Search Results (20,659)

Background: Immune-checkpoint blockade (ICB) is a recent addition to the treatment options for breast cancer, especially the triple-negative (TNBC) subset. Inhibiting immunosuppressive factors in the tumor microenvironment (TME) and preventing or reversing T cell exhaustion may increase the likelihood of a response to ICB. We have shown that decitabine and guadecitabine, DNA methyltransferase inhibitors (DNMTi), prevent the systemic and TME accumulation of myeloid-derived suppressor cells (MDSCs), which are immunosuppressive. Results: Here, we show that adding DNMTi to the neoadjuvant + adjuvant ICB-based treatment of ICB-resistant 4T1 and E0771 murine tumors in Balb/C and C57Bl/6 mice, respectively, effectively reduced the tumor burden, with 52% of 4T1 tumors completely regressing across several studies. DNMTi-based therapy overcame ICB resistance (ICBR) in a selected subline of E0771, and treated tumors showed a reduction in MDSCs. We also show that, in E0771, DNMTi can overcome ICBR to multiple checkpoint inhibitors, and in 4T1, it can modulate anti-tumor immunity by enhancing central memory T cell (Tcm) formation and reducing T cell exhaustion. Conclusion: These pre-clinical findings support the further investigation of incorporating DNMTi as a new immunotherapy modality for TNBC. Full article

Background: Older adults with cancer are at increased risk of severe treatment-related toxicity. CARG, CRASH, and CARG-BC were developed as toxicity-risk prediction models, whereas G8 was developed as a geriatric screening instrument but has also been evaluated as a predictor of treatment-related toxicity. This study aimed to assess, separately for each instrument, the accuracy with which these tools identify older adults who develop severe chemotherapy-related toxicity. Methods: A systematic review and meta-analysis were conducted in accordance with PRISMA 2020 guidelines. Seven databases were searched through May 2026 for observational studies evaluating the predictive accuracy of the CARG, CRASH, CARG-BC and G8 tools in patients aged ≥65 years initiating chemotherapy. Pooled sensitivity and specificity with 95% confidence intervals (CIs) were calculated, and ROC curves were constructed. Risk of bias was assessed using QUADAS-2 and certainty of evidence was evaluated using GRADE. Results: Twenty-one studies were included, with an overall toxicity prevalence of 52.6%. CARG demonstrated a pooled sensitivity of 79.7% and specificity of 38.3% (AUC = 0.632). CRASH showed sensitivity of 86.9% and specificity of 68.2% (AUC = 0.866), but estimates were based on only four studies. CRASH hematological toxicity showed sensitivity of 75.9% and specificity of 53.1% (AUC = 0.694), with substantial heterogeneity. G8 yielded sensitivity of 69.5% and specificity of 41.5% (AUC = 0.666). CARG-BC showed sensitivity of 83.3% and specificity of 54.4% (AUC = 0.763), based on two breast cancer studies. Certainty of evidence ranged from low to very low. Conclusions: The instruments have distinct purposes and were not pooled against one another. CARG and G8 may be useful for initial risk screening, whereas CRASH showed a more balanced profile but remains supported by limited evidence. None should be used as a stand-alone basis to withhold or modify treatment. Full article

Background/Objectives: Triple-negative breast cancer (TNBC) is enriched for germline pathogenic variants in BRCA1/2 and other DNA repair genes, but the additional value of extended germline profiling beyond BRCA1/2 remains insufficiently characterized in Russian patients. We aimed to characterize germline pathogenic/likely pathogenic variants (GPV/LPVs) and variants of uncertain significance (VUSes) in cancer predisposition and homologous recombination repair (HRR)-related genes in Russian TNBC patients and to assess the additional yield of extended germline profiling beyond BRCA1/2. Methods: We retrospectively analyzed germline DNA from 275 patients with histologically confirmed TNBC. Exome sequencing was performed for 204 patients and focused HRR-panel testing for 71 patients on the MGISEQ-G400 platform. Results: Overall, 114 patients (41.5%) harbored at least one germline GPV/LPV. BRCA1/2 GPV/LPVs were detected in 53 patients (19.3%), with BRCA1 predominating over BRCA2 (48 vs. 5 carriers) and the recurrent BRCA1 c.5329dup variant accounting for 23 cases. In the exome subset, 79 of 204 patients (38.7%) carried a GPV/LPV in Groups 1–3, including 48 (23.5%) with BC-related GPV/LPVs; non-BRCA Group 1 genes contributed seven additional carriers beyond BRCA1/2-only analysis. The expanded HRR set identified 52 GPV/LPV carriers (25.5%) versus 45 (22.1%) in the reference HRR panel, while the common HRR gene set identified 68 carriers (24.7%) in the full cohort. In addition, 183 unique VUSes were found in Groups 1–3 in the exome subset, affecting 128 patients (62.7%). Conclusions: Russian TNBC patients show a substantial germline GPV/LPV burden dominated by BRCA1/2 alterations and the recurrent BRCA1 c.5329dup founder variant. Extended germline profiling identified additional non-BRCA and HRR-related findings beyond BRCA1/2, but the incremental yield was moderate and accompanied by a considerable VUS burden. Broader germline testing may therefore support hereditary risk assessment and exploratory HRR-focused stratification, but non-BRCA HRR findings should not be considered sufficient for therapy selection without additional tumor-level or clinical evidence. Full article

