Phosphatase and tensin homolog (PTEN) is one of the highly susceptible genes to breast cancer (BC); however, the role of PTEN-related RNAs in BC remains poorly understood. Understanding the effect of PTEN-related RNAs and their mechanisms may be helpful to clinicians. We screened the differentially expressed RNAs (deRNAs) related to PTEN and established the competitive endogenous RNA (ceRNA) network by integrating several databases. After that, the RNA model, prolactin receptor (PRLR)/calcium voltage-gated channel auxiliary subunit alpha2delta 1 (CACNA2D1), was obtained by KM survival analysis and logistic regression analysis. Finally, mutation, methylation, functional enrichment, and immune correlation were analyzed to explore the roles of these RNAs. Our results showed that PRLR might be harmful to BC, while CACNA2D1 might be beneficial to BC. Furthermore, the abnormal expression of PRLR in BC might result from mutation and hypomethylation, while the aberrant expression of CACNA2D1 might be ascribed to methylation. Mechanistically, PRLR might affect the prognosis of BC by inhibiting the expression of immune checkpoints, while CACNA2D1 might improve the prognosis of BC by increasing the immune cells infiltrating into BC and up-regulating the expression of immune checkpoints. The abnormal expression of PRLR and CACNA2D1 in BC is closely related to the prognosis of BC, and they may serve as targets for the treatment of BC.

Breast cancer has garnered global attention due to its high incidence worldwide, and even more noteworthy is that approximately 90% deaths due to breast cancer are attributed to cancer metastasis. Therefore, the early diagnosis of breast cancer metastasis holds significant importance for reducing mortality outcomes. Biosensors play a crucial role in the early detection of metastatic breast cancer due to their advantages, such as ease of use, portability, and real-time analysis capabilities. This review primarily described various types of sensors for detecting breast cancer metastasis based on biomarkers and cell characteristics, including electrochemical, optical, and microfluidic chips. We offered detailed descriptions of the performance of these various biosensors and made comparisons between them. Furthermore, we described the pathology of breast cancer and summarized commonly used biomarkers for metastatic breast cancer. Finally, we discussed the advantages of current-stage biosensors and the challenges that need to be addressed, as well as prospects for their future development.

Intraglandular dissemination is an important pathological feature of thyroid cancer, yet the biological characteristics of this phenomenon remain relatively underexplored. This paper aims to provide a comprehensive overview of its biological behaviors, protein expressions, and identification methods. Several retrospective studies have found that thyroid cancers with intraglandular dissemination have higher rates of lymph node metastasis, capsule invasion, and vascular invasion, exhibiting more aggressive biological behavior. Immunohistochemistry results show abnormal expression of proteins such as FKBP5, CENPF, CX26, KIF11, PTK7, which are associated with poor prognosis in thyroid cancers with intraglandular dissemination, offering potential guidance for specific targeted therapy in the future. Moreover, adjunctive techniques including ultrasound, fine-needle aspiration, and genetic testing offer valuable support in accurately identifying these cases, facilitating moreproactive treatment and closer follow-up.

Plasma cell mastitis (PCM), a prevalent and refractory form of non-lactating mastitis, is characterized by the pathological triad of ductal ectasia (DE), plasma cell-dominated inflammatory infiltration, and progressive fibrosis. Despite its clinical burden, current surgical interventions yield suboptimal outcomes with recurrence rates up to 43%, underscoring an urgent need for mechanistic insights. This review synthesizes evidence establishing epithelial-mesenchymal transition (EMT) as a central driver of PCM pathogenesis, intricately regulated by the disease-specific immune microenvironment. We demonstrate that autoimmune-mediated DE initiates ductal damage, generating damage-associated molecular patterns (DAMPs) that activate pattern recognition receptors (PRRs). This triggers NF-κB signaling hubs, upregulating pro-inflammatory mediators (IL-1β, IL-6, TGF-β1, ICAM-1, CXCL12) and core EMT-transcription factors (Snail, TWIST). Crucially, IL-6/JAK/STAT3 signaling promotes plasma cell survival via Bcl-2 while concurrently driving EMT in ductal epithelium. Concurrently, IL-1βactivate PI3K/Akt to stabilize EMT effectors and enhance ECM synthesis. A unique, self-amplifying “EMT-fibrosis loop” is identified as a PCM hallmark: EMT-derived fibroblasts secrete CXCL12 and TGF-β1, which activate NF-κB pathways in adjacent epithelia to perpetuate EMT and ECM deposition. This loop, alongside sustained plasma cell activity via IL-6/STAT3/Bcl-2, underpins PCM’s chronicity and distinguishes it from other mastitides like granulomatous lobular mastitis (GLM). We further highlight exosomal involvement in CXCL12 transport and M1 macrophage polarization as amplifiers of inflammation and EMT. Targeting these convergent pathways (NF-κB, JAK/STAT3) or disrupting the EMT-fibrosis loop (e.g., via CXCL12/TGF-β1 inhibitors) represents a promising therapeutic strategy to mitigate fibrosis and recurrence. Future research must validate these mechanisms in human-relevant models and address critical gaps in bacterial-autoimmune interplay and temporal dynamics across PCM stages.

Estrogen receptor-negative/progesterone receptor-positive/human epidermal growth factor receptor 2-negative (ER ^- /PR ⁺ /HER2 ^- )breast cancer is a rare, controversial type that makes up about 0. 3% of all breast cancer cases and does not follow the traditional ER→PR regulatory hierarchy. This review synthesizes the available evidence on the diagnostic evaluation, clinicopathological characteristics, molecular mechanisms, prognosis, and treatment of ER ⁻ /PR ⁺ /HER2 ⁻ (ER ^- /PR ⁺ ) breast cancer. Although there are false-negative ER staining results and pre-analytical/analytical factors, a number of clinical and transcriptomic data support the existence of a reproducible ER ^- /PR ⁺ subgroup with molecular heterogeneity. These tumors often have a high histological grade, elevated Ki-67 expression, TP53 alterations, and basal-like features, and are closer to triple-negative breast cancer than luminal disease. Potential drivers include ER-independent non-canonical PR activation, epigenetic dysregulation, kinase-mediated receptor phosphorylation, membrane-associated progesterone signaling and receptor network reprogramming. Direct subtype-specific evidence remains limited, and the effectiveness of conventional endocrine therapy is unknown. Current guidelines classify these tumors as hormone receptor-positive/HER2-negative, obscuring clinically relevant heterogeneity. Standardized repeat testing and multi-omic characterization are thus required. Future studies should prioritize prospective multicenter cohorts with paired pre-treatment and post-treatment receptor testing, spatial or single-cell characterization, biomarker-guided stratification and adaptive clinical trials. A PR-oriented precision-medicine framework may improve diagnostic classification and help identify therapeutic vulnerabilities in biologically distinct patient subsets. In addition, this rare phenotype may serve as a useful model for investigating lineage plasticity and endocrine resistance.