ReviewInconclusiveLimited evidenceTier 4 · clinical
Therapeutic advances in medical oncology · Dec 2025 · review
epithelial ovarian cancerhigh-grade serous ovarian cancerovarian clear cell carcinomaendometrioid ovarian carcinomamucinous ovarian carcinomalow-grade serous ovarian carcinomaovarian carcinosarcoma
This review describes the main genomic subtypes of epithelial ovarian cancer and how those differences may help match patients to targeted therapies. It highlights PARP inhibitors, MAPK pathway inhibitors, cell cycle checkpoint inhibitors, immune checkpoint inhibitors, and antibody-drug conjugate approaches that are being investigated for specific ovarian cancer types. The article also notes that resistance to PARP inhibitors remains a problem and that more evidence is needed for effective combination therapies.
Key findings
- High-grade serous ovarian cancer is linked mainly to homologous recombination repair gene alterations such as BRCA1 and BRCA2.
- Ovarian clear cell carcinoma is associated with ARID1A and PIK3CA alterations; endometrioid ovarian carcinoma with PIK3CA and KRAS; mucinous ovarian carcinoma with CDKN2A and KRAS; and low-grade serous ovarian carcinoma with MAPK pathway genes such as BRAF and KRAS.
- PARP inhibitor therapy has improved survival for women with homologous recombination repair defects in high-grade serous ovarian cancer, but acquired resistance remains an issue.
- The review emphasizes that genomically targeted combination therapies are urgently needed and that some reported responses are preliminary.
Limitations: Review article only; no new experimental or clinical data presented in the abstract.; No quantitative outcomes or effect sizes are reported in the abstract.; The abstract is broad and does not provide trial-level details, sample sizes, or follow-up durations.; Some therapies discussed are preliminary and require further evidence..
The article is about ovarian cancer genomics and targeted therapies, not a single compound experiment.
AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text
ReviewMechanismInconclusivePreclinical onlyTier 1 · lab
Advanced pharmaceutical bulletin · Oct 2025 · review
ovarian carcinoma
This review discusses purinergic signaling in ovarian carcinoma and summarizes experimental evidence about how ATP and adenosine-related pathways may affect the tumor microenvironment. It describes roles in metastatic behavior, cell proliferation, metabolic changes, and suppression of anti-tumor immune responses. The article does not report new experimental or clinical results.
Key findings
- ATP released by tumor cells can act in the tumor microenvironment through autocrine-paracrine signaling.
- Extracellular ATP is converted to adenosine by CD39 and CD73.
- The review links purinergic signaling to metastatic phenotype, proliferation, metabolic adaptations, and immune suppression in ovarian carcinoma.
Limitations: Review article; no original experimental data.; No human or animal intervention was performed.; No quantitative effect estimates were reported..
The article is about purinergic signaling pathways in ovarian carcinoma and discusses them as potential therapeutic targets, but it is a review rather than a study of a specific compound's effect.
AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text
Human · observationalMechanismReported positiveLimited evidenceTier 3 · early humann = 21
The Journal of pathology · Sep 2025
pancreatic mucinous cystic neoplasmhepatic mucinous cystic neoplasmmucinous ovarian carcinomamucinous borderline ovarian tumor
Researchers performed immunohistochemistry, targeted DNA sequencing, and genome-wide DNA methylation profiling on a cohort of pancreatic and hepatic mucinous cystic neoplasms. They found that both pancreatic and hepatic MCNs have distinct methylation profiles within their organ landscapes and that both group with mucinous ovarian tumors in combined methylation analyses, suggesting possible shared origins.
Reported effects: pancreatic MCNs in cohort 15 · hepatic MCNs in cohort 6 · +9 more
Key findings
- Immunohistochemistry and targeted DNA sequencing were used to confirm MCN diagnoses in the studied cohort.
- Unsupervised DNA methylation analysis placed MCN-P predominantly as a distinct group within the pancreatic tumor methylation landscape.
- MCN-L demonstrated a specific methylation profile within the liver tumor methylation landscape compared with other entities.
- Both MCN-P and MCN-L grouped with mucinous ovarian carcinoma and mucinous borderline ovarian tumors (mBOTs) in the ovarian tumor methylation landscape.
- Low-grade MCNs showed greater DNA methylation similarity to mBOTs, whereas high-grade or invasive MCNs associated primarily with mucinous ovarian carcinomas.
- Across all samples (19 tumor types and four normal tissue types, n=430), MCNs grouped with mucinous ovarian tumors and normal ovarian tissue.
