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Cancer remains a major cause of mortality worldwide, driving ongoing innovation in therapeutic strategies. Immunotherapy has transformed cancer care by leveraging the immune system to target tumors, but its effectiveness is limited by tumor heterogeneity, immune resistance, and unpredictable toxicities. Moreover, the absence of robust biomarkers to predict therapeutic response and manage adverse effects remains a significant challenge. Recent advances in biomarker discovery, including liquid biopsy technologies and gut microbiota profiling, are enhancing the precision of immunotherapy and enabling more personalized cancer management. Here, we present a Comprehensive Oncological Biomarker Framework that integrates genetic and molecular testing, imaging, histopathology, multi-omics, and liquid biopsy to generate a molecular fingerprint for each patient. This holistic approach supports individualized diagnosis, prognosis, treatment selection, and response monitoring. Incorporating emerging biomarkers, such as microbiome signatures, further refines patient stratification, guiding the optimization of therapy. By uniting molecular insights with clinical and social factors, this framework aims to address tumor heterogeneity and immune evasion, ultimately improving patient outcomes through precision oncology.

Pancreatic cancer is a significant cause of cancer-related mortality and often presents with limited treatment options. Pancreatic tumors are also notorious for their immunosuppressive microenvironment. Irreversible electroporation (IRE) is a non-thermal tumor ablation modality that employs high-voltage microsecond pulses to transiently permeabilize cell membranes, ultimately inducing cell death. However, the understanding of IRE’s impact beyond the initiation of focal cell death in tumor tissue remains limited. In this study, we demonstrate that IRE triggers a unique mix of cell death pathways and orchestrates a shift in the local tumor microenvironment driven, in part, by reducing the myeloid-derived suppressor cell (MDSC) and regulatory T cell populations and increasing cytotoxic T lymphocytes and neutrophils. We further show that IRE drives induce cell cycle arrest at the G0/G1 phase in vitro and promote inflammatory cell death pathways consistent with pyroptosis and programmed necrosis in vivo . IRE-treated mice exhibited a substantial extension in progression-free survival. However, within a span of 14 days, the tumor immune cell populations reverted to their pre-treatment composition, which resulted in an attenuation of the systemic immune response targeting contralateral tumors and ultimately resulting in tumor regrowth. Mechanistically, we show that IRE augments IFN- γ signaling, resulting in the up-regulation of the PD-L1 checkpoint in pancreatic cancer cells. Together, these findings shed light on potential mechanisms of tumor regrowth following IRE treatment and offer insights into co-therapeutic targets to improve treatment strategies.

Despite epidermal growth factor receptor (EGFR) is a pivotal oncogene for several cancers, including lung adenocarcinoma (LUAD), how it senses extracellular matrix (ECM) rigidity remain elusive in the context of the increasing role of tissue rigidity on various hallmarks of cancer development. Here it is shown that EGFR dictates tumorigenic agrin expression in lung cancer cell lines, genetically engineered EGFR‐driven mouse models, and human specimens. Agrin expression confers substrate stiffness‐dependent oncogenic attributes to EGFR‐reliant cancer cells. Mechanistically, agrin mechanoactivates EGFR through epidermal growth factor (EGF)‐dependent and independent modes, thereby sensitizing its activity toward localized cancer cell‐ECM adherence and bulk rigidity by fostering interactions with integrin β1. Notably, a feed‐forward loop linking agrin–EGFR rigidity response to YAP–TEAD mechanosensing is essential for tumorigenesis. Together, the combined inhibition of EGFR–YAP/TEAD may offer a strategy to reduce lung tumorigenesis by disrupting agrin‐EGFR mechanotransduction, uncovering a therapeutic vulnerability for EGFR‐addicted lung cancers. The study identifies agrin‐EGFR mechanotransduction as a critical driver of lung adenocarcinoma which enhances EGFR signaling through an integrin‐FAK‐actomyosin dependent positive feedback on YAP/TAZ ‐TEAD in response to matrix stiffness. Targeting this oncogenic loop through combinatorial treatments inhibits lung cancer due to agrin impairment. Thus, agrin may serve as a biomarker for predicting response to these therapies.

Background/Objectives: HER2-low breast cancer has emerged as a clinically meaningful category that challenges the historical HER2-positive versus HER2-negative classification. Although not defined as a distinct biological subtype, HER2-low tumors exhibit unique clinicopathological features and differential sensitivity to novel antibody–drug conjugates. Accurate identification remains difficult due to limitations in immunohistochemistry performance, inter-observer variability, intratumoral heterogeneity, and dynamic shifts in HER2 expression over time. This review synthesizes current evidence on the biological and clinical characteristics of HER2-low breast cancer and evaluates emerging diagnostic innovations, with emphasis on liquid biopsy approaches and evolving technologies that may enhance diagnostic accuracy and monitoring. Methods: A narrative literature review was conducted, examining tissue-based HER2 testing, liquid biopsy modalities, including circulating tumor cells, circulating nucleic acids, extracellular vesicles, and soluble HER2 extracellular domains, and applications of artificial intelligence (AI) across histopathology and multimodal diagnostic systems. Results: Liquid biopsy technologies offer minimally invasive, real-time assessment of HER2 dynamics and may overcome fundamental limitations of tissue-based assays. However, these platforms require rigorous analytical validation and face regulatory and standardization challenges before widespread clinical adoption. Concurrently, AI-enhanced histopathology and multimodal diagnostic systems improve reproducibility, refine HER2 classification, and enable more accurate prediction of treatment response. Emerging biosensor- and AI-enabled monitoring frameworks further support continuous disease evaluation. Conclusions: HER2-low breast cancer sits at the intersection of evolving pathology and technological innovation. Integrating liquid biopsy platforms with AI-driven diagnostics has the potential to advance precision stratification and guide personalized therapeutic strategies for this expanding patient subgroup.

The 50-cent toll on the U.S. 40 bridge over the Susquehanna River should be lifted, the Maryland Transportation Commission has recommended.

Liquor store owners in Cecil county, whose low prices attract out-of-state customers, say Governor Hughes's proposed increase in alcohol and cigarette taxes would undercut the' county's flourishing liquor business and ultimately mean a drop in revenues to the county...

From up on U.S. 40, the view of Perryville is not impressive: There's a gas station, a car dealership, a convenience store.

Building a state prison in Cecil county would shatter a dream for some rural residents, .who worry that having inmates nearby could threaten their safety and change the character of their neighborhoods.

Only The Nose knows or so the saying goes. And when it comes to sniffing out drugs in Cecil county schools, a State Police dog knows best.

The Small Business Adminstration has arranged with several Harford and Cecil county banks to guarantee loans to Conowingo businesses affected by the closing of the Conowingo Dam bridge across the Susquehanna River.