Search Results (210)

Background/Objectives: Epithelial ovarian cancer (EOC) remains a gynecologic malignancy with a poor prognosis, with a 5-year survival of approximately 29% in advanced-stage disease. Despite cytoreductive surgery and platinum- and taxane-based chemotherapy, most patients relapse within 2 years. Major therapeutic barriers include chemoresistance, molecular heterogeneity, and an immunosuppressive peritoneal microenvironment. This review summarizes emerging therapeutic strategies for EOC, their mechanisms of action, and their potential to overcome treatment resistance. Methods: PubMed/MEDLINE was searched for preclinical studies, phase I–III clinical trials, systematic reviews, and meta-analyses addressing novel ovarian cancer therapies and resistance mechanisms. Results: The review covers molecularly targeted therapies, immunotherapies, metabolic and epigenetic approaches, cellular and gene therapies, targeted drug-delivery systems, and locoregional and physical modalities. Strategies include PARP inhibitors, antiangiogenic agents, antibody–drug conjugates, pathway inhibitors, immune checkpoint inhibitors, cancer vaccines, adoptive cell therapies, metabolic and epigenetic modulators, CAR-T, CAR-NK, CRISPR/Cas9, HIPEC, PIPAC, ablation, photodynamic therapy, and sonodynamic therapy. Conclusions: The clinical maturity of these approaches varies substantially. PARP inhibitors, antiangiogenic agents, selected antibody–drug conjugates, MAPK-directed therapy in LGSOC, and HIPEC in selected settings have the strongest clinical support. Most immune combinations, metabolic and epigenetic therapies, adoptive cell therapies, gene-editing approaches, and novel delivery or physical modalities remain early clinical or predominantly preclinical. Progress will depend on biomarker-guided patient selection, reassessment of evolving resistance mechanisms, and rational treatment sequencing and combinations. Full article

Polyploid giant cancer cells (PGCCs) are increasingly recognized as major drivers of therapy resistance and tumor relapse, yet the conserved molecular programs underlying their persistence remain incompletely defined. To identify genes consistently deregulated across eight independent datasets, we performed an integrative transcriptomic analysis of PGCCs derived from prostate, ovarian, and breast cancers. By focusing on consistently up- or down-regulated genes that were expressed in at least five datasets and showed a concordant direction of expression across more than 70% of datasets and met a significance threshold of adjusted p < 0.05, we defined the core regulatory architecture stabilizing the PGCC state under therapeutic stress. Our analysis reveals that PGCCs exhibit a paradoxical ranscriptomic signature consistent with cytolytic activity alongside reduced immune detection. These cells activated pro-inflammatory cytokine and chemokine signaling while simultaneously engaging immune-evasion mechanisms, including PD-L1-associated and virus-like escape programs. Concurrently, PGCCs displayed transcriptional features characteristic of immune-privileged cellular states, including embryonic development, reproductive programs, senescence-associated survival, apoptosis resistance, and deep dormancy marked by coordinated suppression of major housekeeping processes. Notably, PGCCs also activated neuronal differentiation and neurodegeneration-associated pathways, including axon guidance, neurogenesis, and calcium signaling. This neuron-like, calcium-dependent stress adaptation program may further enhance immune privilege and long-term survival capacity. We propose that PGCCs represent an immune-adaptive polyploid survival state in which inflammatory and ontogenetic pathways are repurposed to support immune evasion and tumor persistence. By identifying actionable vulnerabilities within calcium signaling, neuronal mimicry, and checkpoint-associated pathways, this study provides a framework for therapeutic strategies aimed at dismantling the PGCC reservoir and preventing tumor relapse. Full article