- Network analysis of differentially methylated probes showed MCN-P and MCN-L share significant methylation traits resembling mucinous ovarian tumors.
Limitations: Small cohort of primary interest (15 pancreatic MCNs and only 6 hepatic MCNs).; Observational, cross-sectional molecular profiling — cannot establish lineage or causality.; Findings are based on DNA methylation patterns alone (no functional or lineage-tracing experiments reported).; Potential heterogeneity and differences between reference sample sets used for comparative landscapes..
AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text
Animal studyReported positivePreclinical onlyTier 2 · animal
Nature communications · Aug 2025 · xenograft antitumor assays
neuroblastomarhabdomyosarcomacolorectal carcinomamelanomaovarian carcinomabreast carcinoma
This study tested a humanized antibody-drug conjugate called CDX0239-PBD in ALK-expressing cancer models. In cell lines, it was taken up by ALK-positive neuroblastoma cells and killed them in a way that depended on surface ALK expression. In mouse xenograft models, it produced strong antitumor activity and complete responses were maintained in several ALK-expressing cancers.
Key findings
- ALK RNA, protein, and tumor cell surface expression was elevated in multiple pediatric and adult malignancies with minimal expression in childhood normal tissues.
- CDX0239-PBD was internalized in ALK-expressing neuroblastoma cell lines with cell surface expression-dependent cytotoxicity.
- CDX0239-PBD exhibited potent antitumor efficacy including maintained complete responses in ALK-expressing patient and cell line-derived neuroblastoma, fusion-positive rhabdomyosarcoma, and colorectal carcinoma xenograft models.
Limitations: Preclinical study only; no human treatment data are reported in the abstract.; Efficacy was shown in cell lines and xenograft mouse models, which may not predict clinical benefit.; No quantitative effect sizes, dosing details, or toxicity results are provided in the abstract..
The abstract describes a preclinical anticancer antibody-drug conjugate targeting ALK-expressing tumors.
AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text
ReviewMechanismInconclusiveLimited evidenceTier 4 · clinical
Cells · Aug 2025 · review
mucinous ovarian carcinomaovarian cancer
This review summarizes recent treatment ideas and biomarkers for mucinous ovarian carcinoma, a rare type of ovarian cancer. It discusses targeted therapies such as HER2 inhibitors and KRASG12C inhibitors, as well as checkpoint inhibitors and other newer strategies. The abstract does not report results from a new experiment or clinical trial, only a synthesis of the literature.
Key findings
- Mucinous ovarian carcinoma is described as having frequent KRAS mutations and HER2 amplifications.
- The review highlights HER2 inhibitors and KRASG12C inhibitors as targeted therapy options under discussion.
- Checkpoint inhibitors are noted as potentially useful in tumors with high PD-L1 expression or tumor mutational burden.
- The abstract mentions antibody-drug conjugates, synthetic lethality approaches, and Wnt/β-catenin pathway inhibitors as emerging strategies.
Limitations: Review article only; no original patient, animal, or cell-line data in the abstract.; No quantitative outcomes, response rates, or survival data are reported.; The abstract is broad and does not specify which therapies were tested in which settings.; Potential clinical benefit is discussed as promising or potential, not demonstrated in this abstract..
This is a review of therapies and biomarkers in a specific ovarian cancer subtype, not a primary efficacy study.
AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text
Human · observationalMechanismMixed resultsLimited evidenceTier 3 · early humann = 300
Molecular therapy. Oncology · Jul 2025 · proteomic analysis of tumor and control tissue samples
epithelial ovarian cancerovarian carcinomaborderline ovarian tumorbenign ovarian tumor
The authors performed proteomic analysis on 300 patient samples across four main epithelial ovarian cancer histotypes, plus borderline and benign tumors, to find differentially abundant proteins and candidate biomarker panels. They report multiple proteins (e.g., SNCG, S100A1, VWA2, AGR2, CTH, SPINK1) that distinguish tissues, and survival analyses that linked GLYR1, RPL12, GDPGP1, and POLR2M to more favorable outcomes and SDF4, PPP3CC, EIF2AK2, and STX6 to worse outcomes. The study presents histotype-specific protein attributes that the authors propose could inform diagnosis and prognosis, but these candidates require further validation.
Key findings
- Proteomic data from 300 patient samples were used to identify differentially abundant proteins (DAPs) across EOC histotypes and control tissues.
