ReviewReported positivePreclinical onlyTier 1 · lab
Molecular biology reports · May 2026 · narrative review
Genisteinbreast cancerovarian cancerprostate cancergliomaneuroblastomahepatocellular carcinomalung cancerbladder cancerosteosarcomarhabdomyosarcoma This is a narrative review of the biological activities and potential therapeutic roles of soy isoflavones (including genistein and daidzein). The authors summarize proposed anticancer mechanisms (estrogen receptor modulation, apoptosis, anti-angiogenesis, epigenetic effects, etc.) and report that in vitro and in vivo studies have shown promising results across a range of tumor types. They conclude that further research—especially studies combining isoflavones with established chemotherapeutics—is needed.
Studied with: chemotherapeutic agents.
Key findings
- Soy isoflavones (genistein, daidzein) have estrogenic and non-estrogenic activities including anti-inflammatory, antioxidant, and immunomodulatory effects.
- Proposed anticancer mechanisms include modulation of estrogen receptors, copper ion-dependent induction of cell death, promotion of apoptosis, inhibition of angiogenesis and metastasis, regulation of epigenetic processes, and effects on platelet function.
- Because of estrogen receptor interactions, isoflavones have been studied particularly in hormone-dependent cancers such as breast, ovarian, and prostate cancer.
- In vitro and in vivo studies have reported promising results in multiple malignancies (gliomas, neuroblastoma, hepatocellular carcinoma, lung and bladder cancers, osteosarcoma, rhabdomyosarcoma).
- Authors recommend further investigation, particularly combining isoflavones with established chemotherapeutics, to evaluate potential synergy.
Limitations: This article is a narrative review and does not present new clinical trial data.; The evidence summarized is primarily preclinical (in vitro and in vivo) with no clinical trial data provided in the abstract.; Mechanistic proposals are not proven clinical effects and require further experimental and clinical validation.; Safety and efficacy in patients, optimal dosing, and interactions with standard therapies are not established in this review..
AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed · Full text
ReviewReported positivePreclinical onlyTier 1 · lab
Molecular imaging and biology · Apr 2026
triple-negative breast cancer
This review summarizes sonodynamic therapy (SDT) as an ultrasound-driven, reactive-oxygen-species-generating approach combined with immunotherapy for triple-negative breast cancer. It covers SDT physical principles (acoustic cavitation, sonoluminescence, piezocatalysis), cell-death modes (apoptosis, ferroptosis, pyroptosis, mitophagy), innate immune pathways (cGAS-STING), and nanoplatform strategies such as oxygen-generating catalysts and GSH-depleting constructs. The authors discuss durability of anti-tumor immunity with combination therapies and outline preclinical toxicology and pharmacodynamic biomarker needs for translating SDT as an immuno-nanomedicine.
Studied with: immunotherapy.
Key findings
- SDT generates reactive oxygen species (ROS) using ultrasound and can combine localized apoptosis with systemic immune activation.
- The review integrates biophysical SDT mechanisms (acoustic cavitation, sonoluminescence, piezocatalysis) with non-apoptotic cell-death modalities (ferroptosis, pyroptosis, mitophagy).
- Innate nucleic acid receptor-sensing pathways such as cGAS-STING are discussed as immune-activating mechanisms for SDT-enhanced immunotherapy.
- Nanotechnology strategies covered include oxygen-generating catalysts, glutathione (GSH)-depleting constructs, biomimetic and stimulus-responsive carriers, and theranostic probes to address hypoxia and redox suppression.
- The review assesses durability of anti-tumor immunity induced by combination therapies and outlines necessary preclinical toxicology and pharmacodynamic biomarker studies to advance clinical implementation.
Limitations: This is a review article and does not present new primary experimental or clinical trial data.; The discussion is largely mechanistic and preclinical; the abstract does not report human clinical results or quantitative efficacy data.; Recommendations for preclinical toxicology and pharmacodynamics are outlined but specific safety or translational outcomes are not provided in this article..
AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed
Animal studyReported positivePreclinical onlyTier 2 · animal
Advanced materials (Deerfield Beach, Fla.) · Feb 2026
orthotopic breast cancer
The authors developed MeTTh-PAE nanoparticles that form hydrophobic aggregates in acidic environments and enhance cavitation-triggered sonoluminescence under ultrasound, while aggregated MeTTh promotes intersystem crossing to increase ROS generation. These nanoparticles produced enhanced sonodynamic antitumor effects in both cell-based experiments and in vivo orthotopic breast cancer models.
Key findings
- MeTTh-PAE NPs are released as hydrophobic aggregates with a rough surface in response to an acidic environment.
- The aggregated state allows for highly enhanced cavitation-triggered sonoluminescence (SL) under ultrasound.
- As an aggregation-induced emission molecule, MeTTh demonstrates a highly promoted intersystem crossing process at its aggregated state, facilitating efficient SL-to-ROS conversion.
- Combining enhanced cavitation-driven SL generation and efficient SL-to-ROS conversion in MeTTh-PAE NPs results in an excellent sonodynamic antitumor effect in both in vitro and in vivo.
Limitations: Preclinical study only: findings are limited to in vitro experiments and animal (in vivo) models, with no human data reported.; Abstract provides no sample sizes, dosing details, toxicity/safety data, or statistical measures.; Mechanistic interpretations are presented but causality and detailed pathway validation are not shown in the abstract..
AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed
Human trialSupportive careReported positiveModerate evidenceTier 4 · clinicaln = 150
JACC. CardioOncology · Dec 2025 · randomized clinical trial
Supportive carebreast cancerprostate cancer
This randomized clinical trial tested a remotely delivered, behaviorally designed gamification intervention versus attention control in Black and Hispanic breast and prostate cancer survivors with cardiovascular risk factors. Over a 24-week intervention, the gamification group increased mean daily steps and weekly minutes of moderate-to-vigorous physical activity more than the control group; some increases persisted at 12-week follow-up but were smaller and one was not statistically significant.
Reported effects: change in mean daily steps during intervention 759 [209–1309], p=0.007, n=150 · change in mean daily steps at follow-up 581 [-47–1208], p=0.07, n=150 · +2 more
Key findings
- Randomized participants: attention control (n = 76) and gamification (n = 74); mean age 64 years; 81% women; 64% Black; 35% Hispanic.
- Greater change from baseline in mean daily steps during the intervention period for gamification vs control: +759 steps (95% CI: 209-1,309; P = 0.007).
- Change from baseline in mean daily steps at follow-up: +581 steps (95% CI: -47 to 1,208; P = 0.070) for gamification vs control.
- Greater increase in weekly minutes of moderate-vigorous physical activity during intervention: +16 minutes (95% CI: 4-29; P = 0.010) for gamification vs control.
- Increase in weekly minutes of moderate-vigorous physical activity at follow-up: +11 minutes (95% CI: 0-22; P = 0.048) for gamification vs control.
- Trial name and registration: RCT of Strategies to Augment Physical Activity in Black and Hispanic Breast and Prostate Cancer Survivors (ALLSTAR); NCT05176756.
Limitations: Follow-up period after the intervention was limited to 12 weeks (postintervention), so longer-term effects are unknown.; Study population was limited to Black and Hispanic breast and prostate cancer survivors who had received cardiotoxic therapy and ≥1 cardiovascular risk factor, which may limit generalizability to other survivor groups.; Outcomes measured were physical activity metrics (steps and weekly MVPA) rather than clinical cardiovascular events or hard clinical endpoints.; The change in mean daily steps at follow-up did not reach conventional statistical significance (P = 0.070)..
Behavioral gamification was tested to increase physical activity in cancer survivors with cardiovascular risk factors, a strategy intended to lower cardiovascular risk in this population.
AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed · Full text
Case reportMechanismReported positiveLimited evidenceTier 3 · early humann = 1
Tumori · Dec 2025 · case report
breast cancerlarge-cell neuroendocrine carcinoma
This is a case report of a 34-year-old woman initially treated for HR+/HER2- breast cancer in 2012 who developed a mediastinal large-cell neuroendocrine carcinoma (LCNEC) in 2021. Next-generation sequencing identified the same pathogenic PIK3CA variant in both the breast tumor and the LCNEC, suggesting a possible metastatic relationship. The LCNEC progressed on cisplatin/etoposide but had a remarkable and prolonged response to pembrolizumab until treatment was stopped for grade 3 immune-related colitis; the patient had no clinical evidence of disease as of November 2024.
Reported effects: PD-L1 expression 10%, n=1 · tumor mutational burden (TMB) 9.54, n=1 · +1 more
Key findings
- Next-generation sequencing identified shared tumor PIK3CA pathogenic variants in both breast cancer and LCNEC tissues, suggesting a potential relationship as primary tumor and metastasis.
- The mediastinal tumor was a high-grade LCNEC lacking breast-specific markers (GATA3-, HR-, HER2-, mammoglobin-, GCDFP15-).
- PD-L1 expression was 10% and tumor mutational burden (TMB) was 9.54 mut/MB in the LCNEC specimen.
- First-line chemotherapy (cisplatin plus etoposide) led to rapid disease progression; second-line pembrolizumab produced a remarkable and prolonged disease response.
- Treatment was discontinued in 2023 because of grade 3 immune-related colitis; patient had no clinical evidence of disease as of November 2024.
Limitations: Single-patient case report limits generalizability.; Shared PIK3CA mutation suggests but does not definitively prove clonal origin between the two tumors.; No control group or broader cohort for comparison; findings are observational and hypothesis-generating..
AI summary of the abstract, human-reviewed · Aug 2026. Describes what this study reported, not medical advice. View on PubMed
ReviewReported positiveModerate evidenceTier 4 · clinical
The Journal of nutrition · Nov 2025 · review
colorectal cancerbreast cancerendometrial cancerlung cancer
This review summarizes epidemiologic evidence linking red and processed meat consumption with higher risks of multiple chronic diseases, including colorectal, breast, endometrial, and lung cancers, type 2 diabetes, cardiovascular disease, and all-cause mortality. It reports that processed meats show stronger associations than unprocessed red meat, with dose-response relationships indicating elevated risks even at moderate intakes. The authors describe plausible biological mechanisms (carcinogen formation, inflammation, gut microbiome changes, heme iron, TMAO, and metabolic effects) and note inconsistencies such as short-term randomized trial biomarker findings and modification of risk by overall diet, lifestyle, and genetics. The review concludes that minimizing processed meat and replacing red/processed meats with plant proteins, poultry, or fish is expected to reduce disease risk, and it calls for further research on causality, mechanisms, and population diversity.
Studied with: plant proteins, poultry, fish.
Key findings
- Observational studies and meta-analyses show positive associations between red/processed meat consumption and multiple chronic diseases, including colorectal, breast, endometrial, and lung cancers, type 2 diabetes, cardiovascular disease, and all-cause mortality.
- Dose-response relationships indicate elevated risks even at moderate intakes.
- Processed meats consistently show stronger detrimental associations than unprocessed red meats.
- Mechanistic pathways discussed include carcinogen formation, proinflammatory effects, gut microbiome dysbiosis, heme iron, trimethylamine N-oxide (TMAO), saturated fats, and effects on lipid metabolism and insulin resistance.
- Replacing red/processed meats with plant proteins, poultry, or fish is associated with reduced disease risk according to the review.
- Evidence complexities include inconsistent randomized controlled trial findings on short-term biomarkers and substantial modification of risk by processing, cooking methods, overall diet, lifestyle, and genetic factors.