Background/Objectives: Breast cancer biomarker detection through immunohistochemistry (IHC) is essential for treatment planning but faces challenges including turnaround time, variability, and laboratory resource constraints. Large open-source vision-language foundation models offer a potential avenue for inferring biomarker status directly from hematoxylin-and-eosin (H&E)-stained whole-slide images (WSIs). Methods: We evaluated two open-source pathology foundation models—TITAN (Transformer-based Pathology Image and Text Alignment Network, approximately 48.5 M parameters) and CHIEF (Clinical Histopathology Imaging Evaluation Foundation Model, approximately 1.2 M parameters)—for predicting estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER2) status from H&E-stained breast cancer WSIs. WSI data were obtained from The Cancer Genome Atlas Breast Invasive Carcinoma collection (TCGA-BRCA) via the NCI Imaging Data Commons, with biomarker labels from the NCI Genomic Data Commons. In total, 937 cases (995 WSIs; 78.3% ER-positive) were evaluated for ER, 934 cases (992 WSIs; 68.4% PR-positive) for PR, and 646 cases (691 WSIs; 21.1% HER2-positive) for HER2. All evaluation was performed under a strict patient-level 50/25/25 split with 10 independent random partitions; metrics are reported as the mean across partitions with percentile-based 95% confidence intervals. Performance was assessed using area under the receiver operating characteristic curve (AUROC), area under the precision-recall curve (AUPRC), sensitivity, specificity, and positive predictive value (PPV). Results: TITAN and CHIEF achieved comparable performance for ER (TITAN AUROC: 0.885 [95% CI: 0.848, 0.921], AUPRC: 0.954 [0.940, 0.964]; CHIEF AUROC: 0.877 [0.831, 0.914], AUPRC: 0.955 [0.938, 0.969]) and PR (TITAN AUROC: 0.799, AUPRC: 0.868; CHIEF AUROC: 0.791, AUPRC: 0.864). At the default 0.5 operating point, ER PPV was 0.90 and PR PPV was 0.79–0.81. For HER2, both models achieved AUROC values of 0.71–0.74 and AUPRC values of 0.41–0.45—well above the prevalence-based random baseline (approximately 0.211)—but default-threshold sensitivity was very low (approximately 0.07–0.08), reflecting class imbalance and the use of an uncalibrated default threshold rather than a categorical absence of morphologic signal. Conclusions: Under retrospective evaluation, both models demonstrate strong discriminative performance for ER and moderate performance for PR; HER2 prediction at the default operating point is limited and motivates threshold-calibration and multimodal extensions before any clinical use. AUPRC summarizes precision−recall behavior across thresholds and is distinct from threshold-specific precision (PPV); the two should be reported together for clinical-utility assessment in pathology AI. The findings are hypothesis-generating and motivate prospective external validation across independent institutional cohorts before any clinical deployment is considered. Full article