Obesity is a chronic, relapsing disease and a significant oncological risk factor. The correlation is most pronounced and consistent for endometrial cancer. Conversely, evidence linking obesity to ovarian cancer is less robust and varies by histotype, while the association with cervical cancer is influenced by factors related to screening, diagnosis, treatment, and survival. This review examines obesity, particularly class III (morbid) obesity, in relation to the risk of gynaecological cancer, diagnostic approaches, and management strategies. A structured narrative review of PubMed/MEDLINE, Cochrane Library, Scopus and Web of Science Core Collection was conducted for literature published between January 2000 and December 2025. Eligible evidence included systematic reviews, meta-analyses, cohort and case–control studies, mechanistic studies and clinical guidance relevant to obesity and endometrial, ovarian or cervical cancer. Title/abstract screening and full-text selection were conducted using predefined criteria for conceptual relevance and clinical applicability. Excess adiposity contributes to endometrial carcinogenesis through hormonal dysregulation, insulin resistance and hyperinsulinaemia, adipokine imbalance, chronic inflammation, and oxidative stress. In ovarian cancer, associations are generally weaker but appear more relevant for selected histological subtypes and cumulative adiposity exposure. In cervical cancer, obesity should not be interpreted as replacing HPV-driven pathogenesis; rather, it may affect screening adequacy, treatment selection, perioperative risk, and disease-specific survival in morbidly obese patients. Current evidence does not support morbid obesity as an independent driver of all gynaecological cancers. It supports obesity as a major modifiable risk factor and clinical modifier, particularly for endometrial cancer, and highlights the need for pragmatic risk stratification based on BMI class, adiposity distribution, metabolic comorbidity, functional status and cancer-site-specific pathways. Biomarker evidence remains hypothesis-generating, and obesity-integrated oncological pathways require prospective validation in patients with a BMI ≥ 40 kg/m². Full article

Background: Tight junctions are major components of apical junction complexes and are crucial for the maintenance of cell polarity, healthy tissue architecture, adhesion, and permeability. These junctions include the claudin family of transmembrane proteins, which act as paracellular barriers to regulate selective permeability. Abnormal claudin expression disturbs cell adhesions and is associated with cancer through promoting cell invasion, migration, and metastasis. Claudin 6 (CLDN6) overexpression, in particular, is linked to several types of cancer with malignant phenotypes. The present study aimed to investigate the association between CLDN6 protein expression and its copy number variations (CNVs) with clinicopathological features and survival outcomes of ovarian cancer (OC) patients. Methods: A total of 114 formalin-fixed paraffin-embedded blocks from primary OC patients were used to construct tissue microarray slides. Automated immunostaining was used to assess CLDN6 protein expression levels, and next-generation knowledge discovery platforms were used to further evaluate CLDN6 CNV levels using The Cancer Genome Atlas open-source data. The relationships between CLDN6 CNVs and tumor stage, overall survival, disease-specific survival (DSS), and disease-free survival (DFS) were investigated. Results: This study demonstrated that CLDN6 had a mixed membranous-cytoplasmic expression pattern. The cytoplasmic expression of CLDN6 was significantly associated with tumor stage (p = 0.05), tumor size (p = 0.04), and recurrence (p = 0.05). In Univariate analysis, Kaplan–Meier analysis demonstrated that CLDN6 expression was significantly correlated with DFS (p = 0.01). OC patients with lower cytoplasmic CLDN6 expression levels lived longer and had lower recurrence rates. These findings were further confirmed through CLDN6 CNVs analysis, where OC with lower CLDN6 cytoplasmic expression positively correlated with longer DFS and DSS. No independent prognosticator was found when using Cox-regression multivariate analysis (p > 0.05). Conclusions: These results suggest CLDN6 as an interesting prognosticator to identify OC patients at a higher risk of recurrence in order to provide personalized management, alleviate the burden of this disease on women’s health, and improve their survival outcomes. Full article

Epithelial ovarian cancer (EOC) remains one of the most lethal gynecologic malignancies, largely owing to advanced-stage presentation, high rates of relapse, and the eventual emergence of therapeutic resistance. Despite the transformative success of immune checkpoint inhibitors (ICIs) across multiple solid tumors, their clinical impact in ovarian cancer has been comparatively modest. This literature review provides a comprehensive synthesis of recent advances in ICI strategies for ovarian cancer (OC), with particular emphasis on phase II and III clinical trials evaluating programmed cell death protein 1 (PD-1), programmed death-ligand 1 (PD-L1), cytotoxic T-lymphocyte–associated protein 4 (CTLA-4), and T cell immunoglobulin and mucin-domain-containing-3 (TIM-3)-directed therapies. Accumulating evidence indicates that PD-1/PD-L1 monotherapy yields limited clinical activity in unselected OC populations, with low objective response rates and minimal survival benefit. Dual checkpoint blockade with PD-1 and CTLA-4 inhibitors demonstrates enhanced antitumor activity, particularly in clear cell ovarian carcinoma (CCOC), albeit at the expense of increased immune-related toxicity. Large randomized trials incorporating ICI into first-line chemotherapy or maintenance settings have largely failed to improve outcomes in biomarker-unselected cohorts. Available evidence demonstrates that combinatorial approaches integrating ICI with anti-angiogenic agents, PARP inhibitors, or neoadjuvant chemotherapy provide modest benefit in selected molecular and histologic subgroups. Early-phase investigations of TIM-3–targeting strategies further expand the immunotherapeutic landscape, although clinical efficacy remains preliminary. Current evidence underscores that OC is not uniformly responsive to immunotherapy and that rational combination strategies, biomarker-driven patient selection, and improved understanding of tumor immune microenvironment heterogeneity are essential to unlocking the full therapeutic potential of ICI in this disease. Full article

