HER-2 (Human epidermal growth factor receptor 2)

The biological basis arises from the dual function of monocytes in promoting tumor-supportive environments and lymphocytes in facilitating immune monitoring. Through the capture of this immunological interaction, MLR acts as a low-risk and affordable method for risk assessment and treatment choices adapted to molecular subtype traits.

We summarize intensive treatment methods for T1N0M0 HR+/HER2- breast cancer patients, which extend beyond the standard 5-year tamoxifen (TAM)-based adjuvant ET. These methods include intensive ET, poly(ADP-ribose) polymerase (PARP) inhibitors, other targeted therapies, antibody-drug conjugates, oral chemotherapy, immunotherapy, and enhanced prevention of bone metastasis. This review provides a foundation for developing personalized adjuvant treatment strategies for patients with T1N0M0 HR+/HER2- breast cancer.

All enrolled patients received the full treatment protocol consisting of anthracycline followed by 12 months of trastuzumab alone or with pertuzumab. The highest risk was observed when both elevated hs-Tn I (≥82 ng/L after four cycles of anti-HER2 agents) and elevated hs-CRP (after four cycles of anthracyclines) were present. The interaction between both hs-Tn I and hs-CRP demonstrates significant predictive value for cardiotoxicity risk related to HER2+ breast cancer treatment.

EGFR and ALK alterations confer favorable outcomes, while certain alterations such as ROS1 and ERBB2 associate with poorer survival. These findings support the routine integration of biomarker testing into NSCLC management and highlight the need for biomarker-specific therapeutic approaches.

The cooperative GOG 281/LOGS trial showed that trametinib, an MEK inhibitor (MEKi), was significantly more effective than standard-of-care options (including chemotherapy or hormonal therapy) in increasing progression-free survival (median PFS 13.0 months vs. 7.2 months; hazard ratio 0.48, p < 0.001)...Genomic and multi-omic profiling have revealed actionable vulnerabilities and precision oncology approaches. The advent of biomarker-directed trials, molecular subtyping incorporation, and innovative computational strategies is likely to gradually ameliorate therapy selection and, thereby, finally improve long-term outcomes for patients with this complex disease.

This study demonstrates CHCP as a non-thermal (24 °C), non-contact plasma-based IRE platform which induces controlled membrane permeabilization and selective cancer cell death. CHCP offers a translational strategy to eradicate residual tumor cells at the surgical margins, and prevent local recurrence, positioning it as a versatile adjunct in precision surgical oncology.

The discovered LPP phenotype defines a small, high-risk subset warranting external validation. Given the retrospective, single-system design of the study, it is imperative to interpret the discovered phenotype features as hypothesis-generating, rather than as definitive evidence.

The results warrant further investigation on a larger cohort. This framework can be a useful surrogate for participants for whom ODX testing is neither affordable nor available.

We have developed, for the first time, a molecular signature based on cell adhesion, as well as an associated AdhesionScore that can predict patient prognosis in invasive breast cancer, with potential clinical application. We developed a novel adhesion-based molecular signature, the AdhesionScore, that robustly predicts prognosis in breast cancer across independent cohorts, highlighting its potential clinical utility for patient risk stratification.

Conversely, T-DXd administered due to the presence of HER2-low showed excellent effectiveness. Performing a re-biopsy is crucial due to the possible loss of estrogen receptors, which would require a change in therapeutic strategy no longer based on endocrine therapy. In cases that remain luminal, knowledge of the mutational profile may help to offer patients novel targeted treatments.

The strong co-expression of ALKBH7 and NLRP3 suggests a functional association between these molecules that may be critical in shaping the tumor microenvironment. This co-expression set, particularly in aggressive subtypes (HER2+ and TNBC), warrants further mechanistic validation as a potential prognostic marker and a novel therapeutic vulnerability.

We further highlight the role of the tumor microenvironment (TME) and intratumoral heterogeneity in shaping these entities. Collectively, recognition of emerging subtypes as clinically actionable groups represents a paradigm shift from static receptor-based models to dynamic, biomarker-driven frameworks that refine prognosis, enable patient stratification, and support precision oncology in aggressive BC.