Background: Chronic psychological stress drives metastasis in triple-negative breast cancer (TNBC), yet the underlying mechanisms remain poorly understood and effective interventions are lacking. Stress-induced expansion of myeloid-derived suppressor cells (MDSCs) and subsequent immune remodeling play critical roles, with aberrant myeloid differentiation of hematopoietic stem and progenitor cells (HSPCs) serving as a major source of MDSCs. This study investigates whether epicatechin gallate (ECG) suppresses stress-driven TNBC growth and lung metastasis by regulating HSPC myeloid differentiation. Methods: A mouse model of chronic unpredictable mild stress (CUMS) followed by 4T1 tumor implantation was used to evaluate the anti-tumor effects of ECG. CETSA-WB, molecular docking, HSPC differentiation assays, and MDSC functional validation assays, along with immunohistochemistry, immunofluorescence, and flow cytometry, were performed to elucidate how ECG modulates glucocorticoid (GC)/glucocorticoid receptor (GR) signaling and HSPC differentiation. Results: ECG dose-dependently alleviated depressive-like behaviors, reduced serum corticosterone (Cort), and inhibited tumor growth and lung metastasis. Notably, ECG decreased lung metastatic foci by 76.9% relative to the CUMS group. Mechanistically, chronic stress activated GR and induced its nuclear translocation in HSPCs, promoting aberrant HSPC-to-MDSC differentiation. ECG directly bound GR, blocked its nuclear translocation, and suppressed the myeloid differentiation of HSPCs into MDSCs, which was accompanied by downregulation of S100A8/A9, fibronectin, and MMP-2, as well as increased CD8⁺ T cell infiltration. Supernatants from ECG-pretreated and differentiated HSPCs reversed Cort-induced epithelial–mesenchymal transition (EMT) in 4T1 cells. Conclusions: ECG acts as a natural GR signaling blocker that directly targets GR to block chronic stress-driven abnormal myeloid differentiation of HSPCs, thereby remodeling the pulmonary immune microenvironment, suppressing EMT, and reducing breast cancer lung metastasis. These findings identify ECG as a promising GR signaling blocker and a potential adjuvant therapy for cancer patients under high-stress conditions. Full article

Background. Breast and ovarian cancer are among the most common neoplasms in women, and germline variants in the BRCA1 gene markedly increase the risk of developing them. Despite existing studies, the frequency and spectrum of BRCA1 variants in women from Jalisco, Mexico, remain underexplored. Objective. To identify and characterize BRCA1 variants in a cohort of Mexican women with breast and ovarian cancer, and to assess their functional and splicing consequences through computational analysis. Methodology. Genomic DNA from 228 women with breast and/or ovarian cancer, selected by clinical criteria suggestive of hereditary cancer, was analyzed by next-generation sequencing. The functional impact of point variants was predicted with Ensembl VEP, SIFT, PolyPhen-2, REVEL, CADD, and AlphaMissense, and their effect on splicing was evaluated with SpliceAI, using the MANE Select canonical transcript (NM_007294.4). Results. BRCA1 variants were identified in 14.0% of this screening-enriched cohort, with carrier proportions of 16.2% in ovarian and 13.6% in breast cancer; these figures reflect a selected series and do not represent population prevalence. Breast cancer carriers showed a younger age at diagnosis, a higher proportion of the triple-negative phenotype, and a stronger family history. Fourteen-point variants and four large rearrangements were detected, with a predominance of truncating loss-of-function alterations. The recurrent missense variant c.5123C>A (p.Ala1708Glu), located in the BRCT1 domain, was the most relevant finding, present in 28.1% of carriers (9/32). The computational analysis did not reclassify variants on its own but provided complementary evidence (PP3/BP4) consistent with current classifications: it allowed reannotation of c.5243G>A from nonsense to missense, supported the pathogenic nature of the intronic splice variant c.4987-3C>A, and was concordant with the likely benign interpretation of c.2735A>G, while c.3367G>T remained of uncertain significance. Conclusions. This cohort from Western Mexico harbors a distinctive spectrum of BRCA1 variants, including the recurrent c.5123C>A variant, which may reflect a regional founder effect warranting haplotype analysis. These findings underscore the need for local evidence and for genetic panels adapted to the Mexican population, to enable accurate and equitable variant interpretation and access to targeted therapies such as PARP inhibitors. Full article

