Platinum-based chemotherapy resistance is one of the main contributors to the mortality of Ovarian Cancer (OC). It is believed that sensitive biomarkers for identifying the population that is platinum-resistant are urgently needed. This study aims to develop a platinum-resistance gene-based signature to predict OC patients' responses to platinum drugs as well as survival outcomes. A platinum-resistance-related gene model was built by bioinformatics analysis. Then, its predictive power was internally validated. Continually, a nomogram was constructed to confirm the model's predictive ability. Afterward, GSEA was used to explore our model's potential functions. The ESTIMATE, CIBERSORT, TIMER, and ssGSEA were applied to estimate immune conditions. Then, somatic mutation and drug sensitivity were also analyzed. Finally, to gain insights into the roles of targeted genes in drug sensitivity, patient-derived tumor organoids (PDOs) validation was performed. Nine platinum-resistance-related genes, including SLC22A2, TAP1, PC, MCM3, GTF2H2, FXYD5, SUPT6H, IGKC, and MATN2, were anchored to build the predictive model, which was well internally validated. Subsequently, GSEA unveiled that our model genes enriched in the Hedgehog signaling pathway. The predictive signature was associated with immune checkpoint inhibitors such as PD-1, PD-L1, and CTLA4, guiding immunotherapy applications for OC patients. Drugs such as dasatinib, midostaurin, metformin, MK-2206, and mitomycin C might also benefit OC patients with different risk scores. PDOs showed patients with high-risk scores were more resistant to cisplatin than patients with low-risk scores. The platinum-resistance-related gene signature (SLC22A2, TAP1, PC, MCM3, GTF2H2, FXYD5, SUPT6H, IGKC, and MATN2) is valuable for prognosis prediction and guidance of treatment choices for OC patients.

Our previous study demonstrated that training oncologists to provide genetic counselling for ovarian cancer patients in Malaysia, an upper-middle-income Asian country, increased uptake of genetic testing to 80% when the test was free under research. However, in practice, genetic tests are unlikely to be provided for free in low-and-middle-income countries. In this study, we explored the willingness to pay (WTP) for genetic testing among ovarian cancer patients in Malaysia. In this multi-center study, ovarian patients without prior genetic counselling were administered questionnaires on WTP (a contingent valuation exercise), facilitators and barriers to genetic counselling, and followed up for at least 6 months. We estimated the WTP value and explored factors associated with being willing to pay using logistic regression. Of 100 sequential patients recruited, 58% stated WTP for genetic testing at median of MYR1,000 (interquartile range=MYR1,125). Older participants were less likely to be willing to pay (odds ratio=0.95; 95% confidence interval=0.91-0.99). Reasons for being unwilling to pay included affordability (71%), belief that it should be paid by government or insurance (19%) and preference not to know their genetic status (14%). At the end of follow-up (mean 5±17 months), 17% took the test at full price. In this exploratory study, stated WTP for genetic testing was high but only at a reduced price. At follow-up, only a minority of patients paid the full price. A co-payment framework or subsidy scheme may be needed to reduce the significant cost barriers to genetic testing in Malaysia.

Intraperitoneal infusion of stem cell-derived natural killer cells in recurrent epithelial ovarian cancer patients: Results of the phase 1 INTRO-01 trial.

Symptom-related care and diagnoses before ovarian cancer detection: Patterns and differences by cancer stage.

The emergence of drug resistance brings new challenges to the clinical management of ovarian cancer (OC) patients. This study aimed to explore the role and mechanism of ubiquitin-specific peptidase 7 (USP7) on the bevacizumab resistance of OC. The mRNA levels of USP7 and protein tyrosine kinase 2 (PTK2) were measured using quantitative real-time polymerase chain reaction. Western blot analysis was used for detecting the protein levels of USP7, PTK2 and fused in sarcoma (FUS). Cell resistance, proliferation, apoptosis, invasion and angiogenesis were determined by cell counting kit 8 assay, colony formation assay, flow cytometry, transwell assay and tube formation assay. Glucose consumption, lactate production, and ATP/ADP ratio were used to evaluate glycolysis. The interactions between USP7 and PTK2/FUS were detected by co-immunoprecipitation assay. Mice xenograft model was also constructed to explore USP7 roles in vivo. USP7 was upregulated in OC tissues and bevacizumab-resistant cells. USP7 knockdown or its inhibitor P22077 inhibited the bevacizumab resistance of OC cells via suppressing cell growth, metastasis, angiogenesis and glycolysis. USP7 stabilized PTK2 protein expression via deubiquitinating. PTK2 overexpression reversed the effect of USP7 knockdown on the bevacizumab resistance of OC cells. Besides, FUS stabilized USP7 mRNA to regulate its protein level, and it could affect PTK2 expression by mediating USP7. USP7 knockdown enhanced the sensitivity of OC tumors to bevacizumab in vivo. FUS-stabilized USP7 enhanced the bevacizumab resistance of OC by deubiquitinating PTK2, providing a new idea for overcoming bevacizumab resistance in OC.

