression-free survival (PFS) and overall survival (OS) of the patients were observed. Results: The all-RAS wild-type mCRC patients were divided into group A (n=10), group B (including the TP53, APC, PTEN, BRCA2, and SMAD4 variants) (n=42), and group C (including the ERBB2, BRAF, PIK3CA, and RET variants) (n=8). The median PFS of groups A, B, and C were 15.0, 12.0, and 3.0 months, respectively (P=0.007). Fitting sex as a stratified variable to the Cox survival analysis model showed that only the PFS of groups B and C differed significantly (P=0.011). In the left-sided mCRC patients, the median PFS of groups A, B, C were 3.0, 13.0, and 3.0 months, respectively (P=0.009). Among the patients in group B, the median PFS of the metastatic local intervention subgroup was 14.0 months, and the non-local intervention subgroup was 12.0 months (P=0.55). Only the type of combined gene mutation was an independent factor affecting PFS. Conclusions: The PFS and OS of mCRC patients with all-RAS wild-type and no combined mutations treated with cetuximab were not better than those of patients with combined mutations. Compared to mCRC patients with all-RAS wild-type and oncogenic driver gene mutations, cetuximab significantly prolonged the PFS of all-RAS wild-type patients with the tumor suppressor gene mutations.