Biomarkers are vital in healthcare as they provide valuable insights into disease diagnosis, prognosis, treatment response, and personalized medicine. They serve as objective indicators, enabling early detection and intervention, leading to improved patient outcomes and reduced costs. Biomarkers also guide treatment decisions by predicting disease outcomes and facilitating individualized treatment plans. They play a role in monitoring disease progression, adjusting treatments, and detecting early signs of recurrence. Furthermore, biomarkers enhance drug development and clinical trials by identifying suitable patients and accelerating the approval process. In this review paper, we described a variety of biomarkers applicable for cancer detection and diagnosis, such as imaging-based diagnosis (CT, SPECT, MRI, and PET), blood-based biomarkers (proteins, genes, mRNA, and peptides), cell imaging-based diagnosis (needle biopsy and CTC), tissue imaging-based diagnosis (IHC), and genetic-based biomarkers (RNAseq, scRNAseq, and spatial transcriptomics).

A biomarker is a physiological observable marker that acts as a stand-in and, in the best-case scenario, forecasts a clinically significant outcome. Diagnostic biomarkers are more convenient and cost-effective than directly measuring the ultimate clinical outcome. Cancer is among the most prominent global health problems and a major cause of morbidity and death globally. Therefore, cancer biomarker assays that are trustworthy, consistent, precise, and verified are desperately needed. Biomarker-based tumor detection holds a lot of promise for improving disease knowledge at the molecular scale and early detection and surveillance. In contrast to conventional approaches, surface plasmon resonance (SPR) allows for the quick and less invasive screening of a variety of circulating indicators, such as circulating tumor DNA (ctDNA), microRNA (miRNA), circulating tumor cells (CTCs), lipids, and proteins. With several advantages, the SPR technique is a particularly beneficial choice for the point-of-care identification of biomarkers. As a result, it enables the timely detection of tumor markers, which could be used to track cancer development and suppress the relapse of malignant tumors. This review emphasizes advancements in SPR biosensing technologies for cancer detection.

Angiogenesis and epithelial–mesenchymal transition (EMT) are key hallmarks that contribute to the progression of oral squamous cell carcinoma (OSCC), but whether the two programs vary simultaneously across tumors and how much of this reflects tumor composition remain unclear. We scored predefined, non-overlapping 20-gene angiogenesis and EMT signatures with a rank-based method in 342 primary oral cavity tumors from The Cancer Genome Atlas (TCGA-OSCC). The two programs were strongly correlated (Spearman ρ = 0.809, P = 2.7 × 10 ⁻⁸⁰ ), and 2,396 bridge genes were associated with both programs across the transcriptome. The bridge genes were enriched in pathways associated with focal adhesion and extracellular matrix– receptor interaction. In the cellular case, fibroblast and endothelial marker scores were prominent and correlated with the program scores. The coupling was attenuated but remained positive after joint adjustment for tumor purity and stromal and immune scores (partial ρ = 0.406) and with an epithelial-restricted EMT score (ρ = 0.710). Further correlation was performed with a partial EMT (pEMT), which shows a significant positive correlation (ρ = 0.59) and an inverse correlation with tumor purity (ρ = −0.70). 146 final gene candidates were found using multi-omic evidence and candidate-level testing on the external cohort GSE30784; after adjusting for inferred cell fractions, 101 of these candidates supported the dual program. For thorough characterization, three candidates with an emphasis on OSMR, MICAL2, and LHFPL2 were chosen. Additional CPTAC data were used to confirm protein-level support, which was strongest for MICAL2. No significant connection was seen between the Interface score and overall survival (hazard ratio per 1-SD increase, 0.92; 95% CI, 0.78–1.08). These results describe a coordinated angiogenesis–EMT transcriptional state in OSCC that is attenuated but retained after accounting for tumor composition, and nominate candidate genes for experimental study.