Ovarian cancer is the most lethal gynaecological cancer, largely because it is often diagnosed late and shows strong tumour heterogeneity, therapy resistance, and rapid metastatic spread. A key driver of this aggressive behaviour is the tumour’s ability to reshape its surrounding microenvironment to support invasion, angiogenesis, and escape from treatment. Cathepsin L (CTSL), a lysosomal cysteine protease, has emerged as an important mediator of these processes and is gaining attention as both a prognostic marker and a potential therapeutic target. This review examines the diverse roles of CTSL in ovarian cancer progression, focusing on how its expression, localisation, and extracellular release are altered within the hypoxic and acidic conditions typical of the tumour microenvironment. It also outlines emerging therapeutic strategies aimed at targeting CTSL, including selective inhibitors, multi-cathepsin approaches, CTSL-activated prodrugs and antibody-drug conjugate linkers, and nanomedicine systems designed for tumour-specific delivery. Overall, the evidence highlights CTSL as a central regulator of invasion, angiogenesis, and relapse in ovarian cancer, underscoring its potential as a target for new therapies in aggressive disease. Full article

Background: Recurrence poses a major challenge in epithelial ovarian cancer (EOC), often occurring despite optimal first-line therapy. Dormant cancer cells are believed to play a key role, yet the mechanisms driving their reactivation remain unclear. This study examined whether exosomes released by normal peritoneal mesothelial cells (PMCs) and fibroblasts (PFBs) undergoing iatrogenic senescence after carboplatin and paclitaxel exposure contribute to EOC recurrence. Methods and Results: Senescent PMCs and PFBs secreted markedly more exosomes, identified by CD9, CD63, and CD81, compared with young cells. Exosomes from both cell types more effectively reactivated dormant EOC cells (pEOCs, A2780, OVCAR-3, SKOV-3) than non-exosomal medium constituents. Importantly, senescent PMC-derived exosomes most strongly reactivated pEOCs and SKOV-3, whereas those from senescent PFBs exerted greater effects on pEOCs, OVCAR-3, and SKOV-3. Kinetic studies of exosome internalization revealed that this process was generally more efficient in the presence of exosomes derived from senescent cells compared with those from young donor cells. Compositional analysis revealed distinct profiles between young and senescent exosomes compared in two variants: young PMCs/senescent PMCs and young PFBs/senescent PFBS. Senescent PMC exosomes displayed reduced miR-210-3p, miR-409-3p, and miR-421, alongside elevated MMP1, MMP3, and VEGF, while senescent PFB exosomes showed increased amphiregulin and osteopontin but lower MMP1, MMP3, TIMP1, bFGF, VEGF, and HGF. Functionally, senescent PMC exosomes enhanced pEOC migration, invasion, and spheroid formation, and induced the expression of CCL11 and ABCB1. Senescent PFB exosomes promoted migration and upregulated CCL11, TGF-β1, BIRC5, and CHEK1. Conclusions: These findings suggest that therapy-induced senescence in peritoneal cells may contribute to EOC recurrence by reactivating dormant tumor cells through exosomal signaling. Full article

