Rapid and accurate identification of Candida species is critical for guiding antifungal therapy, especially with the emergence of intrinsically resistant pathogens. However, diagnostics using culture-based methods remain slow and labor-intensive, limiting timely treatment decisions. This systematic review evaluated the diagnostic performance and clinical applicability of nucleic acid amplification tests (NAATs) for Candida species identification using a PubMed search completed on 23 June 2025. A total of 888 records were screened, 333 full-text articles were assessed, and 158 studies were included based on criteria including comparison with standard diagnostic methods, diagnostic performance reporting, and involvement of clinical samples. PCR-based approaches were the most widely used, including conventional, nested, multiplex, real-time, and droplet digital PCR. Isothermal methods such as loop-mediated isothermal amplification (LAMP) and recombinase polymerase amplification (RPA) were increasingly represented. Common molecular targets included the ITS and 18S/28S rDNA regions. The risk of bias assessment was completed with the QUADAS-2 tool. Diagnostic performance varied depending on assay design, specimen type, gene target, and reference method. Excellent specificity and low limits of detection were achieved, especially with isothermal platforms offering the shortest turnaround times and greatest potential for point-of-care implementation. Multiplex assays were particularly advantageous for detecting mixed-species samples, while highly specific assays were optimal for distinguishing clinically important species such as Candidozyma auris, Nakaseomyces glabratus, and Pichia kudriavzevii. Overall, NAATs represent a promising diagnostic tool for Candida species identification, but broader clinical adoption will require improved standardization, validation across diverse patient populations, and clearer interpretation of fungal burden in the context of colonization versus infection.

Triple-negative breast cancer (TNBC) is an aggressive breast cancer subtype lacking estrogen receptor, progesterone receptor, and HER2 expression. Although ionizing radiation (IR) is widely used to treat TNBC, tumour radioresistance remains a major therapeutic barrier. Tumour hypoxia contributes to resistance by limiting IR-induced reactive oxygen species generation and activating pathways that promote tumour survival, progression, and aggressiveness. Hypoxia-inducible factors (HIFs) are oxygen-sensitive transcription factors that regulate many of these pathways; however, the mechanisms underlying HIF-mediated radioresistance in TNBC remain incompletely characterized. This review examines the role of HIF signalling in TNBC radiation resistance and emerging strategies for overcoming hypoxia-mediated radioresistance. PubMed and Web of Science were searched for studies investigating HIFs, TNBC, and radiation response. Relevant studies were screened against the eligibility criteria and analyzed for mechanistic findings and therapeutic interventions targeting HIF-associated pathways. The literature indicates that HIF activation promotes radioresistance through multiple mechanisms, including altered ferroptosis and pH regulation. Proposed countermeasures include pharmacologic inhibition of HIF signalling, nanotechnology-based delivery systems, and alternative radiation-based modalities, including photodynamic and radiodynamic therapies. Collectively, these findings identify HIF signalling as a central mediator of TNBC radioresistance and a promising therapeutic target for improving radiotherapy outcomes.