RECQL4 as a novel drug target against ovarian cancer.

Bisphenol A exposure modulates ovarian cancer gene expression and oxidative stress markers: a case-control study.

Objectives: BRCA1-mutated ovarian cancer is characterized by impaired DNA double-strand break repair and homologous recombination deficiency, leading to distinct tumor biology and therapeutic responses. Competing endogenous RNA networks have emerged as important regulatory mechanisms in cancer progression. This study aimed to investigate the functional and clinical significance of the HOTAIR–miR34a–CCND1 axis in BRCA1-mutated ovarian cancer. Methods: Transcriptomic and clinical data of high-grade serous ovarian cancer patients were obtained from the TCGA-OV cohort via the GDC portal. Differential gene expression analysis was performed using edgeR, while pathway enrichment analysis was conducted with clusterProfiler and KEGG. Survival analyses were evaluated using Kaplan–Meier curves. Results: The HOTAIR–miR34a–CCND1 axis displayed distinct expression profiles in BRCA1-mutated ovarian cancer tissues compared to wild-type cases. Kaplan–Meier survival analysis revealed no statistically significant differences in overall survival based on the expression levels of these genes (p > 0.05). However, KEGG pathway enrichment analysis demonstrated that these genes are involved in cancer-associated microRNA pathways, suggesting their potential role in tumor progression despite the lack of direct survival association. Conclusion: The HOTAIR–miR-34a–CCND1 axis may represent a potential prognostic biomarker and therapeutic target in BRCA1-mutated ovarian cancer, supporting the development of novel strategies such as HOTAIR inhibition, miR-34a replacement, or combination with PARP and CDK4/6 inhibitors.

ABSTRACT While our prior study identified the HLA-A *0201-restricted ACRBP epitope peptide and demonstrated its capacity to generate cytotoxic T lymphocytes (CTLs) in vitro, the clinical relevance of the peptide-induced T cell reactivity in ovarian cancer (OC) patients and the in vivo anti-tumor efficacy of these CTLs remain unexplored. In this study, dendritic cells were sensitized with ACRBP peptide (ALLVLCYSI) and co-cultured with autologous CD8+T cells to induce the production of specific cytotoxic T lymphocytes (Pep-CTLs). The anti-tumor effects of Pep-CTLs were evaluated in SCID mice bearing human ovarian cancer (OC) OVCAR-3 cells. Concurrently, we co-cultured ALLVLCYSI peptide with peripheral blood mononuclear cells (PBMCs) from OC patients (HLA-A2+, ACRBP+) and assessed the number of specific T cells using ELISPOT assays. The immunological impact of the ACRBP peptide against human OC was validated through both in vitro and in vivo experiments. These findings establish a preclinical foundationfor developing ACRBP peptide-based vaccines in OC immunotherapy. To further elucidate ACRBP’s role in OC treatment, the study analyzed single-cell RNA sequencing data from 8 OC patients and bulk RNA sequencing data from the Cancer Genome Atlas Project (TCGA) comprising 308 ovarian cancer cases. This analysis aimed to explore the heterogeneity among ACRBP-expressing tumor cell populations and to investigate the correlation between ACRBP expression and immune molecule expression (including MHC and chemokines) alongside chemotherapy response. These insights furnish a theoretical framework supporting the future application of ACRBP in tumor immunotherapy and strategies to prevent immune escape.

