These are reviewed studies whose abstracts concern Breast Invasive Ductal Carcinoma (IDC). Each describes only what that study reported. This is not a claim by OncoForge that any compound helps or harms Breast Invasive Ductal Carcinoma (IDC). Most are early lab, animal, or small human studies, and findings often conflict.
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
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
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
Lab · in vitroReported positivePreclinical onlyTier 1 · lab
Journal of medical physics · Oct 2024
breast cancer (MCF-7 cell line)
Researchers synthesized cobalt ferrite (CoFe2O4) nanoparticles by chemical co-precipitation, characterized their structural and magnetic properties, and measured a zeta potential of -0.0048 V (4.8 mV). In vitro tests on MCF-7 breast cancer cells showed decreased cell viability with increasing nanoparticle concentrations; antimicrobial activity was also reported. The authors state the zeta potential was higher than that of MCF-7 cells and interpreted this as indicating effectiveness.
Reported effect: zeta potential -0.0048
Key findings
- CoFe2O4 nanoparticles synthesized by chemical co-precipitation showed cubic structure, ferrite phase, and spherical magnetic nature.
- The zeta potential was found to be - 0.0048V (4.8 mV).
- Cytotoxicity analysis exhibited decreased cell viability with increasing concentrations of CoFe2O4 nanoparticles (in vitro, MCF-7 cells).
- Antimicrobial studies displayed good inhibiting properties.
- The authors state the zeta potential of the synthesized CoFe2O4 nanoparticles was higher than that of the breast cancer cells (MCF-7) and interpreted this as proof of effectiveness.
Limitations: In vitro study only (no animal or human data).; Abstract does not report quantitative cytotoxicity metrics (no percent viability values, no concentrations, no sample sizes, no statistical values).; No experiments described that apply magnetic hyperthermia (despite the stated aim).; No control or comparator details reported in the abstract.; Zeta potential value presentation is internally inconsistent (reported as "- 0.0048V (4.8 mV)") and lacks context for biological interpretation.; No mechanistic molecular data reported; conclusions about efficacy appear to be interpretive rather than demonstrated in vivo..
AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed · Full text
Animal studyReported positivePreclinical onlyTier 2 · animal
Advanced science (Weinheim, Baden-Wurttemberg, Germany) · Jul 2024
breast cancer (4T1 murine model)
This preclinical mouse study tested layered double hydroxide nanosheets loaded with the PAD4 inhibitor YW3-56 combined with ultrasound (sonodynamic therapy). The nanoagent generated reactive oxygen species under ultrasound, induced immunogenic cell death, inhibited PAD4-mediated citrullinated histone H3 and NET release, boosted immune-activated cells and M1 macrophages, lowered PD-1 expression, reduced primary tumor growth (69.5% tumor inhibition rate) and decreased lung metastases in a 4T1 model. These results are from an animal model and not from human trials.
Reported effect: tumor inhibition rate 69.5%
Studied with: ultrasound (sonodynamic therapy), a-CoW-LDH nanosheets (nanostructure delivery).
Key findings
- a-CoW-LDH nanosheets act as a sonosensitizer to generate abundant ROS under ultrasound irradiation.
- Loading YW3-56 onto a-CoW-LDH (a-LDH@356) plus ultrasound induced ROS generation and immunogenic cell death.
- YW3-56 inhibited elevation of citrullinated histone H3 (H3cit) and the release of neutrophil extracellular traps (NETs).
- Combination therapy upregulated the proportion of immune-activated cells and induced M1 macrophage polarization.
- Combination therapy downregulated PD-1 expression on immune cells under ultrasound irradiation.
- In the 4T1 tumor model the combination arrested primary tumor progression with a tumor inhibition rate of 69.5%.
- The combination also prevented tumor metastasis, producing the least number of lung metastatic nodules among groups tested.
Limitations: Study performed in a single animal tumor model (4T1 murine breast cancer); no human data.; Abstract does not report sample sizes, randomization, or blinding.; Dose, dosing schedule and detailed toxicity/safety data are not reported in the abstract.; Long-term outcomes and durability of anti-metastatic effect are not described.; Mechanistic and translational relevance to humans remains unproven..
Preclinical demonstration that PAD4 inhibition delivered via LDH nanosheets can augment sonodynamic therapy, reduce NETs, and enhance anti-tumor immune responses to limit primary tumor growth and metastasis in a murine breast cancer model.
AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed · Full text
Animal studyReported positivePreclinical onlyTier 2 · animal
Journal of nanobiotechnology · Jun 2024
breast cancerbreast cancer bone metastasis
The authors created IR780-loaded PLGA nanoparticles coated with a hybrid membrane made from breast cancer cell membranes and bacterial outer membrane vesicles (IR780@PLGA@HM). In cell and mouse (4T1) experiments the nanoparticles showed good biocompatibility, targeted tumors, promoted macrophage type I polarization and dendritic cell activation, increased anti-tumor inflammatory factor expression, and reduced tumor burden in vitro and in vivo, suggesting potential for sonodynamic therapy against breast cancer bone metastasis.
Studied with: sonodynamic therapy, PLGA nanoparticle delivery.
Key findings
- Constructed IR780@PLGA@HM nanoparticles combining cancer cell membrane and bacterial OMV.