Limitations: Predominantly observational epidemiologic evidence, which is susceptible to confounding and cannot establish causality.; Inconsistent randomized controlled trial findings limited to short-term biomarkers rather than clinical endpoints.; Heterogeneity introduced by differences in processing methods, cooking techniques, and definitions of processed versus unprocessed meat.; Potential modification of associations by overall diet, lifestyle, and genetic factors, complicating interpretation.; Identified gaps include need for greater mechanistic specificity, more diverse populations, and integrated health-environment assessments..
AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed
Animal studyReported positivePreclinical onlyTier 2 · animal
ACS applied materials & interfaces · Oct 2025 · In vitro assays (ROS generation, cytotoxicity) and in vivo murine tumor model with comparisons to monotherapy and single-membrane-coated controls; PET pretargeting imaging of membrane components.
triple-negative breast cancer
The authors developed a hybrid erythrocyte/tumor cell membrane-coated nanoprobe carrying chlorin e6 for sonodynamic therapy and tirapazamine, a hypoxia-activated prodrug. In vitro the nanoprobe generated reactive oxygen species under ultrasound and showed potent cytotoxicity; in mouse TNBC models it accumulated in tumors and produced greater tumor growth inhibition and prolonged survival versus monotherapy or single-membrane-coated controls. PET pretargeting imaging indicated immune evasion and tumor-specific accumulation of the biomimetic membrane components. Treated mice showed reduced splenomegaly and normalization of aberrant immune cell counts, and negligible toxicity was reported in the absence of ultrasound.
Studied with: sonodynamic therapy (Ce6 + ultrasound), tirapazamine (TPZ).
Key findings
- RBCm/4T1m@D-Ce6-TPZ generated reactive oxygen species (ROS) under ultrasound activation and exerted potent cytotoxicity in vitro.
- Safety evaluation reported negligible toxicity without ultrasound stimulation.
- A click-chemistry-enabled pretargeting PET imaging strategy visualized in vivo distribution of the biomimetic membrane components, validating immune evasion and tumor-specific accumulation.
- Combination sonodynamic therapy and hypoxia-responsive chemotherapy with RBCm/4T1m@D-Ce6-TPZ achieved superior tumor growth inhibition and prolonged survival in murine models compared to monotherapy or single-membrane-coated controls; ultrasound activation further enhanced efficacy.
- Treatment mitigated splenomegaly and normalized aberrant immune cell counts in treated mice, suggesting an immunomodulatory effect.
Limitations: Preclinical only: findings are from in vitro assays and mouse models; no human data reported in the abstract.; Abstract does not report sample sizes, detailed statistical results, or quantitative effect sizes.; No dosing regimen, concentration, or treatment schedule details are provided in the abstract.; Safety assessment appears limited in the abstract (notes negligible toxicity without ultrasound) with no detailed toxicology or long-term safety data.; Translatability to humans is uncertain given the murine model and absence of clinical data..
AI summary of the abstract, human-reviewed · Sep 2026. Describes what this study reported, not medical advice. View on PubMed
ReviewMechanismInconclusiveLimited evidenceTier 3 · early human
Cells · Aug 2025 · review
uterine serous carcinomaendometrial cancerbreast cancer
This is a narrative review of HER2/neu as a signaling and therapeutic marker in uterine serous carcinoma (USC). It summarizes HER2 expression and amplification in USC, compares USC HER2 features to breast cancer, evaluates preclinical and clinical evidence for HER2-directed therapies (including monoclonal antibodies and ADCs), and discusses possible mechanisms of resistance.
Studied with: monoclonal antibodies, antibody-drug conjugates, chemotherapy.
Key findings
- HER2/neu coordinates cell growth and differentiation and when overexpressed and/or amplified its downstream tyrosine kinase can become constitutively activated, causing dysregulated gene transcription.
- HER2/neu has been successfully targeted in breast cancer with monoclonal antibodies and antibody-drug conjugates.
- Use of HER2-directed therapies in gynecologic malignancies has been slower, in part due to unique characteristics of HER2 protein expression and gene amplification in USC such as major heterogeneity and lack of apical staining compared to breast cancer.