Prospective parallel genetic testing of both germline and tumour DNA in ovarian cancer patients (OC) is the recommended model in several different countries across the globe and the UK. The high (∼67%) chance of identifying germline PVs in patients with tumour PVs has led to a discourse surrounding the need for consent for tumour genetic testing in OC. We discussed with OC patients during focus group workshops, physicians, and charity representatives about consent options for tumour testing in OC patients: verbal consent prior to testing (Option 1) and reflex testing (Option 2). Most patients (97%; 33/34) did not feel that consent was required and were happy with reflex testing (Option 2). Physician consensus was that reflex testing was preferred and most charity representatives (4/5; 80%) agreed. All groups wanted an opt-out option and a patient information sheet about tumour testing. This can inform new recommendations in the UK and foster further discussions regarding consent for OC tumour testing.

Ovarian cancer (OC), continues to be a maximum frequent etiological factor of cancer- correlated demises in view of late-stage diagnosis and resistance to therapies. Whereas surgery and chemotherapy are canonical therapies, botherations for instance platinum resistance, tumor heterogeneity, and restricted therapeutic modalities continue. Antibody-drug conjugates (ADCs) have got advented as attractive therapeutic option regarding OC treatment specifically in patients of platinum-resistant ovarian cancer (PROC). ADCs combine monoclonal antibodies with robust cytotoxic payloads, illustrating significant plausibility in therapy of gynecologic malignancies. By selectively targeting tumor- correlated antigens, ADCs allow preciseness of drug administration whereas minimizing off-target toxicity. Presently, mirvetuximab soravtansine tisotumab vedotin got approval by the FDA for therapy of folate receptoralpha-positive PROC/ recurrent cervical cancer, In OC, ADCs targeting antigens for instance folate receptor alpha (FRα), trophoblast cell surface antigen 2 (TROP-2), mesothelin (MSLN), sodium-dependent phosphate transport protein 2B (NaPi2b), and human epidermal growth factor receptor 2 (HER2) have demonstrated promising preclinical outcomes and significant clinical activity. Nevertheless, concerns like i) antigen heterogeneity, ii) off-target toxicity, and iii) resistance mechanistic modes persist. This review emphasizes the present ADCs utilized in the clinical scenario regarding OC treatment, their botherations, and the future plausibility of ADC-based treatments in tackling resistance and leading to improved patient results. After earlier reviewing the advances in therapy of advanced OC with special emphasis on the PD1/PDL1 pathway, update on high grade serous ovarian carcinoma(HGSOC) stressing– on intra tumor heterogeneity(ITH); homologous recombination repair (HRR) pathway ; homologous recombination deficiency(HRD)and therapy with PARP hampering agents BRCA mutations in such cases following neoadjuvant chemotherapy (NACT) platinum-based chemotherapy, immune checkpoint hampering agents (ICIs), iv)chimeric antigen receptor T (CAR-T) cell therapy here we try to complete full topography of OC therapy includingADCs. Nevertheless, overcoming hurdles is needed for optimization of PROC outcomes.

