Preoperational hemogram parameters have been reported to be associated with the prognosis of several types of cancers. This study aimed to investigate the prognostic value of hematological parameters in gastric cancer in a Chinese population. A total of 870 gastric cancer patients who underwent radical tumorectomy were recruited from January 2008 to December 2012. Preoperative hematological parameters were recorded and dichotomized by time-dependent receiver operating characteristic curves. The survival curves of patients stratified by each hematological parameter were plotted by the Kaplan–Meier method and compared by log-rank test. Multivariate Cox proportional hazards models were used to select parameters independently correlated with prognosis. The median age of the patients was 60 years. The median follow-up time was 59.9 months, and the 5-year survival rate was 56.4%. Results from the univariate analyses showed that low lymphocyte count (<2.05 × 109/L), high neutrophil-to-white blood cell ratio (NWR > 0.55), low lymphocyte-to-white blood cell ratio (LWR < 0.23), low lymphocyte-to-monocyte ratio (LMR < 5.43), high neutrophil-to-lymphocyte ratio (NLR > 1.44), and high platelet-to-lymphocyte ratio (PLR > 115) were associated with poor survival of gastric cancer patients. Multivariate analysis showed that low LMR (HR: 1.49, 95% CI: 1.17–1.89, P = .001) was the only hematological factor independently predicting poor survival. These results indicate that preoperational LMR is an independent prognostic factor for patients with resectable gastric cancer.
Persistent infection with the carcinogenic human papillomavirus (HPV) is a prerequisite for the progression of cervical lesions and cancer. A growing body of research has focused on the functional role of the vaginal microbiota in the persistence of HPV infection. Understanding the microbial composition and structure in women with high-risk (hr)-HPV infection may help reveal associations between the vaginal microbiota and HPV infection, and identify potential biomarkers. Our study investigated the vaginal microbial community in women with and without hr-HPV infection, by using 16s rRNA gene sequencing. We found that microbial perturbations occurred in the early phase of hr-HPV infection. Lactobacillus and Sporolactobacillus were decreased, while bacteria related to bacterial vaginosis (BV), such as Gardnerella, Prevotella, Dialister, Slackia, Actinomyces, Porphyromonas, Peptoniphilus, Anaerococcus, Peptostreptococcus, Streptococcus, Ureaplasma, Megasphaera, and Mycoplasma were increased. Our results could offer insights into the correlations between hr-HPV and the vaginal microbiota in the early infection period, and provide indications that the predominance of some BV-associated bacteria during hr-HPV infection may increase the risk for cervical neoplasia.
Cervical cancer is one of the most common gynecologic malignancies and poses a serious health problem worldwide. Identification and characterization of cervical cancer stem cells may facilitate the development of novel strategies for the treatment of advanced and metastatic cervical cancer. Breast cancer-resistance protein (Bcrp1)-positive cells were selected from a population of parent HeLa cells using flow cytometry. The invasion capacity of Bcrp1-positive and -negative cells was analyzed with a Boyden chamber invasion test. The tumorigenicity of these cells was determined by in vivo transplantation in non-obesity diabetes/severe combined immunodeficiency (NOD/SCID) mice. The Bcrp1-positive subpopulation accounted for about 7% of the parent HeLa cell population. The proliferative capacity of the Bcrp1-positive cells was greater than that of the Bcrp1-negative cells (P \ 0.05). In the invasion assay, the Bcrp1-positive cells demonstrated a greater invasive capacity through the artificial basement membrane than their Bcrp1-negative counterparts. Following transplantation of 10 4 cells, only the Bcrp1-positive cells formed tumors in NOD/SCID mice. When 10 5 or 10 6 cells were transplanted, the tumor incidence and the tumor mass were greater in the Bcrp1-positive groups than those in the Bcrp1-negative groups (P \ 0.05). The Bcrp1-positive subpopulation cervical cancer stem cells.
Helicobacter pylori (H. pylori) is the definite carcinogen of gastric cancer. H. pylori infection induces chronic inflammation, causes DNA damage and aberrant methylation of genes and these pathways are involved in H. pylori-related gastric carcinogenesis. Polymorphisms of the genes involved in these pathways could alter susceptibility to gastric cancer. In this mini review, we focused on the role of polymorphisms in these genes on the susceptibility to gastric cancer, with a particular emphasis on their possible interactions with H. pylori infection. We found that many studies on this theme did not simultaneously report H. pylori infection and the interactions remained inconclusive.
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