Background/Objectives: High-grade serous ovarian cancer (HGSOC) is usually discovered in advanced stages and often relapses shortly after initial conventional therapy. Survival in HGSOC patients might be improved with the use of novel immune therapies, which potentiate autologous anti-tumor responses. Dendritic cells (DCs) are potent antigen-presenting cells that can initiate immune responses, activate cytotoxic T cells and drive T-cell differentiation. This pilot trial evaluated the safety and efficacy of a unique DC vaccine (α-DC-1) in relapsed, advanced HGSOC patients with minimal tumor burden. Methods: Monocytes from patient leukaphereses were used to propagate a unique autologous DC, the α-DC-1, generated with granulocyte–macrophage colony-stimulating factor and interleukin-4, pulsed with keyhole limpet hemocyanin (KLH) and tumor lysate (from debulking surgery) on day 5, and matured with a cocktail of cytokines and chemokines on day 6. Mature α-DC-1 were harvested on day 7 and administered intranodally (inguinal nodes) every other week for three doses/cycle for up to three DC vaccine cycles (nine vaccines). The primary endpoints were progression-free survival (PFS) and overall survival (OS). Results: In 19 patients treated, the median PFS was 9.7 months (95% CI: (5, NA)) and the median OS was 42.2 months (95% CI: (31.2, 68.3)). In 5/19 (26.3%) patients, OS exceeded five years. Administration of six or more vaccines was associated with a significant improvement in PFS. No grade 2 or higher toxicities were noted. Conclusions: Our α-DC-1 vaccine was safe, and 94.2% elicited an immune response to KLH. The long OS, exceeding 5 years in some patients, suggests this DC vaccine may improve survival for some with relapsed HGSOC. Full article

Ovarian cancer (OC) remains one of the leading causes of gynecologic cancer mortality, largely due to late diagnosis, frequent relapse, and the emergence of chemoresistance. An important but often-overlooked contributor to treatment failure is the heterogeneous penetration of anticancer drugs within tumors. Structural and biochemical barriers—including abnormal vasculature, elevated interstitial pressure, dense extracellular matrix, drug efflux transporters, and malignant ascites—generate steep intratumoral concentration gradients that conventional preclinical models fail to capture. As a result, systemic pharmacokinetic measurements frequently provide limited insight into tumor-level drug exposure. Patient-derived organoids (PDOs) have emerged as physiologically relevant 3D models that preserve the genetic, architectural, and functional characteristics of the original tumor. These systems enable controlled investigation of pharmacokinetic and pharmacodynamic processes, including drug penetration, metabolism, retention, and exposure–response relationships. Adding cell-free malignant ascites supernatant enhances PDOs’ ability to mimic the metastatic peritoneal microenvironment of OC. This review discusses recent advances in PDO technologies and examines how PDO-derived data can inform intratumoral pharmacokinetics and dosing strategies using physiologically based pharmacokinetic modeling and in vitro–in vivo extrapolation. Emerging hybrid platforms, including organoid-on-chip systems, vascularized co-cultures, and multi-omics integration, are crucial to improve translational prediction and support precision oncology. Full article

Background/Objectives: Ovarian cancer (OC) remains the most lethal gynecologic malignancy, largely due to late-stage diagnosis and high rates of recurrence following platinum-based chemotherapy. Growing evidence implicates cancer stem-like cells (CSCs) in OC relapse, as these cells exhibit enhanced chemoresistance, stemness, epithelial–mesenchymal transition (EMT), and the capacity to remodel the tumor microenvironment. Inhibitors of DNA-binding (ID) 1-4 proteins are transcription factors with known redundancy; however, their collective role in OC chemotherapy response remains poorly defined. Here, we examined how ID family signaling responds to chemotherapy and contributes to CSC-associated features and microenvironment remodeling. Methods: Publicly available patient data, OC cell lines, and a subcutaneous xenograft mouse model were used to correlate changes in ID1-4 expression with CSCs, EMT, and the tumor microenvironment (TME). OC cell lines were used for in vitro assays to evaluate CSC features and IL-6 production in the presence of carboplatin and/or a small molecule inhibitor of ID proteins, AGX51. Results: Analysis of clinical datasets, cell lines, and in vivo models revealed enrichment of ID1-4 following chemotherapy, with additive increases across treatment cycles. In vivo ID2 and ID4 expression was associated with IL-6 secretion and loss of anti-tumoral macrophages. Pan-ID inhibition demonstrated that cumulative ID activity minimally supports CSC maintenance during chemotherapy, while more strongly regulating IL-6 secretion. Conclusions: IL-6 production from cancer cells was at least partially dependent on ID proteins, linking collective ID signaling to microenvironment remodeling and relapse potential in ovarian cancer. Full article