Objective: To investigate the expression of microfibril-associated protein 5 (MFAP5) in ovarian cancer and its influence on malignant behavior of ovarian cancer cells. Methods: GEPIA, CSIOVDB and Kaplan-Meier Plotter online databases were used to analyze the expression of MFAP5 in various tumor tissues, especially in ovarian cancer. Immunohistochemistry was used to detect the expression level of MFAP5 in ovarian cancer tissue chip (The tissue microarray was commissioned to Zhongke Guanghua [Xi'an] Intelligent Biotechnology Co., Ltd. for processing. The specimens were sourced from Henan Provincial People's Hospital from January 2018 to March 2023), and the relationship between MFAP5 expression and the clinical characteristics of patients with ovarian cancer was analyzed using SPSS software. Kaplan-Meier Plotter online database was used to analyze the relationship between MFAP5 expression and survival prognosis of ovarian cancer patients. The ovarian cancer data sets GSE9891 and TCGA594 were downloaded from GEO and TCGA respectively, and ssGSEA was used to analyze the scores of gene sets related to epithelial mesenchymal transition, migration and invasion in ovarian cancer data sets. Next, the relationship between MFAP5 expression and the above scores was analyzed using GraphPad Prism. The expression of MFAP5 in normal fibroblasts (NFs) and cancer associated fibroblasts (CAFs) was verified by western blot. MFAP5 expression in CAFs was reduced by MFAP5-si RNA, and influence of CAFs with high or low expression of MFAP5 on malignant behavior of ovarian cancer cell SKOV3 was verified by transwell test. The influence of CAFs with high or low expression of MFAP5 on epithelial mesenchymal transition markers of ovarian cancer cell SKOV3 was verified by western blot. The CCK8 assay and 3D co-culture model were used to verify the effects of CAFs with high and low MFAP5 expression on the chemoresistance of ovarian cancer cells SKOV3. Transwell assay, western blot, and 3D co-culture model were used to explore and verify the related pathways through which MFAP5 affects the malignant behavior and drug resistance of ovarian cancer cells SKOV3. Results: Online data analysis showed that the expression of MFAP5 in ovarian cancer tissue was significantly higher than that in normal ovarian tissue (P＜0.001). Immunohistochemistry showed that the expression of MFAP5 was mainly concentrated in ovarian cancer stroma, and the later stage and the higher grade ovarian cancer tissues showed higher MFAP5 expression. Survival analysis showed that the high expression of MFAP5 was related to the poor prognosis of patients, and it was only significant in later stages and higher grades. ssGSEA analysis showed that the expression of MFAP5 was positively correlated with the scores of gene sets related to epithelial-mesenchymal transition, migration and invasion of ovarian cancer. In vitro experiments showed that reducing the expression of MFAP5 in CAFs could not only partially reduce its supportive effect on the malignant behaviors such as migration and invasion of ovarian cancer epithelial cells SKOV3 (The number of migrating cells in the control group, si-NC group, and si-MFAP5-group was 73.44±7.80, 199.74±18.26, and 91.21±6.70, respectively. The number of invading cells in the control group, si-NC group, and si-MFAP5-group was 61.62±8.76, 174.81±15.23, and 67.17±9.83, respectively), but also increase the sensitivity of ovarian cancer epithelial cells SKOV3 to chemotherapy and maintenance therapy. Further research showed that MFAP5 could activate the AKT signaling pathway in ovarian cancer cells SKOV3, and inhibiting the AKT pathway could block the supportive effect of MFAP5 on the malignant behavior and drug resistance of ovarian cancer cells. Conclusions: MFAP5 is highly expressed in ovarian cancer, especially in the stromal tissue of ovarian cancer, where the expression level is the highest. High expression of MFAP5 often indicates a poor prognosis for ovarian cancer patients. By reducing the expression of MFAP5 in CAFs, the supportive effect on the malignant biological behavior and drug resistance of ovarian cancer epithelial cells can be weakened. The underlying mechanism of this phenomenon may be related to the blockade of the AKT signaling pathway in ovarian cancer cells.

Background. Ovarian cancer is one of the most lethal gynecological malignancies. Primary cytoreductive surgery remains the standard treatment, but in high-risk patients the complication rate is substantial. Multimodal prehabilitation within ERAS protocols is a promising approach to optimize patients’ condition before surgery. The purpose was to evaluate the impact of multimodal prehabilitation on perioperative outcomes in patients with advanced ovarian cancer undergoing primary cytoreduction. Materials and methods. In this prospective observational study (2022–2024), 150 patients with FIGO stage IIIC–IV ovarian cancer and ASA III–IV status were included. Seventy-five patients completed a 7–14-day prehabilitation program (nutritional support, anemia correction, exercise, psychological counseling), while 75 historical controls received standard ERAS care only. Primary endpoints were postoperative complications; secondary endpoints included hospital stay and time to chemotherapy initiation. Results. Prehabilitation significantly improved nutritional and functional parameters, reduced hospital stay (8 vs. 14 days; p < 0.005), accelerated chemotherapy initiation (8 vs. 15 days; p < 0.005), lowered the incidence of severe complications and 30-day mortality (1 vs. 10 %). Optimal benefit was achieved with ~ 10-day programs. Conclusions. Multimodal prehabilitation improves functional status, reduces morbidity, and shortens recovery in patients with advanced ovarian cancer, supporting its integration into ERAS pathways.