Background/Objectives: Prospective studies of omega-3 supplementation during breast cancer chemotherapy differ in intervention composition, co-supplementation, dose, treatment setting, and outcomes. We summarized and critically appraised interventions comprising DHA alone, EPA + DHA, EPA + DHA + GLA, or EPA + DHA with or without vitamin D, stratified by intervention composition and outcome domain. Methods: PubMed/MEDLINE, the Cochrane Library/CENTRAL, ClinicalTrials.gov, Scopus, Web of Science Core Collection, and Embase were last searched on 8 July 2026, supplemented by citation searching. Eligible studies prospectively administered EPA and/or DHA during chemotherapy and reported inflammatory/biological, nutritional/functional, quality-of-life, treatment-related, anticancer-response, or safety outcomes. Active co-supplementation was analyzed separately. Owing to clinical and methodological heterogeneity, findings were synthesized narratively; risk of bias and outcome-specific certainty were assessed using RoB 2-informed and GRADE approaches. Results: Fourteen reports representing ten prospective interventional trials were included. No eligible EPA-only trial was found. Interventions comprised EPA + DHA/fish oil without another active nutrient, DHA alone, EPA + DHA plus gamma-linolenic acid, and a factorial trial of EPA + DHA with or without vitamin D. One trial reported lower paclitaxel-induced neuropathy, whereas another found no benefit for paclitaxel-associated acute pain or neuropathic symptoms. Biomarker, nutritional, functional, and quality-of-life findings were inconsistent and often derived from small trials, exploratory or compliance-restricted analyses, companion reports, or co-supplementation designs. No consistent improvement in treatment response or survival was demonstrated. Serious supplementation-related adverse events were not reported, although adverse-event reporting varied. Certainty was low for safety and very low for efficacy-related domains. Conclusions: Current evidence is preliminary. The evaluated interventions appeared generally tolerated, but independent clinical efficacy of DHA alone, EPA + DHA without another active nutrient, EPA + DHA + GLA, or EPA + DHA with or without vitamin D during breast cancer chemotherapy remains unproven. Full article

Despite the development of new drugs, chemoresistance constitutes a major obstacle in cancer treatment. To investigate mechanisms of resistance and potential therapeutic targets, we developed doxorubicin-resistant models of HER2− (D2F2/Dox) and HER2+ (D2F2E2/Dox) breast cancer cells. Compared with parental cells, the D2F2/Dox and D2F2E2/Dox differed in morphology, increased migratory potential, elevated levels of the transcription factor signal transducer and activator of transcription 3 (Stat3), and a lower proliferation rate in D2F2E2/Dox. Moreover, D2F2/Dox and D2F2E2/Dox differed in the expression profiles of genes related to cell stemness, apoptosis, and drug efflux. Stat3 gene silencing in both doxorubicin-resistant cell types reversed the expression profiles of some genes (different in each resistant cell line), and decreased migratory potential was observed only in D2F2 cells. These data indicate that the acquired doxorubicin resistance was associated with Stat3 status; however, HER2− and HER2+ breast cancer cells did not indicate the same mechanism of chemoresistance acquisition. Importantly, Stat3 silencing did not substantially restore doxorubicin sensitivity, suggesting that effective therapy may require simultaneous targeting of multiple pathways. Furthermore, we demonstrated that siStat3 therapeutics could be selectively delivered to HER2+ cancer cells using H2.1MS1:MS2KN silk spheres, indicating their potential for targeted drug delivery in vivo. Full article

Background/Objectives: Exercise is increasingly recognized as an effective supportive intervention in breast cancer (BC), with substantial evidence demonstrating benefits on cancer-related fatigue, physical function, and quality of life. However, despite this strong scientific basis, its implementation in routine clinical practice remains inconsistent. Existing exercise oncology frameworks have primarily focused on screening, risk stratification, and referral, with limited availability of practical tools to guide individualized exercise prescription across the BC continuum. Accordingly, this narrative review aimed to synthesize current evidence to develop a clinically applicable, stepwise algorithm for individualized exercise prescription in women with BC. Methods: Current evidence from randomized controlled trials, systematic reviews, meta-analyses, and international clinical guidelines on exercise interventions in women with BC was synthesized narratively, with emphasis on exercise modality, intensity, progression, safety considerations, treatment phase, and patient-specific factors. Results: Aerobic and resistance exercise are safe and effective across different phases of BC care, including active treatment, survivorship, and advanced disease, with consistent improvements in fatigue, physical function, cardiorespiratory fitness, and health-related quality of life. However, heterogeneity in interventions, patient populations, and clinical contexts limits direct translation into clinical practice. To address this implementation gap, the available evidence was translated into a structured clinical algorithm based on the FITT principle (frequency, intensity, time, and type), treatment phase, risk stratification, patient-specific characteristics, treatment-related toxicities, and safety considerations, allowing individualized adaptation to different clinical scenarios. Conclusions: Exercise should be considered a core component of BC care rather than a general lifestyle recommendation. Bridging the evidence-to-implementation gap requires structured, individualized, and clinically applicable approaches to exercise prescription. The proposed algorithm translates current evidence into a structured clinical decision-support framework that may facilitate the routine implementation of individualized exercise prescription across the BC continuum. Full article

