Candidiasis is a highly pervasive infection posing major health risks, especially for immunocompromised populations. Pathogenic Candida species have evolved intrinsic and acquired resistance to a variety of antifungal medications. The primary goal of this literature review is to summarize the molecular mechanisms associated with antifungal resistance in Candida species. Resistance can be conferred via gain-of-function mutations in target pathway genes or their transcriptional regulators. Therefore, an overview of the known gene mutations is presented for the following antifungals: azoles (fluconazole, voriconazole, posaconazole and itraconazole), echinocandins (caspofungin, anidulafungin and micafungin), polyenes (amphotericin B and nystatin) and 5-fluorocytosine (5-FC). The following mutation hot spots were identified: (1) ergosterol biosynthesis pathway mutations (ERG11 and UPC2), resulting in azole resistance; (2) overexpression of the efflux pumps, promoting azole resistance (transcription factor genes: tac1 and mrr1; transporter genes: CDR1, CDR2, MDR1, PDR16 and SNQ2); (3) cell wall biosynthesis mutations (FKS1, FKS2 and PDR1), conferring resistance to echinocandins; (4) mutations of nucleic acid synthesis/repair genes (FCY1, FCY2 and FUR1), resulting in 5-FC resistance; and (5) biofilm production, promoting general antifungal resistance. This review also provides a summary of standardized inhibitory breakpoints obtained from international guidelines for prominent Candida species. Notably, N. glabrata, P. kudriavzevii and C. auris demonstrate fluconazole resistance.

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.

Candida auris is a multidrug-resistant fungal pathogen for which echinocandins are recommended first-line therapy, yet its adaptive responses to this drug class remain incompletely understood. This study defined the genome-wide transcriptional responses of C. auris strain B11244 (Clade IV) to subinhibitory caspofungin, micafungin, and anidulafungin and examined whether shared responses corresponded to cell-wall remodeling. Growth-based broth microdilution indicated susceptibility to all three drugs by MIC (caspofungin, approximately 0.5–1 µg/mL; micafungin, 0.125 µg/mL; anidulafungin, approximately 0.03125 µg/mL), but caspofungin uniquely produced marked paradoxical growth at 4–8 µg/mL, consistent with caspofungin tolerance. RNA sequencing identified 2920, 2130, and 2149 differentially expressed genes following caspofungin, micafungin, and anidulafungin exposure, respectively, including 283 co-upregulated and 157 co-downregulated genes. All three drugs induced a conserved cell-wall integrity program marked by transcriptional induction of Bck1-Mkc1 and Hog1 MAPK pathway components and an 18-gene signature involved in chitin synthesis and cell-wall cross-linking. The response was strongest with caspofungin, and RT-qPCR corroborated representative transcriptional changes. No canonical FKS1 hotspot mutation was detected; an I1572L substitution was predicted to be structurally neutral. Calcofluor White microscopy showed qualitatively enhanced peripheral fluorescence following each treatment, whereas colorimetric glucosamine measurement demonstrated significantly increased bulk chitin only with caspofungin (149% of control); micafungin (120%) and anidulafungin (98%) did not differ significantly from control. Taken together, these findings are consistent with inducible, MAPK-associated cell-wall remodeling as a potential FKS1-independent contributor to echinocandin tolerance, while showing that transcriptional convergence does not imply uniform phenotypic outcomes.

Minimal residual disease (MRD) is a major contributor to colorectal cancer (CRC) recurrence following curative-intent treatment, yet conventional surveillance methods may fail to detect residual disease at its earliest stages. Circulating tumor DNA (ctDNA) has emerged as a minimally invasive biomarker for MRD detection and postoperative monitoring. We conducted a structured PubMed-based literature review and included 94 publications evaluating ctDNA in CRC. Across the literature, postoperative ctDNA positivity was consistently associated with increased recurrence risk and poorer disease-free and overall survival, while serial monitoring improved detection sensitivity and enabled assessment of treatment response. ctDNA frequently identified molecular recurrence approximately 2.5–11.5 months before conventional surveillance. Both tumor-informed and tumor-naive strategies were represented, using PCR/ddPCR, targeted next-generation sequencing, whole-exome or whole-genome sequencing, methylation-based assays, and emerging multiomic approaches. Although ctDNA demonstrates strong prognostic value, evidence supporting treatment modification based solely on ctDNA status remains limited. Further prospective randomized trials, assay standardization, and consensus clinical guidelines are required before routine implementation. Overall, ctDNA is a promising tool for recurrence prediction, surveillance, and precision management of CRC.