Background: At present, the characteristics of mucinous breast carcinoma (MBC) and the factors affecting its prognosis are controversial. We compared the clinical features of MBC with those of infiltrating ductal carcinoma (IDC) and summarized the relevant prognostic factors. Methods: The Surveillance, Epidemiology, and End Results (SEER) database includes information on 10,593 patients diagnosed with MBC between 2004 and 2016. Chi-square tests and analyses were used to analyze differences in variables between the MBC and IDC groups. Univariate and multivariate Cox proportional hazards models were used to assess the relative impacts of risk factors on cancer-specific survival (CSS) in patients. Kaplan-Meier survival curves were constructed to assess cancer-specific mortality and were compared using the log-rank test. Results: From 2004 to 2016, 10,593 people were diagnosed with MBC, and 402,797 were diagnosed with IDC. Patients with MBC had significantly higher 5−/10-year CSS rates (96.4%/93.4%) than those with IDC (89%/83.8%). Compared with IDC patients, MBC patients had less lymph node metastasis, an earlier stage, a higher rate of hormone receptor positivity and a lower expression rate of HER2. Univariate and multivariate analyses showed that age ≥ 60 years old (HR = 1.574, 95%CI: 1.238–2.001, P < 0.001), singled status (HR = 1.676, 95%CI: 1.330–2.112, P < 0.001) and advanced TNM/SEER stage were independent prognostic risk factors for MBC. In addition, positive estrogen receptor (HR = 0.577, 95%CI: 0.334–0.997, P = 0.049), positive progesterone receptor (HR = 0.740, 95%CI: 0.552–0.992, P = 0.044), surgical treatment (HR = 0.395, 95%CI: 0.288–0.542, P < 0.001) and radiotherapy (HR = 0.589, 95%CI: 0.459–0.756, P < 0.001) were identified as protective factors. Conclusion: Compared with IDC, MBC has a better prognosis. For patients with MBC, we identified prognostic factors that can help clinicians better assess patient outcomes and guide individualized treatment.

Breast cancer is posing a serious threat to the health of the female workforce as one of the most prevalent malignancies. Emerging epidemiological evidence suggests that insufficient intake of the trace element, iodine, is associated with breast oncogenesis. In this paper, we propose a potential link between iodine deficiency and increased breast cancer risk. A central element of this mechanism may involve the cytoplasmic mislocalization and oncogenic function of the sodium/iodide symporter (NIS), which primarily mediates iodine transport under physiological conditions in the human body. We propose a three-stage model: (1) Initiation: Iodine deficiency triggers systemic alterations in the hypothalamic-pituitary-thyroid (HPT) and gonadal (HPG) axes, as well as lactogenic signaling, establishing a proliferative and inflamed breast microenvironment. (2) Heterogeneous subtype-specific evolution: For hormone receptor-positive (HR+) breast cancer, sustained PI3K/AKT activation driven by the relative dominance of estrogen disrupts normal glycosylation, leading to the cytoplasmic retention of NIS. For triple-negative breast cancer, TP53 and FOXA1 mutations primarily contribute to significant upregulation of NIS. (3) Malignant evolution: Cytoplasmic NIS associates with the leukemia-associated RhoA guanine exchange factor (LARG) and hyperactivates the RhoA-ROCK signaling pathway, driving cytoskeletal rearrangement, tumor invasion and metastasis. Deciphering the contributions of iodine status toward breast carcinoma development is assumed to open new avenues for novel therapeutic measures for breast cancer.

Despite growing recognition that nutritional factors modulate breast cancer risk and prognosis through endocrine and metabolic pathways, existing reviews have predominantly focused on individual nutrients or single hormonal axes, lacking an integrated framework that systematically connects nutritional biomarkers across biological scales to clinical prediction models. Furthermore, the translational gap between biomarker discovery and clinical implementation—compounded by pre-analytical variability, population heterogeneity, and the absence of standardized testing protocols—remains inadequately addressed in the current literature. This review synthesizes contemporary evidence on nutritional biomarkers and their interactions with endocrine-related mechanisms in breast cancer, with a specific focus on risk assessment and prognosis prediction. We systematically integrate four core endocrine-metabolic axes (estrogen signaling, insulin/IGF-1 pathway, adipokine homeostasis, and inflammatory-oxidative stress) with four functional classes of nutritional biomarkers (recovery, concentration, replacement, and predictive), delineating their hierarchical relationships and complementary clinical roles. We further examine subtype-specific metabolomic signatures associated with differential prognosis across triple-negative, luminal-like, and HER2-enriched breast cancer, and evaluate the clinical utility of integrating multi-dimensional biomarkers into prognostic prediction models including nomograms. Our analysis reveals that while circulating vitamins, fatty acid profiles, and inflammatory biomarkers demonstrate consistent associations with breast cancer risk, their prognostic value varies substantially by molecular subtype and menopausal status; composite metabolomic signatures outperform single biomarkers in prognostic discrimination, yet most evidence derives from retrospective single-center cohorts with limited external validation. We conclude that biomarker-guided precision nutrition holds substantial promise for advancing personalized breast cancer prevention and management, but critical barriers—including non-standardized assay protocols, underrepresentation of non-Western populations, and a paucity of prospective intervention trials—must be addressed before widespread clinical translation.