Gastrointestinal (GI) cancers represent a heterogeneous group of malignant neoplasms arising from the digestive tract, including gastric, colorectal, hepatic, pancreatic, and biliary cancers. These tumors represent a major public health challenge due to their aggressive nature and poor prognosis. Although significant progress has been made in diagnostic imaging, endoscopy, and multimodal therapies, early detection remains difficult. Conventional serum biomarkers often lack sufficient sensitivity and specificity for reliable diagnosis, prompting a growing interest in identifying novel, minimally invasive biomarkers. In this context, liquid biopsy is emerging as a revolutionary tool in oncology. Among its components, extracellular vesicles (EVs) have gained increasing attention because they carry a wide range of molecular cargoes that reflect the biological state of their tumor of origin. In particular, EV-associated microRNAs (miRNAs) hold great promise as biomarkers for early cancer detection, real-time monitoring of disease progression, and assessment of therapeutic response. This review discusses the diagnostic and prognostic potential of EVs as novel biomarkers in GI cancers, emphasizing EV-contained miRNAs as a key resource for the development of personalized and precision medicine strategies.

Cadmium (Cd), a heavy metal known to act as an endocrine disruptor, has been implicated in breast cancer (BC) via mechanisms that involve both estrogen receptor (ER)-dependent and -independent pathways. We used BALB-neuT transgenic mice, a model of aggressive ErbB2-driven mammary carcinogenesis, to evaluate the effects of chronic exposure to an environmentally relevant, low-dose of Cd on tumor onset, multiplicity, progression, immune microenvironment, and metastasis. Cd exposure significantly accelerated tumor onset and increased tumor multiplicity and weight, reducing both tumor-free and overall survival. Cd-exposed mice displayed elevated serum estrogen levels, and increased expression of progesterone receptor and tumor progression markers, including CD31, Ki67, and phosphorylated Akt, in tumor tissues. Despite the increased recruitment of CD4⁺ and CD8⁺ T cells to the peritumoral stroma, Cd exposure fostered an immunosuppressive microenvironment with elevated Tregs and PD-1⁺ exhausted T cells, both locally and systemically. Notably, lung metastases were threefold more frequent in Cd-exposed mice. Our results demonstrate that low-dose Cd exposure promotes the development and progression of ErbB2-driven breast tumors through hormonal, proliferative, and immune-modulating mechanisms. These findings reveal that exposure to environmentally relevant doses of Cd not only accelerates ErbB2-driven breast cancer but also reshapes the immune landscape toward dysfunction and immunosuppression, likely compromising both anti-tumor immunity and response to immunotherapies. These data advocate for tighter regulation of Cd exposure in populations at risk for breast cancer.