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Introduction/Background Recent studies in China have reported an incidence of approximately 1% for multiple primary tumors. However, it is important to note that the current prevalence in China might be underestimated due to regional variations and limited case numbers. Synchronous primary cancers of the endometrium and cervix with different histomorphology are particularly rare in the female reproductive system. Methodology A 73-year-old woman was admitted to Gansu Provincial Maternity and Child-care Hospital with complaints of vaginal bleeding for two weeks, occasional lower abdominal discomfort, and dizziness. We performed serological, imaging, and histopathological tests on this patient. To further investigate whether cancer sites were primary or metastatic, we utilized a dual-gene methylation detection system (CISPOLY, China) to analyze pathological tissues from different areas. Results Serological tests revealed elevated levels of carcinoembryonic antigen and CA-125. Transvaginal ultrasound (TVS) showed abnormalities in the uterine cavity and cervical canal. Pelvic MRI revealed diffuse occupancy of the uterine cavity and cervical canal, indicating a likelihood of endometrial cancer. Pathological biopsy revealed the presence of inflammatory cells, consistent with endometrial cancer. Surgical and pathological results confirmed tumor sites as follows: invasion of the muscle layer in the uterine cavity, adenocarcinoma in situ, and chronic cervicitis. We observed positive gene methylation results in other sites, indicating molecular-level changes that have not yet manifested as tissue alterations. Conclusion Both gene methylation technology and traditional histopathology were employed for simultaneous detection. The results of gene methylation analysis may provide further insights in determining whether the reproductive tract tumors originate primarily or secondarily. Essentially, the presence of positive methylation in other areas may suggest a potential cancer progression within a specific timeframe, which can serve as a basis for assessing the likelihood of cancer metastasis. However, further clinical cases are needed to substantiate the role of methylation in considering the cancer foci metastasis possibility. Disclosures No potential conflict of interest was reported by the authors.

Background: Microchromosome maintenance protein 10 (MCM10) is required for DNA replication in all eukaryotes, and it plays a key role in the development of many types of malignancies. However, we currently still do not know the relationship between MCM10 and ovarian cancer (OV) prognosis and immune checkpoints.Methods: The Gene Expression Profiling Interactive Analysis and Tumor Immunology Estimation Resource (TIMER) databases were used to investigate MCM10 expression in Fan cancer. The Kaplan-Meier Plotter and PrognoScan were used to assess the relationship between MCM10 and OV prognosis. The LinkedOmics database was used to analyze the MCM10 co-expression network and explore GO term annotation and the KEGG pathway. The relationship between MCM10 expression and immune infiltration in OV was investigated using the Tumor Immunology Estimation Resource database. cBioPortal database was used to explore the relationship between MCM10 expression and 25 immune checkpoints. Finally, quantitative real-time polymerase chain reaction (qRT-PCR) was performed to detect MCM10 expression. The prognosis was also analyzed by distinguishing between high and low expression groups based on median expression values.Results: The results of the three data sets (220,651_s_at, 222,962_s_at and 223,570_at) in KM Plotter all indicated that the overall survivalof the high MCM10 expression group was lower than that of the low expression group OV, and the results of GSE9891 also reached the same conclusion. The expression level of MCM10 was negatively correlated with B cells and CD8+T cells, and positively correlated with CD4+T Cells and Macrophages. GO term annotation and KEGG pathway analysis showed that the co-expressed genes of MCM10 were mainly enriched in cell cycle and DNA replication. The alterations in MCM10 coexisted statistically with the immune checkpoints CTLA4, TNFSF4, TNFSF18, CD80, ICOSLG, LILRB1 and CD200. PCR results displayed that MCM10 was highly expressed in OV tissues, and the increased expression of MCM10 was significantly associated with poor overall survival.Conclusion: These results demonstrated that high expression of MCM10 was associated with poor prognosis in OV and correlated with immune checkpoints.

Our previous study has demonstrated that two low molecular weight-polycyclic aromatic hydrocarbons (LMW-PAHs), phenanthrene (Phe) and fluorene (Flu), alone and as a mixture could induce oxidative damage and inflammation in A549 cells. However, the associated mechanisms have not been well discussed. The aim of this study was to further investigate the roles of PI3K/AKT and NF-κB signaling pathways in the inflammatory effects in A549 cells induced by Phe, Flu and their mixture. The results indicated that Phe, Flu and their mixture significantly activated PI3K/AKT and NF-κB signaling pathways by increasing the phosphorylation levels of PI3K, AKT, IκBα and NF-κB p65. In addition, pro-inflammatory cytokine expressions of TNF-α and IL-6 induced by the binary mixture of Phe and Flu were all alleviated by co-treatment with PI3K/AKT and NF-κB specific inhibitors (LY294002 and BAY11-7082). The results suggested that PI3K/AKT and NF-κB signaling pathways played an important role in LMW-PAHs induced inflammation in A549 cells.

Low molecular weight-Polycyclic aromatic hydrocarbons (LMW-PAHs) are ubiquitous environmental pollutants, which may contribute to respiratory diseases. However, studies of the relative mechanisms are limited. This study aimed to explore the effects of two LMW-PAHs [phenanthrene (Phe) and fluorene (Flu)], separately and as binary PAH mixture on oxidative stress and inflammation in A549 cells. Cell viability was firstly detected at various concentrations (200-800 μM) by Phe, Flu, and the mixture of Phe and Flu. ROS level, MDA content, SOD and CAT activities were then determined to evaluate oxidative damage. The protein and mRNA expressions of IL-6, TNF-α, TGF-β, and the protein content of SP-A were further determined to evaluate inflammation. Results showed that Phe, Flu, and their mixture triggered ROS generation and induced abnormal productions of MDA, SOD, and CAT. And the protein and mRNA expressions of TNF-α and IL-6 were increased by Phe, Flu, and their mixture, respectively. In addition, SP-A was also increased by Phe and Flu, while it was decreased by their mixture at 600 μM. The results demonstrated that Phe, Flu, and their mixture could induce oxidative stress and subsequent inflammation in A549 cells, while combined inflammatory response was stronger than single actions.

Phenanthrene (Phe) female rat model was established to explore the effects of Phe on oxidative stress and inflammation. The rats were randomly divided into three groups including control (C), low (L), and high (H) group. Phe was supplied to L and H groups at the dosage of 180 mg/kg and 900 mg/kg orally at first day, and with the dose 90 mg/kg and 450 mg/kg by intraperitoneal injection at the last 2 days. The C group was enriched with the same volume of corn oil. The blood, lung, and liver tissues were collected. The superoxide dismutase (SOD), malonaldehyde (MDA), and 8-hydroxy-2-deoxyguanosine (8-OHdG) were detected to evaluate oxidative stress. The protein and mRNA expressions of interleukin 6 (IL-6), tumor necrosis factor-α (TNF-α), transforming growth factor-β (TGF-β), and interleukin 10 (IL-10) were detected to evaluate inflammation. Further, the forkhead box transcription factor 3 (Foxp3) was analyzed to hint the injury mechanism of inflammation. The results showed SOD and MDA in lung and liver, and serum 8-OHdG elevated significantly in H groups (P < .05). Meanwhile, there were significant increases in the protein and mRNA expression of TNF-α and IL-6 in lung and liver of H groups (P < .05). In addition, the protein and mRNA expressions of TGF-β and Foxp3 were all decreased significantly in both lung and liver of H groups (P < .05). Results demonstrated that an obvious change of Phe exposure could induce oxidative stress and inflammation in female rats. This is a first pilot study to explore the association between Phe exposure and oxidative stress and inflammation using a female rat model.