The presence and impact of toxins have been detected in various regions worldwide ever since the discovery of azaspiracids (AZAs) in 1995. These toxins have had detrimental effects on marine resource utilization, marine environmental protection, and fishery production. Over the course of more than two decades of research and development, scientists from all over the world have conducted comprehensive studies on the in vivo metabolism, in vitro synthesis methods, pathogenic mechanisms, and toxicology of these toxins. This paper aims to provide a systematic introduction to the discovery, distribution, pathogenic mechanism, in vivo biosynthesis, and in vitro artificial synthesis of AZA toxins. Additionally, it will summarize various detection methods employed over the past 20 years, along with their advantages and disadvantages. This effort will contribute to the future development of rapid detection technologies and the invention of detection devices for AZAs in marine environmental samples.

Bladder cancer (BLCA) is a prevalent malignancy of the urinary system, associated with a high recurrence rate and poor prognosis. FAM111B, which encodes a protein containing a trypsin-like cysteine/serine peptidase domain, has been implicated in the progression of various human cancers; however, its involvement in BLCA remains unclear. In this study, we investigated the expression of FAM111B gene in tumor tissues compared to para-tumor tissues using immunohistochemistry and observed a significantly higher FAM111B gene expression in tumor tissues. Furthermore, analysis of clinical characteristics indicated that the increased FAM111B gene expression correlated with lymphatic metastasis and reduced overall survival. To investigate its functional role, we employed FAM111B-knockdown BLCA cell models and performed cell proliferation, wound-healing, transwell, and flow cytometry assays. The results showed that decreased FAM111B gene expression inhibited proliferation and migration but induced apoptosis in BLCA cells. In vivo experiments further validated that FAM111B knockdown suppressed tumor growth. Overall, our findings suggest that FAM111B acts as an oncogene in BLCA, playing a critical role in tumorigenesis, progression, and metastasis of BLCA. In conclusion, we have demonstrated a strong correlation between the expression of FAM111B gene and the development, progression, and metastasis of bladder cancer (BLCA). Thus, FAM111B is an oncogene associated with BLCA and holds promise as a molecular target for future treatment of this cancer.

Antibody–drug conjugates (ADCs) represent a paradigm shift in precision oncology, ingeniously coupling the targeting capability of monoclonal antibodies with the lethal potency of cytotoxic payloads to selectively eradicate tumor cells. While ADCs have demonstrated transformative efficacy across a spectrum of malignancies, the emergence of intrinsic and acquired resistance remains a formidable obstacle, frequently culminating in treatment failure and disease progression. The landscape of ADC resistance is highly complex, governed by a diverse array of molecular mechanisms. These range from alterations in antigen dynamics—such as downregulation or impaired trafficking—to intracellular adaptations, including the upregulation of multi-drug resistance efflux pumps, enhanced DNA damage repair capacity, and the blockade of apoptotic cell death. Moreover, tumor cells often exploit compensatory signaling networks to bypass therapeutic inhibition. Consequently, elucidating the intricate signaling cascades that drive these resistance phenotypes is critical for clinical advancement. This review comprehensively examines the pivotal signaling pathways underpinning ADC resistance and evaluates novel therapeutic strategies designed to circumvent these molecular barriers, aiming to optimize patient outcomes.

Azaspiracids are a type of polyether toxin. Currently, the existing detection methods for azaspiracids all have certain drawbacks. Aptamers offer a cost-effective and convenient approach for the detection of azaspiracids. By employing the Capture-SELEX (Systematic evolution of ligands by exponential enrichment) method to screen aptamers specific to azaspiracid-2, a high-affinity aptamer can be identified for toxin detection. The bin ding affinity of the toxin is verified using biolayer interferometry (BLI) technology. Additionally, computer simulations are utilized to explore the binding sites of the aptamer and conduct molecular dynamics simulations to investigate the stability of the aptamer–toxin complex. Further optimization of the obtained aptamers is carried out to enhance their affinity for the toxin. Ultimately, two aptamers, JD2-RM3-27C28T and JD3-RMM1, are obtained, with dissociation constants (K_D) improved by two orders of magnitude (K_D = 8.7 × 10⁻⁸ M and K_D = 6.8 × 10⁻⁸ M, respectively). These aptamers have the advantage of being incorporated into a new AZA2 assay that is more accurate and ethical than biological monitoring methods, and more economical than LC-MS. In the future, this is expected to demonstrate significant advantages in the fields of food safety, environmental toxin monitoring, toxin exposure diagnosis, and public health monitoring.

Domoic acid (DA) is a neurotoxic terpenoid compound produced by certain marine algae. It accumulates through the food web and poses a significant threat to humans and animals by selectively targeting hippocampal neurons, leading to neuronal degeneration, necrosis, and subsequent memory impairment. The primary mechanism involves its potent agonism at glutamate receptors, which induces excessive calcium influx, resulting in excitotoxic cell swelling and death. Recent studies have further elucidated the critical role of downstream oxidative stress and other pathogenic factors in DA-induced neurotoxicity. These insights into its multifaceted mechanism have paved the way for novel therapeutic strategies, highlighting promising directions for future treatment development.

Introduction: Antibody-drug conjugate (ADC) has become the standard of treatment for metastatic urothelial cancer. Current trials generally test the combination or sequential use of antibody-drug conjugates with different targets and different chemotherapeutic reagents. Case description: We show that in three patients with metastatic urothelial cancer who have progressed on anti-HER2 antibody-drug conjugates, two showed responses when treated with EV (the same monomethyl auristatin E-containing ADC, but with different targets). Conclusion: This result showed the therapeutic potential of sequential use of ADC containing the same chemotherapeutic reagents with different targets for metastatic urothelial cancer.