Theranostic nanoparticles, which integrate diagnostic imaging and therapeutic delivery within a single nanoplatform, represent a transformative paradigm in oncological nanomedicine. Despite substantial preclinical progress, the field faces persistent gaps in rational nanoparticle design informed by tumor biology, preclinical model fidelity, and clinical translation. This review critically synthesizes theranostic nanoparticle research across three underexplored domains. First, we examine tumor microenvironment features—reactive oxygen species dynamics, glutathione gradients, hypoxia, and proteasomal dysregulation—as mechanistic drivers of nanoparticle responsiveness. Second, we evaluate redox-responsive and proteasome-targeted nanoplatforms that exploit these cues for stimuli-triggered drug release and simultaneous imaging readout. Third, we address the unmet need for three-dimensional organoid and microfluidic tumor models as predictive preclinical testing environments, given the well-documented limitations of conventional two-dimensional cultures. Cancer subtype-specific applications are discussed for breast cancer, HPV-associated malignancies, colorectal cancer, and prostate cancer. Clinical translation barriers—including pharmacokinetic constraints, protein corona formation, immune clearance, anti-PEG antibodies, complement activation-related pseudoallergy, and FDA/EMA regulatory pathways—are addressed from a clinical oncology perspective. The review concludes with a research roadmap integrating proteomics-guided nanoparticle engineering, patient-derived organoid biobanks, and artificial intelligence-assisted design as priority areas for next-generation oncological theranostics. Full article

The performance of AI solutions in mammography is largely determined by data quality, preprocessing methods, and augmentation strategies. However, systematic evaluation of these factors for models trained on aggregated multicenter datasets remains underexplored. This article presents a comparative assessment of the effects of different stages of the training pipeline on the final diagnostic accuracy. Using a pooled dataset (VinDr-Mammo, INBreast, CMMD, CBIS-DDSM), we evaluated each pipeline step—from filtering to architecture selection (EfficientNet-B3, CLIP). External testing was conducted on the MosMed database. Among the tested preprocessing steps, filtering the darkest 5% of images proved most effective. For EfficientNet-B3, optimal geometric and photometric augmentations increased test AUROC on the prepared MosMed test set from 0.844 to 0.900. Domain-specific pretraining and high resolution yielded the best performance: Mammo-CLIP achieved an AUROC of 0.949 ± 0.012, and EfficientNet-B3 reached 0.934 ± 0.013. Overall, this study developed a standardized pipeline that includes sequential data filtering and harmonization, augmentation optimization, and architecture selection. This approach ensures reliable and reproducible results for automated mammogram classification. Full article

Breast cancer is a highly heterogeneous disease characterized by distinct molecular subtypes, dynamic tumor–microenvironment interactions, and variable therapeutic responses. Despite the availability of multiple preclinical platforms, a major challenge remains the lack of a coherent multiscale framework capable of integrating biological complexity across experimental systems. This limitation reduces the predictive power of individual models and highlights the need for complementary strategies that reproduce disease progression across multiple biological scales. In this context, advanced imaging technologies have emerged as essential tools for linking preclinical platforms and enhancing their translational relevance. This review examines how multimodal imaging supports the integration of in vitro, ex vivo, and in vivo breast cancer models. We discuss how optical imaging, high-frequency ultrasound, magnetic resonance imaging, positron emission tomography/computed tomography, and intravital microscopy provide complementary molecular, functional, anatomical, and cellular information for the longitudinal assessment of tumor growth, metastatic dissemination, microenvironment remodeling, and therapeutic response. Particular attention is given to emerging translational workflows that combine patient-derived models with advanced imaging to investigate drug sensitivity, treatment resistance, and tumor progression within a precision oncology perspective. We also highlight the role of multimodal imaging in biomarker validation across platforms and in the development of clinically relevant preclinical pipelines. Overall, advanced imaging represents a critical translational bridge across breast cancer model systems, improving the predictive value of preclinical studies and supporting imaging-guided precision oncology from bench to bedside. Full article