- Nanoparticles had good biocompatibility (as reported).
- Effectively targeted 4T1 tumors (as reported).
- Promoted macrophage type I polarization and dendritic cell activation.
- Enhanced expression of anti-tumor inflammatory factors.
- Demonstrated the ability to effectively kill tumors both in vitro and in vivo in the reported experiments.
Limitations: Preclinical study only: results reported from in vitro and mouse models, no human data.; Abstract provides no sample sizes, quantitative outcome measures, or statistical values.; No dosing regimen, safety/toxicity details, or follow-up duration provided in the abstract.; Unclear whether appropriate controls or randomized comparisons were used (not described in abstract).; Translation from mouse 4T1 model to human breast cancer bone metastasis is uncertain..
AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed · Full text
Human · observationalReported positiveModerate evidenceTier 3 · early humann = 4332
JAMA oncology · Apr 2024 · International longitudinal cohort study
breast cancerovarian cancerperitoneal cancer
This international cohort study followed 4,332 women with pathogenic BRCA1 or BRCA2 variants (no prior cancer) to evaluate whether self-reported bilateral oophorectomy was associated with mortality. After a mean 9.0 years, oophorectomy was associated with lower age-adjusted all-cause mortality (HR 0.32); HRs were 0.28 for BRCA1 and 0.43 for BRCA2 carriers. Estimated cumulative all-cause mortality to age 75 was lower for women who had oophorectomy at age 35 versus those who did not (BRCA1: 25% vs 62%; BRCA2: 14% vs 28%).
Reported effects: cohort_size 4332, n=4332 · deaths_total 228, n=4332 · +5 more
Key findings
- Cohort included 4,332 women (mean age, 42.6 years); 2,932 (67.8%) underwent preventive oophorectomy at a mean age of 45.4 years.
- After mean follow-up of 9.0 years, 851 women developed cancer and 228 died (57 ovarian/fallopian tube cancer, 58 breast cancer, 16 peritoneal cancer, 97 other causes).
- Age-adjusted HR for all-cause mortality associated with oophorectomy: 0.32 (95% CI, 0.24-0.42; P < .001).
- Age-adjusted HR for all-cause mortality for BRCA1: 0.28 (95% CI, 0.20-0.38; P < .001); for BRCA2: 0.43 (95% CI, 0.22-0.90; P = .03).
- Estimated cumulative all-cause mortality to age 75 for oophorectomy at age 35 versus no oophorectomy: BRCA1 25% vs 62%; BRCA2 14% vs 28%.
Limitations: Observational cohort design with no randomization, so results may be affected by confounding.; Oophorectomy status was self-reported via questionnaire.; Potential for residual confounding or selection bias not addressed in the abstract.; Mean follow-up of 9.0 years may limit capture of longer-term outcomes..
AI summary of the abstract, human-reviewed · Jul 2026. Describes what this study reported, not medical advice. View on PubMed · Full text
Human · observationalMechanismReported positiveLimited evidenceTier 3 · early humann = 500
Biochemical genetics · Dec 2023 · Retrospective computational analysis of TCGA and TCGASpliceSeq RNA-seq and ASE data
prostate adenocarcinomabreast cancer
The authors analyzed RNA-seq and alternative splicing event data for 500 prostate adenocarcinoma patients from TCGA and used LASSO regression to select five genes to build a prognostic prediction model. The model showed good reliability by ROC analysis and was significant in both univariate and multivariate Cox regression (both P<0.001). They constructed a putative splicing regulatory network and report that HSPB1 up-regulating PIP5K1C-46,721-AT (P<0.001) may be linked to tumorigenesis, progression and metastasis via Alzheimer’s-disease-pathway members (SRC, EGFR, MAPT, APP, PRKCA) (P<0.001).
Reported effects: sample_size 500, n=500 · Cox regression p-value, p <0.001 · +2 more
Key findings
- RNA sequencing data and ASEs data from 500 PRAD patients were retrieved from TCGA and TCGASpliceSeq.
- Five genes were selected by LASSO regression to construct a prognostic prediction model.
- The prediction model had good reliability on ROC analysis (ROC curve reported as supportive in abstract).
- Both univariate and multivariate Cox regression analyses confirmed prognostic efficacy of the model (both P<0.001).
- A splicing regulatory network was proposed and, after multiple-database validation, HSPB1 up-regulating PIP5K1C-46,721-AT was associated with PRAD progression (P<0.001).
- The authors suggest involvement of key members of the Alzheimer's disease pathway (SRC, EGFR, MAPT, APP, PRKCA) in this axis (P<0.001).
Limitations: Retrospective computational analysis of public datasets (TCGA/TCGASpliceSeq) without prospective clinical validation reported.; No experimental (in vitro or in vivo) functional validation of the proposed splicing events or regulatory axis is reported in the abstract.; Prognostic model performance details (e.g., AUC values, independent external cohort performance metrics) are not provided in the abstract.; Associations reported are correlative and the proposed mechanistic links are speculative based on database analyses..
This study identifies alternative splicing events and builds a prognostic splicing-signature/model associated with metastasis and prognosis in prostate adenocarcinoma using TCGA data.
AI summary of the abstract, human-reviewed · Jun 2026. Describes what this study reported, not medical advice. View on PubMed · Full text