- Identified DAPs included SNCG, S100A1, VWA2, AGR2, CTH, and SPINK1 that contributed to biomarker panels stratifying tissues.
- Enrichment of biological processes was observed to profile histotypes and involve the identified DAPs.
- Survival analysis identified candidate prognostic biomarkers with histotype-specific associations: GLYR1, RPL12, GDPGP1, and POLR2M were associated with favorable outcomes.
- Survival analysis also linked SDF4, PPP3CC, EIF2AK2, and STX6 with unfavorable outcomes.
Limitations: Observational proteomic profiling without interventional or functional validation experiments reported in the abstract.; No independent external validation cohort is mentioned in the abstract.; Abstract does not report adjustment for clinical confounders in the survival analyses.; Clinical utility of identified biomarkers is not established by this study; further validation is required..
AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed · Full text
ReviewMechanismReported positiveModerate evidenceTier 4 · clinical
International journal of molecular sciences · May 2025 · review
Mirvetuximab-soravtansineepithelial ovarian cancerhigh-grade serous ovarian carcinomaplatinum-resistant epithelial ovarian cancerovarian neoplasms This review summarizes the role of folate receptor alpha (FRα) in ovarian cancer, noting that FRα is frequently overexpressed in high-grade serous ovarian carcinoma. It describes that a VENTANA IHC assay is approved as a companion diagnostic to select patients (≥75% tumor cells with moderate to strong membrane staining) for the FRα-targeted antibody-drug conjugate mirvetuximab soravtansine, and discusses biological significance, IHC technical issues, and heterogeneity of expression across subtypes and tissue samples.
Key findings
- FRα is frequently overexpressed in several epithelial malignancies, particularly in high-grade serous ovarian carcinoma.
- The VENTANA FOLR1 (FOLR1-2.1) RxDx Assay (IHC) is now approved as a companion diagnostic for selecting patients eligible for mirvetuximab soravtansine.
- Clinical trials (SORAYA and MIRASOL) demonstrated significant clinical benefit in platinum-resistant epithelial ovarian cancer patients with high FRα expression (≥75% of tumor cells with moderate to strong membrane staining).
- The review summarizes biological significance of FRα in ovarian cancer progression and its predictive value for targeted therapy.
- Technical aspects of IHC assessment, including scoring interpretation and pre-analytical variables, are discussed.
- Heterogeneity in FRα expression across histological subtypes and tumor sites, and differences between archival versus fresh tissue, are important considerations.
Limitations: This is a review article and does not present new, individual patient-level data.; FRα expression heterogeneity across histologic subtypes and tumor sites may limit generalizability of biomarker-based selection.; IHC technical factors and pre-analytical variables can affect assessment of FRα and thus patient selection.; The companion diagnostic and demonstrated benefit apply specifically to patients with high FRα expression (≥75%), so findings may not extend to lower expressors..
AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed · Full text
ReviewInconclusiveLimited evidenceTier 4 · clinical
Biomedicines · May 2025 · narrative review
mucinous ovarian carcinomaepithelial ovarian cancer
This review summarizes what is known about mucinous ovarian carcinoma, a rare subtype of ovarian cancer with distinct molecular features such as KRAS mutations and HER2 amplifications. It discusses surgery, fertility-sparing approaches, and adjuvant therapy, and notes that targeted strategies like MEK inhibitors and HER2-directed therapies are being investigated for selected molecular subgroups. The abstract does not report new patient data or trial results.
Key findings
- MOC has frequent KRAS mutations and HER2 amplifications.
- Expansile and infiltrative histologic subtypes may guide lymphadenectomy decisions.
- Fertility-sparing surgery appears safe in FIGO stage IA expansile MOC.
- The role of adjuvant therapy in early-stage disease remains debated because of chemoresistance.
- MEK inhibitors and HER2-directed therapies are under investigation for selected molecular subgroups.
Limitations: Narrative review rather than original study.; No new experimental or clinical outcome data reported in the abstract.; No quantitative effect estimates or trial results provided.; Conclusions depend on heterogeneous retrospective cohorts, molecular studies, and guidelines..
Provides a review of molecularly informed management options for mucinous ovarian carcinoma, including discussion of targeted therapies.
AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text
ReviewMechanismInconclusiveLimited evidenceTier 4 · clinical
The Journal of pathology · May 2025 · narrative review
mucinous ovarian carcinoma
This narrative review summarizes pathological, epidemiological and molecular evidence about the cellular origins of mucinous ovarian carcinoma (MOC). The authors propose a model distinguishing Müllerian-type from gastrointestinal-type mucinous differentiation and outline possible origins including teratoma-derived tumours, lesions associated with Brenner tumours/Walthard nests, mucinous metaplasia in Müllerian tumours, and gastrointestinal metaplasia of ovarian inclusions. The model is hypothetical and the authors state it requires validation and mechanistic study.
Key findings
- MOC is a rare histotype of epithelial ovarian cancer and its cellular origin is not well established.
- The review distinguishes Müllerian from gastrointestinal-type mucinous differentiation.
- A small proportion of gastrointestinal-type mucinous tumours arise from teratoma.
- Some gastrointestinal mucinous tumours are associated with Brenner tumours and arise from associated benign lesions (Walthard nests).
- Other mucinous tumours may develop through mucinous metaplasia in established Müllerian tumours or via gastrointestinal metaplasia of epithelial or mesothelial ovarian inclusions.
- The proposed model remains to be validated and its mechanistic basis is not yet understood.
Limitations: Narrative review — no new primary experimental or clinical data presented.; Proposed model is hypothetical and unvalidated according to the authors.; Mechanistic pathways underlying the model are not established.; MOC is a rare tumour type, limiting the available direct evidence (as noted in the abstract)..
AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed · Full text
ReviewMixed resultsLimited evidenceTier 4 · clinical
International journal of gynecological cancer : official journal of the International Gynecological Cancer Society · Mar 2025
mucinous ovarian carcinoma (MOC)epithelial ovarian cancer
This narrative review summarizes controversies in diagnosis, surgery, and systemic therapy for mucinous ovarian carcinoma (MOC), a rare subtype of epithelial ovarian cancer. The authors emphasize difficulties distinguishing primary from metastatic mucinous tumors, debate fertility-sparing surgery and lymphadenectomy approaches, and note poor response to standard ovarian chemotherapy with several unvalidated alternative strategies (gastrointestinal regimens, HER2-targeted ADCs, immune checkpoint inhibitors for MSI, and combinations targeting RAS/WEE1). They recommend histologic subtyping, molecular profiling, multidisciplinary care, and international collaboration to enable larger studies and improve management.
Studied with: RAS pathway inhibitors + WEE1 inhibitors.
Key findings
- MOC is rare (<5% of epithelial ovarian cancers) and has distinct molecular, histologic, and clinical features leading to controversies in diagnosis and treatment.
- Distinguishing primary MOC from metastatic mucinous tumors (eg, gastrointestinal primaries) is challenging and misclassification can impair management, emphasizing the need for high-quality pathologic review.
- Surgical management is controversial: fertility-sparing surgery should be considered in young patients with early-stage disease, but feasibility requires careful selection; systematic lymphadenectomy has been de-escalated for expansile MOC but is recommended for early-stage infiltrative MOC.
- Advanced-stage MOC tumors are often bulky and chemoresistant; the benefit of extensive cytoreduction must be weighed against surgical morbidity.
- Systemic therapy responses to standard ovarian cancer regimens are poor; alternative approaches discussed include gastrointestinal-based chemotherapy regimens, HER2-targeted antibody-drug conjugates (eg, trastuzumab deruxtecan), immune checkpoint inhibitors for microsatellite unstable MOC, and preclinical/early-phase combination strategies targeting RAS and WEE1.
Limitations: MOC rarity limits the size of studies and clinical trial evidence available.; Diagnostic overlap with gastrointestinal primaries can lead to misclassification in clinical series.; Many alternative therapeutic strategies cited lack robust clinical validation (reliance on pre-clinical and early-phase data).; This is a narrative review and does not present new primary patient-level data or a systematic meta-analysis..
AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed
Human · observationalReported positiveLimited evidenceTier 3 · early humann = 10
BMC cancer · Dec 2024 · retrospective cohort
Trastuzumab-deruxtecan-t-dxdTrastuzumab-deruxtecanendometrial neoplasmsovarian neoplasmscervical neoplasmsuterine carcinosarcomauterine leiomyosarcomauterine serous carcinomaovarian carcinosarcomahigh-grade serous ovarian carcinomamucinous ovarian carcinomasquamous cervical carcinoma This retrospective single-center study identified 10 patients with HER2-expressing (IHC 2+/3+) recurrent or metastatic gynecological cancers who received trastuzumab deruxtecan (5.4 mg/kg IV every 3 weeks). The cohort had a median progression-free survival of 5.4 months (95% CI 0.8-9.8). Five patients had a partial response, one had stable disease at 12 weeks, and four had disease progression at initial assessment. Clinical benefit was observed mainly in tumors with HER2 IHC 3+.