- Optimal testing algorithms for HER2/neu status in USC may have important implications for developing targeted therapies.
- The review evaluates efficacy of HER2-directed therapies in both preclinical and clinical settings and discusses possible mechanisms of resistance.
Limitations: Narrative review rather than original experimental or systematic/meta-analytic data.; Abstract contains no quantitative results or study-level sample sizes.; Conclusions depend on heterogeneous preclinical and clinical studies in the literature rather than a single controlled dataset.; Field limitations noted (e.g., heterogeneity of HER2 expression in USC) may limit generalizability of testing and therapeutic approaches..
Reviews HER2/neu expression and the potential of HER2-directed therapies in uterine serous carcinoma, with attention to diagnostic testing and resistance.
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
Human · observationalSupportive careMixed resultsModerate evidenceTier 3 · early humann = 267586
Journal of the National Cancer Institute · Aug 2025 · prospective cohort study
Supportive carecervical cancerHodgkin lymphomaprostate cancerbreast cancercolorectal cancerlung cancerendometrial canceroral cavity and pharynx cancerkidney cancerovarian cancersarcomamelanomaleukemia
Researchers followed participants in three large prospective cohorts for up to 36 years to examine whether a cancer diagnosis was associated with later atherosclerotic cardiovascular disease (ASCVD). They documented 4,334 new ASCVD events among 49,603 incident cancer cases and found that cervical cancer and Hodgkin lymphoma were associated with higher ASCVD risk, prostate cancer with slightly lower risk, and that ASCVD risk trajectories over time varied by cancer type (for example, breast cancer survivors had lower ASCVD risk for the first 7.5 years, then risk increased).
Reported effects: new-onset ASCVD events among incident cancer cases 4334, n=49603 · cervical cancer HR 1.56 [1.06–2.29] · +6 more
Key findings
- During up to 36 years of follow-up, 4,334 new-onset ASCVD events among 49,603 incident cancer cases were documented.
- Cervical cancer was associated with increased ASCVD incidence (HR = 1.56, 95% CI = 1.06 to 2.29).
- Hodgkin lymphoma was associated with increased ASCVD incidence (HR = 2.80, 95% CI = 1.89 to 4.15).
- Prostate cancer was associated with lower ASCVD incidence (HR = 0.91, 95% CI = 0.85 to 0.97).
- Breast cancer survivors experienced lower ASCVD risk during the first 7.5 years after diagnosis, but risk gradually increased afterward (Pnonlinearity = .01).
- ASCVD risk increased over time among patients with cancers of the colorectum (P = .003), lung (P = .002), and endometrium (P = .04).
- No statistically significant association with ASCVD risk was observed for cancers of the oral cavity and pharynx, kidney, or ovary; sarcoma; melanoma; or leukemia.
Limitations: Observational cohort design cannot establish causality.; Potential for residual confounding despite multivariable adjustment.; Cohorts consist of nurses and health professionals, which may limit generalizability to other populations.; Abstract does not report details on cancer stage or treatments, which could influence ASCVD risk..
AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text
ReviewInconclusiveModerate evidenceTier 4 · clinical
Breast care (Basel, Switzerland) · Jun 2025 · guideline update
early breast cancer
This paper presents the AGO (German Gynecological Oncology Group) Breast Committee's 2025 update of evidence-based recommendations for diagnosis and treatment of patients with early breast cancer. The abstract does not provide details of specific recommendations, methods, or results.
Key findings
- The article presents the 2025 update of evidence-based recommendations for the diagnosis and treatment of patients with early breast cancer.
- The abstract does not report specific recommendations, levels of evidence, or details of changes from prior guidelines.
Limitations: Abstract contains only a brief statement and provides no detail on methods, literature search, or recommendation content.; No specific recommendations, evidence grades, or actionable clinical details are reported in the abstract.; This is a guideline/review document and not a primary study of any compound or intervention..
Guideline update relevant to clinical management of early breast cancer.
AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed · Full text