Substantial clinical evidence supports the efficacy of cognitive behavioral therapy (CBT) for various diseases, particularly in oncology. However, the true impact of CBT interventions on cancer-related fatigue and mental health in patients with ovarian cancer remains unknown. To evaluate the effects of CBT on fatigue, anxiety, depression and quality of life in patients with ovarian cancer. Randomized controlled trials (RCTs) on CBT for patients with ovarian cancer were searched in the PubMed, EMBASE, Web of Science and Cochrane Library databases. According to the preferred reporting items for systematic reviews and meta-analyses statement, we formulated the inclusion and exclusion criteria, strictly screened the literatures, extracted data and performed a meta-analysis. Six RCTs with 332 ovarian cancer patients were included. Compared with the control group, cancer fatigue [mean difference (MD) = -0.98, 95% confidence interval (CI): -1.47 to -0.50], anxiety [standardized mean difference (SMD) = -0.64, 95%CI: -0.91 to -0.36] and depression levels (SMD = -0.41, 95%CI: -0.76 to -0.06) of the patients in the experimental group reduced after CBT intervention. Quality of life (MD = 1.28, 95%CI: 0.65 to 1.90) and sleep quality (MD = -0.49, 95%CI: -0.66 to -0.33) of the patients improved, and the differences between the groups were statistically significant (P < 0.01). The quality evaluation results suggested that the quality of the included RCTs was low. The meta-regression results showed that patient age and nurse guidance affected treatment outcomes, especially anxiety, whereas the specific method of CBT had a non-significant effect. CBT effectively improves mental status and cancer-related fatigue in patients with ovarian cancer undergoing chemotherapy. Future research should prioritize adequately powered RCTs with standardized outcome measures and longitudinal designs to establish sustained efficacy.

Background: Ovarian cancer (OC) remains one of the most lethal gynecologic malignancies due to its often-late diagnosis and complex molecular heterogeneity. Understanding the metabolic alterations in OC can provide insights into its pathophysiology and potential therapeutic targets. This study aimed to explore serum metabolomic profiles and their correlation with clinical and pathological features in OC patients. Materials and Methods: Thirty serum samples were collected from patients diagnosed with ovarian tumors (OTs) (n = 24 malignant, n = 6 benign) and undergoing treatment at Careggi University Hospital. Additionally, 47 samples were obtained from age-matched healthy female donors. Serum samples underwent processing and analysis using an H-NMR (Nuclear Magnetic Resonance) platform to identify a panel of metabolites. Correlation analysis between the metabolomic data and clinical parameters was performed using R software (v.4.4.0). Results: Differential metabolomic profiling showed a significant upregulation of metabolites associated with the purine salvage pathway (i.e., hypoxanthine and inosine) and the ketone bodies axis (i.e., acetone, 3-hydroxybutyrate, and acetate) in samples from ovarian tumor (OT) patients compared to healthy donors. Within malignant OC samples, metabolomic profiles significantly correlated with BRCA1/2 mutation status (BRCA1/2-mutated vs. wild-type) and homologous recombination deficiency (HRD) status. Conclusions: The analysis revealed significant variation in specific metabolites such as betaine, creatinine, carnitine, glycerol, and mannose; notably, a downregulation of these metabolites was observed in HRD-positive patients. The study identifies significant metabolomic alterations in OC, implicating pathways such as purine salvage and ketone bodies. Intriguingly, consistent variation in specific metabolites across BRCA/HRD phenotypes underscores their potential as OC biomarkers. Further research is needed to validate these findings and explore their prognostic and therapeutic implications.

Ovarian cancer is currently the gynaecological malignancy with the highest mortality rate, with a five-year survival rate of less than 50%. Combination chemotherapy regimens primarily based on platinum remain the main treatment for advanced ovarian cancer. However, while most patients initially respond sensitively to chemotherapy drugs, approximately 80% of patients develop resistance to chemotherapy drugs after repeated cycles of chemotherapy. Chemotherapy resistance is a key reason for treatment failure in patients with advanced ovarian cancer or recurrent ovarian cancer. There are many reasons for chemotherapy resistance in ovarian cancer patients, with tumor microenvironment emerging as a key focus. This "neighbor" has previously been regarded as a bystander during tumor initiation and growth. Through technological advances and deeper research, tumor microenvironment is now recognized as a critical active contributor to cancer progression, as well as chemotherapy resistance. Therefore, this paper reviews the research progress on the cellular and non-cellular components in the tumor microenvironment that contribute to chemotherapy resistance in ovarian cancer. Furthermore, we reviewed the impact of chemotherapy resistance from the perspectives of tumor hypoxia and tumor energy metabolism. Summarized the latest strategies for targeted tumor microenvironment therapy. With the aim of improving the prognosis of ovarian cancer patients, reversing chemotherapy resistance, and identifying drug treatment targets in the tumor microenvironment, this study provides new insights.