Reported effects: median PFS 5.4 mo [0.8–9.8], n=10 · partial responses 5, n=10 · +2 more
Key findings
- 10 patients with recurrent/metastatic HER2-expressing gynecological malignancies were treated with T-DXd.
- Histologies included uterine neoplasms (n=5), cervical squamous carcinoma (n=1) and ovarian cancers (n=4).
- Median age was 65.4 years (25th-75th percentile, 58.1-75.2 years).
- HER2 by IHC: 5 patients were 3+ and 5 patients were 2+.
- Median number of prior therapy lines was 4 (range 2-6); 2 uterine serous carcinoma patients were pretreated with trastuzumab and 4 patients had prior immunotherapy.
- Dose: T-DXd 5.4 mg/kg IV every 3 weeks until progression/toxicity.
- Median progression-free survival (PFS) in the cohort was 5.4 months (95% CI 0.8-9.8 months).
- Responses: 5 patients had partial response (including 2 previously treated with trastuzumab), 1 patient had stable disease at 12 weeks, 4 patients had disease progression at initial assessment.
- Most patients who derived clinical benefit had HER2 IHC 3+ expression.
Limitations: Retrospective, single-center design; Very small sample size (n=10); No control or comparator arm; Heterogeneous mix of gynecologic histologies; Heavily pre-treated population limits generalizability; Limited/absent reporting of safety or adverse event data in the abstract; Potential selection and reporting bias inherent to retrospective series.
AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text
ReviewMechanismInconclusiveLimited evidenceTier 4 · clinical
Minerva obstetrics and gynecology · Dec 2024 · literature review
epithelial ovarian carcinomaovarian cancer
This review examined published data on using laparoscopy and other minimally invasive methods to predict whether primary debulking surgery can achieve no residual tumor (RT=0) in advanced epithelial ovarian cancer. The authors report that accurate assessment of intra- and extra-abdominal disease using a combination of imaging (MRI, PET, CT), surgical approaches (laparoscopy, mini-laparotomy), and blood markers (CA-125, HE4) helps determine tumor extent and can aid in personalizing the therapeutic approach. The article is a review and does not present new primary quantitative data on predictive accuracy.
Studied with: magnetic resonance imaging, positron emission tomography, computed tomography, laparoscopy, mini-laparotomy, CA-125, HE4.
Key findings
- Laparoscopy and other minimally invasive surgical methods have been analyzed as tools to predict the possibility of obtaining residual tumor of 0 (RT=0) in primary debulking surgery for advanced epithelial ovarian carcinoma.
- Accurate assessment of intra- and extra-abdominal pathology is essential to guide the surgeon in therapeutic choice.
- Combining radiological methods (MRI, PET, CT), surgical approaches (mini-laparotomy, laparoscopy), and serological markers (CA-125, HE4) provides a more complete picture for determining tumor extent and personalizing therapy.
Limitations: This publication is a literature review and presents no new primary patient-level data.; Abstract does not state whether the review was systematic or the methods used for study selection or quality assessment.; No quantitative accuracy metrics (sensitivity, specificity, predictive values) or pooled estimates are reported in the abstract..
AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed
Meta-analysisMixed resultsModerate evidenceTier 4 · clinical
Taiwanese journal of obstetrics & gynecology · Sep 2024 · systematic review and meta-analysis
Rucaparibrecurrent high-grade ovarian carcinomaovarian cancer This systematic review and meta-analysis pooled seven studies of rucaparib in patients with recurrent high-grade ovarian carcinoma. The pooled objective response rate (ORR) was 0.331 (95% CI 0.221–0.449) with high between-study heterogeneity (I2 = 92.4%), and the authors report improvements in PFS and OS versus controls. Safety signals were substantial: 98.7% experienced any treatment-emergent adverse event and 61% had grade ≥3 events; common AEs and hematologic abnormalities were reported.
Reported effects: number_of_articles 7 · ORR 0.331 [0.221–0.449] · +10 more
Key findings
- The meta-analysis of seven articles revealed a pooled objective response rate (ORR) of 0.331 (95% CI, 0.221-0.449; I2=92.4%), particularly evident in the BRCA-mutated cohort.
- Rucaparib consistently outperformed controls in progression-free survival (PFS) and overall survival (OS).
