Objective: This study evaluates the preoperative and postoperative systemic immune-inflammation index (SII) capacity to predict the prognosis of patients with endometrial carcinoma after the operation and build a nomogram model to assist clinical practice.Methods: The retrospective study included 362 consecutive patients with surgically resected endometrial cancer between January 2010 and June 2015 at The Affiliated Cancer Hospital of Shantou University Medical College. Blood routine was examined within 1 week before surgery to calculate SII, NLR, PLR, and MLR and 3 days after surgery to measure SII. The Pearson's χ²-test or Fisher's exact test was used to explore their relationship to clinical variables. The univariate and multivariate survival analyses were performed by Cox regression to identify the independent prognostic indicators. The Kaplan–Meier method with the log-rank test was used to generate the overall survival (OS) curves. R software was used to generate the receiver operating characteristic (ROC) curve and then it got the optimum cutoff value through the maximum Youden index. A nomogram model was formed with systemic immune inflammation and clinical factors.Results: The preoperative SII was related to age (p = 0.009), FIGO stage (p = 0.02) and menopause (p = 0.014). The postoperative SII was associated with menopause (p = 0.014). Univariate analysis indicated that FIGO stage, lymphatic invasion, depth of myometrial invasion, postoperative chemotherapy, postoperative radiotherapy, preoperative SII, NLR, PLR, MLR, CRP, CA125, and postoperative SII were predictors of OS (p < 0.05). Multivariate analysis showed that lymphatic invasion and postoperative SII were independent prognostic factors of OS (p < 0.05). The nomogram model was visualized precisely to reflect the prognosis with a C-index value of 0.866 in this model.Conclusion: The postoperative SII is the independent prognostic factor in patients with endometrial carcinoma after the operation and contributes to poor outcomes. However, after surgery, the preoperative SII and preoperative NLR, PLR, and MLR are not associated with OS endometrial carcinoma. Making good use of the nomogram model would contribute to better subsequent therapy.

The role of farnesoid X receptor (FXR) in cervical cancer and the underlying molecular mechanism remain largely unknown. Therefore, this study aimed to assess the mechanism of FXR in cervical cancer. Western blot, qRT-PCR, and immunohistochemistry demonstrated that FXR was significantly reduced in squamous cell carcinoma tissues, although there were no associations of metastasis and TNM stage with FXR. In Lenti-FXR cells obtained by lentiviral transfection, the overexpression of FXR reduced cell viability and colony formation. Compared with the Lenti-Vector groups, the overexpression of FXR induced early and late apoptosis and promoted G1 arrest. With time, early apoptosis decreased, and late apoptosis increased. In tumor xenograft experiments, overexpression of FXR upregulated small heterodimer partner (SHP), murine double minute-2 (MDM2), and p53 in the nucleus. Co-immunoprecipitation (Co-IP) showed that SHP directly interacted with MDM2, which is important to protect p53 from ubiquitination. Nutlin3a increased MDM2 and p53 amounts in the Lenti-Vector groups, without effects in the Lenti-FXR groups. Silencing SHP reduced MDM2 and p53 levels in the Lenti-FXR groups, and Nutlin3a counteracted these effects. Taken together, these findings suggest that FXR inhibits cervical cancer via upregulation of SHP, MDM2, and p53.

Background: Estrogen receptor (ER) is essential in reproductive development and is also the primary driver of breast cancers. Deregulation of ER may also be involved in tumorigenesis of other organs. To understand the role of ER in different tumor types, pan‐cancer analysis of estrogen receptor alpha (ESR1) and estrogen receptor beta (ESR2) in various tumors and association with patients' survival were conducted using The Cancer Genome Atlas (TCGA) data.Results: Gene methylation level was evaluated by the mean methylation level of CpG sites in the promoter region. The significant different DNA methylation between tumor and healthy tissues was shown in 10 tumor types for ESR1 and eight tumor types for ESR2. The methylation pattern was also varied across different TCGA tumors. The pan‐cancer analysis showed significantly different mRNA expression of ESR1 in nine tumor types and ESR2 in four tumor types. Survival analysis showed that the effects of ERs expression on survival are diverse in different tumors. The expression of ERs was associated with tumor molecular subtypes and various clinical characteristics. ER correlated genes were mainly enriched in cancer and immune‐related pathways.Conclusions: Our pan‐cancer analysis data indicated that ERs might be significantly associated with carcinogenesis and progression of some tumors, which may be potential therapeutic targets and prognosis biomarkers.

Introduction: In cancer treatment, every minute counts. Due to the unpredictable behavior of cancer cells caused by continuous mutations, each cancer patient has a unique situation and may or may not respond to a specific drug or treatment. The process of finding an effective therapy can be time-consuming, but cancer patients do not have the luxury of time for trial and error. Therefore, a novel technology to fast generate a patient relevant organoid for the therapies selecting is urgently needed.Methods: Utilizing the new organoid technology by specially dissolving the mesenchyme in tumor tissues acquired from cancer patients, we realized the work of creating patient-specific organoids (PSO) within one day.Results: PSO properties reflect those of its respective original in vivo tumor tissue and can be utilized to perform various in vitro drug sensitivity tests to identify the most effective clinical treatment for patients. Additionally, PSO can aid in assessing the efficacy of immune cell therapies.Discussion: Organoid technology has advanced significantly in recent years. However, current cancer organoid methods involve creating 3D tumor tissue from 2D cancer cells or cell clusters, primarily for cancer research purposes aimed at investigating related molecular and cellular mechanisms of tumor development. These methods are research-driven, not tailored towards clinical applications, and cannot provide personalized information for individual patients. PSO filled the gap of clinic-driven and time-saving method for the personalized therapies selecting to the cancer patients.

Aim: This study aimed to explore using peripheral blood mononuclear cell (PBMC)-derived chimeric antigen receptor (CAR) NK cells targeting ROBO1 as a personalized medicine approach for ovarian cancer. Methods: A two-step strategy generated ROBO1-targeted CAR NK cells from PBMCs of ovarian cancer patients. Efficacy was evaluated using xCELLigence RTCA, CCK-8 and Live/Dead fluorescence assays. Results: ROBO1-NK cells exhibited higher efficiency in eradicating primary ovarian cancer cells and lysing ovarian tumor organoids compared with primary NK cells without ROBO1-CAR modification. Conclusion: These findings highlight the potential of developing ROBO1-targeted CAR-NK cells from patients' PBMCs as a personalized treatment option for ovarian cancer.