TEST:

nCounter® Breast Cancer 360™ Panel

Endocrine resistance in luminal breast cancer is characterized by elevated immune signatures, increased proliferation, and specific genomic alterations. The integration of clinical information, gene expression patterns, and genetic data enhances patient stratification and potentially informs treatment decisions. These findings support the use of integrative analyses to guide personalized endocrine therapy and improve outcomes.

Patients from deprived areas exhibited higher inflammation and antioxidant depletion even within the same tumor grade (p < 0.05). Neighborhood deprivation correlates with pro-inflammatory, proliferative multiomic profiles that may underlie worsened outcomes.

Using multiplex IHC and transcriptome analyses, this study demonstrated that PABC was associated with a higher abundance of immune cells, including increased infiltration of T cells, B cells, and macrophages, in the breast tumor microenvironment. Future research is required to focus on the role of immune cells in pregnancy-associated breast cancer patients.

This study highlights the unique molecular and biological features of metastatic EMPD, emphasizing the need for tailored treatment approaches. This information should be used to guide future clinical strategies for metastatic EMPD.

Non-luminal intrinsic subtypes are prevalent in BCBMs and basal-like genomic features are associated with worse survival. Recurrent gene expression modifications with potential therapeutic implications were observed in BCBMs.

This study reinforces the prognostic utility of histological grading and reveals a set of cell cycle-related genes whose overexpression is linked to adverse outcomes in breast cancer. These findings suggest potential biomarkers for risk stratification and therapeutic targeting, offering insights for personalized management of patients beyond traditional histological assessments.

ER-negative, HER2-positive breast cancer has unique molecular and immunologic features that may predict pCR after neoadjuvant HP. Validation of these potential biomarkers and composite biomarker analyses may guide design of future clinical trials.

Interestingly, differences emerged when comparing patients diagnosed during gestation (PABC-GS) and the postpartum period (PABC-PP), with PABC-PP showing increased expression of immune-related genes, including PD-1, and greater immune cell infiltration (Tregs, macrophages, neutrophils, B-cells). These findings suggest an enhanced proliferative capacity and impaired DNA repair in PABC, and underscore the role of immune infiltration in postpartum cases; providing insights into its aggressive nature and potential targets.

In this study, we analyzed the intrinsic subtype of HR positive, HER2 positive breast cancer based on prediction analysis of microarray 50 (PAM50) and Breast Cancer 360 panel (nanostring) between durable and poor responder in first-line docetaxel + trastuzumab + pertuzumab (THP) treated patients. Conclusions Other than HER2 pathway, ER pathway and inflammatory signal may influence the tumor response of HR(+), HER2 (+) breast cancer. Further clinical trials should be designed based not only on HER2 status, ER status and other molecular subtypes should be considered to maximize the clinical benefit.

We found a downregulation of GE signatures related to the immune system and tumour ME in BM compared with PT. This was validated by the lower levels of TILs, CD4+ and CD8+ T cells in BM. The lower immunogenicity of BM may partly explain the reduced effect by immunotherapy intracranially.

Methods Pre/perimenopausal pts with no prior systemic therapy for aggressive HR+/HER2− ABC were randomized 1:1 to RIB + letrozole/anastrozole + goserelin or physician's choice of combo CT. Contrary results in the CT arm suggest that these signatures warrant further studies on their potential predictive value. These data are hypothesis generating and should be interpreted with caution due to small sample sizes.

Excess visceral adiposity was associated with shorter survival and increased expression of stroma and mammary stemness genes in tumors of patients with HER2-enriched breast cancer, suggesting adiposity's contribution to breast cancer progression differs by molecular intrinsic subtype. This translational study provides additional evidence for the importance of excess adiposity as is a major modifiable risk factor for patient survival.