Dokyoung Kim

Cervical cancer remains a leading cause of cancer-related mortality among women worldwide, with mortality disproportionately concentrated in low-and middle-income countries (LMICs), where screening infrastructure is limited. Although persistent high-risk human papillomavirus (hrHPV) infection drives nearly all cervical cancers through a prolonged preinvasive window, making the disease both preventable and detectable, current screening modalities face biological and operational limitations that constrain their global impact. Cytology-based methods suffer from moderate sensitivity and subjective interpretations. HPV DNA testing is highly sensitive, it lacks specificity for transforming infections and shifts the diagnostic burden toward triage and colposcopy. Meanwhile, visual inspection methods are accessible, they offer limited reproducibility. In this review, we adopt a target-centric diagnostic framework that organizes cervical cancer screening not by detection platform but by the biological class of the marker being interrogated. We first examined the molecular pathogenesis of cervical carcinogenesis, including HPV genotype-specific biology, viral integration dynamics, oncogene-driven transformation, and epigenetic consolidation, to establish the biological rationale for each biomarker category. We then systematically evaluated conventional screening modalities and their limitations before reviewing emerging diagnostic technologies across four target domains: HPV-derived markers (DNA, mRNA, capsid proteins), host cell-cycle regulators (p16^INK4a, Ki-67), non-protein biomarkers (biothiols, volatile metabolites), and marker-free platforms (Raman/FT-IR spectroscopy, AI-assisted cytopathology). Particular emphasis is placed on point-of-care (POC) deployability, noninvasive sampling strategies, and the integration of multilayered risk stratification into scalable screening pathways. By mapping diagnostic innovation onto the biological continuum of cervical carcinogenesis, this review provides a conceptual foundation for developing next-generation screening approaches that align molecular precision with global accessibility, thereby supporting progress toward the World Health Organization goal of cervical cancer elimination.

Objectives/Background: This study aimed to systematically summarize and pool the available evidence on the risk of incident hypertension associated with calcitonin gene‐related peptide (CGRP)–targeted therapies. CGRP‐targeted therapies have emerged as effective preventive treatments for migraine; however, concerns have been raised regarding their potential hypertensive effects. Prior studies have been limited by small sample sizes, inconsistent definitions of hypertension, and incomplete trial inclusion. Methods: We systematically searched MEDLINE, Embase, and ClinicalTrials.gov up to September 25, 2024. We included randomized controlled trials comparing CGRP‐targeted therapies with placebo or another intervention arm in adult patients with migraine. The primary outcome was incident hypertension as defined by each individual study. Two reviewers independently assessed risk of bias using the Cochrane Risk of Bias 2 tool and rated the certainty of evidence using the Grading of Recommendations Assessment, Development, and Evaluation approach. Results: Eight publications or trial reports, comprising 19 underlying randomized controlled trials, were included. The pooled relative risk (RR) for hypertension with CGRP‐targeted therapies versus control was 0.91 (95% confidence interval [CI] 0.58–1.43; I ² = 0.0%), indicating no statistically significant increased risk. The certainty of evidence for this outcome was rated as very low. Erenumab showed no significant increase in risk (RR 0.71, 95% CI 0.30–1.70), whereas galcanezumab also showed no statistically significant association (RR 1.14, 95% CI 0.54–2.39). Conclusion: CGRP‐targeted therapies were not associated with a statistically significant increase in hypertension risk in patients with migraine, particularly among relatively healthy populations enrolled in short‐term randomized controlled trials. However, the certainty of evidence was very low, and possible variation across agents warrants further study. Longer term comparative studies and real‐world observational studies with standardized blood pressure monitoring are needed to confirm these findings and better define hypertension risk in higher risk patient subgroups.

Organic fluorescent dyes are indispensable tools in bioimaging; however, their translational viability increasingly depends on pharmacokinetic performance rather than optical brightness alone. For systemically administered small-molecule dyes, the dominant elimination route, renal versus hepatobiliary, is largely encoded by a compact set of structural and physicochemical variables that can be deliberately programmed during the synthetic stage. This review presents a chemical design framework for controlling clearance by examining four interconnected determinants: (i) the serum state of the dye, governed by protein binding and aggregation propensity, which defines effective hydrodynamic behavior in circulation; (ii) charge distribution and charge topology, which regulate the hydration shell and nonspecific adsorption to biological surfaces; (iii) lipophilicity and solvent-exposed aromatic surface area, which bias hepatic uptake and biliary processing; and (iv) scaffold stability and susceptibility to biotransformation, which determine whether dyes are eliminated intact or as polar metabolites. Practical structure–clearance design rules and emerging opportunities in data-driven clearance prediction and standardized pharmacokinetic reporting are discussed to accelerate the rational development of clearance-tunable imaging agents for clinical use.