- Safety evaluations indicated that 98.7% of patients experienced treatment-emergent adverse events (TEAEs), with 61% being grade 65;3.
- Notable TEAEs included nausea (69.0%), fatigue (66.8%), vomiting (37.3%), and constipation (32.1%).
- Hematological concerns comprised anemia (47.9%), thrombocytopenia, elevated AST/ALT (37.3%), and serum creatinine levels (19.7%).
- The authors note that the rucaparib group recorded higher event rates across various metrics than controls and recommend careful monitoring and dose adjustments.
Limitations: High between-study heterogeneity (I2 = 92.4%) reported for the pooled ORR.; Pooled estimate derived from seven articles only, which may limit generalizability.; Abstract reports no numeric effect sizes (HRs/CIs) for PFS or OS despite stating improvements versus controls.; High rates of treatment-emergent adverse events and grade 65;3 events raise tolerability concerns affecting applicability..
AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed
Human · observationalMechanismReported positiveLimited evidenceTier 3 · early humann = 1
Journal of Zhejiang University. Science. B · Aug 2024 · single-cell RNA sequencing (scRNA-seq) analysis of resected primary tumor with comparison to published scRNA-seq datasets
ovarian carcinosarcomahigh-grade serous ovarian carcinoma
The authors performed single-cell RNA sequencing on a resected primary ovarian carcinosarcoma and compared the data with published high-grade serous ovarian carcinoma and other OCS datasets. They identified malignant epithelial and malignant mesenchymal cells, four epithelial subclusters (one with high BRCA1 and TOP2A expression linked to cell cycle and drug-resistance features), and a mesenchymal subcluster C14 with an OCS-specific expression pattern. They also report FGF and PTN signaling as major pathways mediating epithelial–mesenchymal communication. The study provides a single-cell transcriptomic resource for exploring OCS heterogeneity.
Key findings
- Both malignant epithelial and malignant mesenchymal cells were observed in the OCS patient sample.
- Four epithelial cell subclusters were identified; epithelial subcluster 4 had high BRCA1 and TOP2A expression and was related to drug resistance and cell cycle.
- Intercellular interaction analysis indicated FGF and PTN signaling as main pathways contributing to communication between epithelial and mesenchymal cells.
- A mesenchymal subcluster (C14) showed OCS-specific expression (elevated CYP24A1, COL23A1, CCK, BMP7, PTN, WIF1, and IGF2) and distinct characteristics compared with another published OCS tumor and normal ovarian tissue.
Limitations: Analysis appears to be from a single resected tumor/patient, limiting generalizability.; Observational transcriptomic profiling without functional validation of identified pathways or subclusters.; No clinical outcome, treatment response, or longitudinal data reported.; Comparisons rely on previously published datasets rather than additional contemporaneous samples..
AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text
Lab · in vitroFormulationReported positivePreclinical onlyTier 1 · lab
Nanoscale · Jul 2024
The authors developed zwitterionic thermoresponsive nanoparticles with an upper critical solution temperature (UCST) tuned to 43 °C to deliver paclitaxel intracellularly and release it upon hyperthermia. In cell experiments, the nanoparticles released nearly all encapsulated drug after 1 hour at 43 °C while retaining more than 95% of the payload at 37 °C, and paclitaxel-loaded nanoparticles produced greater therapeutic effects on ovarian cancer cells than non-encapsulated paclitaxel.
Reported effects: payload release after 1 h at 43 °C · payload retained at 37 °C
Studied with: paclitaxel.
Key findings
- Thermoresponsive nanoparticles (NPs) with UCST behavior were synthesized via RAFT emulsion polymerization combining polyzwitterionic stabilizers and an oligoester biodegradable core.
- The cloud point (Tcp) of the NPs was tuned to match hyperthermia treatment needs at 43 °C and used to control paclitaxel delivery.
- "The NPs released almost entirely the encapsulated drug only following 1 h incubation at 43 °C, whereas they retained more than 95% of the payload in the physiological environment (37 °C), thus demonstrating their efficacy as on-demand drug delivery systems."
- Administration of drug-loaded NPs to ovarian cancer cells produced therapeutic effects that outperformed conventional administration of non-encapsulated paclitaxel.
Limitations: In vitro cell-based study only; no in vivo or human data reported in the abstract.; Abstract does not report quantitative cytotoxicity metrics, cell line identities, sample sizes, or statistical analysis details.; No pharmacokinetic, biodistribution, safety, or long-term efficacy data presented..
AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed · Full text