Ovarian cancer (OC) is frequently diagnosed at an advanced stage and characterized by high rates of recurrence despite aggressive cytoreductive surgery and chemotherapy. Relapse is driven by microscopic residual tumors that are disseminated most often throughout the peritoneal cavity, posing significant challenges with conventional systemic therapy. Targeted alpha-particle therapy (TAT) combines molecular targeting with alpha-emitting radionuclides to deliver highly potent and localized cellular damage, uniquely suited for the eradication of small OC tumor clusters within the peritoneal cavity. We conducted an extensive literature search for clinical trials (clinicaltrials.gov) and pre-clinical studies (PubMed, Scopus, Google Scholar) between September 2025 and November 2025. Peer-reviewed articles published in English over the past 20 years that used OC mouse models with reported treatment data were included. Review articles without original data and clinical trials that have been terminated or withdrawn were excluded. In this review, we (1) summarize the biological and physical rationale supporting the use of TAT in OC, (2) discuss the relevant molecular and immunological anti-tumor mechanisms, and (3) critically evaluate early treatment outcomes of 19 pre-clinical and four clinical studies with respect to efficacy, safety, and feasibility. Despite the progress and promising survival outcomes, several challenges remain, including heterogeneous antigen expression, delivery and retention within the peritoneal cavity, off-target toxicity, radiation resistance, radionuclide availability, dosimetry uncertainties, and limitations in clinical trial design. We highlight future directions to overcome these barriers and the continued multidisciplinary efforts essential to translate TAT into effective clinical strategies to treat advanced stages of OC and other solid tumors resistant to conventional treatment. This work was supported with funding available to Kurt R. Zinn as the Hickman Family Endowed Chair in Oncology at Michigan State University. Full article

Background: Poly(ADP-ribose) polymerase inhibitor (PARPi) treatment in ovarian cancer patients after first-line chemotherapy and following the response to platinum-based chemotherapy at relapse is associated with survival benefits. Maintenance therapies can be administered over extended periods, making treatment tolerability assessment essential in optimizing patient outcomes. This cohort study aimed to evaluate the agreement between physician and patient reporting of PARP inhibitor-related toxicities and the rate of underestimation of each symptom considered. Methods: Patients treated with PARPis in the first-line or recurrent setting were included. A specific Patient-Reported Outcomes Common Terminology Criteria for Adverse Events (PRO-CTCAE) questionnaire was generated and administered to the cohort. For each toxicity, agreement between patients and physicians was assessed using Cohen’s kappa and Gwet’s AC1; in addition, the rate of toxicity under-reporting by physicians was calculated. Results: Seventy-seven ovarian cancer patients were included; 39 (50.6%) received PARPis in the first-line setting, while 38 (49.4%) were treated for recurrence. Cohen’s kappa values for agreement between patients and physicians across 12 reported toxicities ranged from 0 to 0.15, indicating poor agreement (κ < 0.20) for all assessed toxicities, with the lowest levels of agreement for decreased appetite (κ = 0), rash (κ = 0.02), headache (κ = 0.00), arthralgia (κ = 0.03), insomnia (κ = 0.03), and fatigue (κ = 0.04). When agreement was assessed using Gwet’s AC1, agreement remained poor to moderate for the majority of the symptoms evaluated. Physician under-reporting rates were higher for nausea (51.9%), rash (57.1%), headache (49.3%), arthralgia (70.2%), insomnia (48.1%), and fatigue (67.5%). Conclusions: Our results underscore the importance of systematically integrating patient-reported outcomes into clinical practice, including in maintenance settings, to ensure an accurate assessment of treatment-related toxicities. Full article