Background: Germline PALB2 variants are associated with hereditary breast cancer risk, but their clinical impact in Central Asian populations remains largely uncharacterized. This case study aims to evaluate the clinical significance of PALB2 variants in two Kazakh women with early-onset breast cancer. Methods: Molecular genetic testing identified germline PALB2 pathogenic variants (NM_024675.4:c.18_22delGAAGC and NM_024675.4:c.1034T>G) in two Kazakh women with early-onset invasive ductal carcinoma. Clinical courses, treatment responses, and outcomes were followed. Results: Neither patient had a reported family history of breast or other malignancies. Patient 1, a 26-year-old pregnant woman, was diagnosed with stage IIIB luminal B, HER2-negative invasive ductal carcinoma and received neoadjuvant chemotherapy, radical surgery, radiotherapy, endocrine therapy, and subsequent treatment for metastatic disease. Despite an initial response, she developed extensive skeletal metastases and died from metastatic breast cancer. Patient 2, a 33-year-old woman, presented with de novo stage IV luminal B, HER2-negative invasive ductal carcinoma with hepatic metastases. Following multimodal treatment, including chemotherapy, surgery, radiotherapy, endocrine suppression, and systemic therapy for disease progression, she experienced further metastatic spread and ultimately died from breast cancer-related complications. Conclusions: Both patients exhibited aggressive clinical courses characterized by early disease onset, metastatic progression, and poor outcomes despite comprehensive treatment. These cases highlight the potential clinical significance of germline PALB2 variants in apparently sporadic breast cancer and underscore the importance of genetic testing, risk assessment, and genetic counselling in young breast cancer patients, particularly in underrepresented. Full article

Background/Objectives: Mammary adipose tissue functions as an active endocrine organ, potentially influencing breast carcinogenesis through metabolic and inflammatory mechanisms. This systematic review synthesized evidence on associations between mammary adipocyte size, obesity-related adipose tissue dysfunction, and breast cancer. Methods: A comprehensive literature search was conducted across MEDLINE, EMBASE, CENTRAL, CINAHL and Web of Science (January 2010–September 2025) for observational studies measuring mammary adipocyte size in human breast tissue. Two reviewers independently conducted screening following the Cochrane Review’s rigorous methodology, and bias assessment using the ROBINS-E (Risk Of Bias In Non-randomized Studies of Exposure) tool. Random-effects meta-analyses were performed for quantifiable outcomes, with heterogeneity assessed using the I² statistic. Results: Twenty-one studies were included in the systematic review. Meta-analyses indicated that mammary adipocyte diameter was positively correlated with body mass index (8 studies; n = 720; correlation coefficient (r) = 0.44, 95% CI: 0.29–0.56), crown-like structure (CLS) density (5 studies; n = 383; r = 0.45, 95% confidence interval (CI): 0.36–0.54), aromatase expression (3 studies; n = 333; r = 0.36, 95% CI: 0.05–0.61), and three studies compared adipocyte diameter between CLS-positive and CLS-negative tissue (n = 297; mean difference = 9.69 μm, 95% CI: 4.94–14.44). Conclusions: This review summarizes moderate positive correlations of mammary adipocyte size with systemic adiposity, local breast inflammation, and aromatase expression, supporting a potential role for mammary adipose tissue in obesity-related metabolic dysfunction. Future prospective studies with standardized measurement protocols and improved control for confounding variables are needed to strengthen causal inference and clinical applications. Full article

Young breast cancer survivors often develop post-breast surgery pain syndrome (PBSPS). Despite potential benefit from physical activity, access to in-person programs is often limited by competing work and caregiving responsibilities. We assessed the feasibility and acceptability of a remotely delivered physical activity intervention for young Hispanic breast cancer survivors with PBSPS. Our single-arm, 12-week feasibility study enrolled Hispanic women aged ≤60, at least 3 months post-treatment for invasive breast cancer or ductal carcinoma in situ (DCIS), with PBSPS. Using a Fitbit Inspire 3 activity tracker and health coaching, the program encouraged whole-of-day movement to increase activity. Feasibility outcomes included recruitment, retention, and adherence. Secondary outcomes assessed pain measures, daily steps, and quality of life (QOL). Twenty-five breast cancer survivors enrolled (mean age 47.4 years [SD 6.3]), with 76% selecting Spanish-language health coaching. Retention at 12 weeks was 79% (19/24). Engagement with health coaching was high, with 95% completing at least 4 of 5 pre-planned calls. The mean change in daily step count was 1502 (−348, 3353), with twelve (66.7%) increasing in step count (median 2334.5, range: 14, 13,422). Each additional 1000-step increase was associated with a 2.67-point increase in pain self-efficacy scores (β = 2.669, 95% CI: 0.884 to 4.454, p = 0.006). A remotely delivered, health coaching physical activity intervention was feasible and acceptable for young Hispanic breast cancer survivors with PBSPS. This supports further evaluation in a larger trial. Accessible survivorship interventions for young breast cancer patients in their preferred language are needed. Full article