Platinum resistance remains a major obstacle to effective treatment and improved prognosis in ovarian cancer. Although 5-methylcytosine (m5C) RNA modification has been implicated in chemoresistance, its precise functional role in ovarian cancer remains unclear. In this study, we integrated RNA-Seq and single-cell transcriptomic data from cisplatin-resistant ovarian cancer cell lines and patient samples, identifying the m5C reader protein ALYREF as a key regulator of platinum resistance. Functional studies using ALYREF and NSUN2 knockdown, overexpression, and mutant constructs-combined with multi-omics analyses (RNA-Seq, m5C-BIS-Seq, and RIP-Seq)-revealed that ALYREF binds to m5C-modified LGR4 mRNA, enhancing its stability and promoting activation of the Wnt/β-catenin signaling pathway. Critically, this regulatory mechanism is dependent on NSUN2-mediated m5C modification of LGR4 mRNA. Together, our findings demonstrate that the NSUN2/ALYREF/LGR4 axis mediates platinum resistance through m5C-dependent stabilization of LGR4 and downstream Wnt signaling activation. Thus, targeting ALYREF may represent a promising strategy to overcome platinum resistance in ovarian cancer.

Ovarian cancer is characterized by aggressive metastasis, chemoresistance, and poor survival outcomes. Gaps in understanding of factors that drive these phenotypes have hindered the development of actionable therapeutic targets. We demonstrate that Zinc Finger Protein 217 (ZNF217) is a key pro-metastatic factor in ovarian cancer cells. ZNF217 overexpression dramatically increases proliferation, metastasis, and chemoresistance while its depletion impairs these phenotypes. Consistently, ZNF217 overexpression is associated with poor prognosis in both mouse models and ovarian cancer patients. Interestingly, ZNF217 induces metastatic phenotypes in fallopian tube cells, suggesting potential role in the transition of early-stage tumors to aggressive carcinoma. ZNF217's oncogenic activity is dependent on its ability to bind DNA and alter multiple processes, including EMT, that are critical in driving different aspects of cancer progression. Thus, our data establishes ZNF217 as a potent oncogene in ovarian cancer cells that impacts multiple steps in the metastatic process and a potential therapeutic target.

miR-98-3p/VEGFA axis mediates MALAT1-induced angiogenesis in ovarian tumors.

IntroductionFor ovarian cancer patients undergoing preoperative Neoadjuvant Chemotherapy (NACT), the toxicity of chemotherapeutic agents may cause hepatic and renal function impairment, altered sensitivity of the central nervous system or abnormal pain perception thresholds. These changes can further affect the metabolism and efficacy of intraoperative anaesthetics. However, the optimal intraoperative opioid dosage regimen for this specific patient population remains unclear. Currently, nociceptive stimulation monitoring technology has achieved certain progress in guiding intraoperative opioid administration. Among this technology, the index of consciousness 2 (IOC2), as a representative monitoring indicator in this field, provides important references for optimising opioid dosage regimens. This trial will investigate the opioid requirements and patient outcomes in the anaesthetic management of ovarian cancer patients undergoing preoperative NACT guided by IOC2.Methods and analysisThis prospective, single-blind, single-centre randomised controlled trial will randomly recruit 90 patients undergoing open ovarian cancer cytoreductive surgery under general anaesthesia, with equal numbers assigned to the control and experimental groups. The experimental group will adjust the remifentanil plasma target concentration based on the IOC2 value, while the control group will adjust according to the patients’ mean arterial pressure. The primary outcome will be intraoperative opioid use (calculated in morphine equivalents per hour). Secondary outcomes include the average intraoperative propofol dose, post-anaesthesia care unit (PACU)-related metrics (including extubation time, time to spontaneous eye opening and morphine consumption in PACU), pain levels at 4, 24 and 48 hours postoperatively, as well as the use of analgesics and antiemetics. Postoperative recovery quality will also be assessed, including time to first flatus, time to ambulation, length of hospital stay and the 24-hour Quality of Recovery-15 (QoR-15) score.Ethics and disseminationThis study involves human participants and was approved by the Ethics Committee of the Jiangsu Cancer Hospital (ethics no: XJS-2024-017). Patients gave informed consent to participate in the study before taking part. The study results will be published in peer-reviewed journals and presented at relevant academic conferences.Trial registration numberChiCTR2400091897.