Ovarian cancer (OC) remains the leading cause of death among gynecologic cancers. Most women diagnosed with OC at advanced stages eventually develop relapse and chemoresistance, leading to poor clinical outcomes. While piRNAs have emerged as critical regulators of gene expression and tumor biology, their specific roles in OC remain to be fully elucidated. This study integrated clinical and computational analyses to investigate the expression pattern and functional relevance of P-element-induced wimpy testis (PIWI)-interacting RNA-823 (piR-823) and its associated protein piwi-like RNA-mediated gene silencing 1 (PIWIL1)/DNA methyltransferase 3B (DNMT3B)/E-cadherin (CDH1) axis in OC tissues from 40 patients, with 20 non-cancer control samples. Expression profiling was performed using qPCR on OC and normal ovarian tissues, followed by correlation and regression analyses. Public databases, including GEPIA, TNM plot, and MethBank, were explored to validate gene expression, methylation status, and pathway enrichment. Our results revealed that piR-823, PIWIL1, and DNMT3B were significantly upregulated in OC tissues (p < 0.001, p = 0.009, and p < 0.001, respectively), and they correlated positively with each other and inversely with CDH1 expression. CDH2, OCT4, and NANOG were significantly upregulated (p = 0.011, p = 0.03, and p < 0.001, respectively), whereas CDH1 expression was significantly downregulated (p < 0.001) in OC tissues. In silico analyses supported DNMT3B-mediated CDH1 promoter methylation, epithelial–mesenchymal transition (EMT), and stemness pathway enrichment. Our integrated computational and clinical analyses indicate that the piR-823/PIWIL1/DNMT3B/CDH1 axis is a putative epigenetic regulator of EMT and cancer stemness in ovarian cancer. Additionally, piR-823 may serve as a promising prognostic biomarker and therapeutic target, offering novel insights into OC pathogenesis and treatment. Full article

The ovary, as the primary organ responsible for reproduction and new life, plays a central role in female development, maturation, and health. Neoplasms arising from the ovary and its associated tissues exhibit substantial heterogeneity in their histopathological and molecular profiles, many of which remain poorly understood. This review aims to summarize recent advances in the understanding of genetic alterations underlying ovarian neoplasms and to explore therapeutic strategies informed by molecular biomarkers and tumor microenvironmental factors. A comprehensive literature search was performed, focusing on genomic alterations, biomarker-guided therapies, and tumor microenvironmental modulation in ovarian cancers. Emphasis was placed on studies addressing lipid mediator pathways and their roles in immune regulation and therapeutic response. Based on diagnostic classifications, recurrent alterations in TP53, MYC, PIK3CA, and KRAS are consistently observed across epithelial and germ cell ovarian tumors, whereas non-epithelial subtypes such as sex cord–stromal tumors (SCSTs) and small-cell carcinoma of the ovary, hypercalcemic type (SCCOHT), are predominantly associated with ARID1A and SMARCA4 mutations, respectively. These findings highlight distinct pathogenic mechanisms linked to specific genetic alterations and reveal potential therapeutic vulnerabilities. Moreover, lipid metabolism has been closely implicated in immune surveillance through STING signaling cascades within innate immune cells, suggesting that lipid mediators and their associated genes may represent promising therapeutic targets in ovarian cancers (OCs). Targeting lipid mediators could be particularly effective in relapsed OCs, as modulating innate immune cells within the tumor microenvironment (TME) may enhance immune surveillance and improve antitumor responses. Integrating genetic and microenvironmental insights offers a promising direction for developing more effective and personalized therapeutic strategies in OC. Full article

High-grade serous ovarian carcinoma is the most common and aggressive form of ovarian cancer, accounting for over 60% of cases and nearly 75% of deaths, mainly due to late diagnosis and tumor aggressiveness. Standard treatment is platinum-based chemotherapy with paclitaxel, but relapse is frequent. This study aimed to identify prognostic biomarkers for patients with poor survival outcomes after Taxol treatment using bioinformatics analysis. We examined the effects of TGFB2 mRNA expression and other markers on overall survival in serous ovarian cancer using the TCGA database, applying a multivariate Cox model that included interaction terms to identify TGFB2-dependent and independent prognostic markers, and controlling for age and treatment type. Candidate TGFB2-independent prognostic markers from TCGA were further validated using patient data from the KMplotter database. High TGFB2 mRNA expression emerged as a prognostic biomarker for three potential gene targets (TRPV4, STAU2, and HOXC4) associated with improved OS at low levels of gene target expression, we identified four additional markers (CLIC3, ANPEP/LAP1, RIN2, and EMP1) that exhibited a TGFB2-independent negative correlation between mRNA expression and OS across the full spectrum of gene expression values in the ovarian cancer cohort validated using independent dataset from KMplotter, for Taxol-treated ovarian cancer patients. This study proposes a panel of potential prognostic biomarkers for the treatment of ovarian cancer patients, particularly by leveraging TGFB2-dependent mRNA expression as a significant biomarker, alongside four additional TGFB2-independent prognostic markers, for patients undergoing Taxol-based therapies. Future prospective clinical trials will be required to validate these prognostic markers. Full article