Gynecologic cancers remain a major global health burden, particularly in low- and middle-income countries, with high incidence and mortality rates around 45–50%. The detection of minimal residual disease (MRD) is transforming the management of recurrence risk in gynecologic cancers through highly sensitive molecular technologies. MRD encompasses small populations of residual cancer cells or post-treatment molecular traces but remain undetectable by conventional methods. Its detection relies on circulating tumor DNA (ctDNA), circulating tumor cells (CTCs), and advanced next-generation sequencing (NGS), with ctDNA-based MRD assays having sensitivity levels between 85% and over 99%. Other technologies, such as liquid biopsies and digital PCR, are also in development. MRD status has demonstrated high predictors of recurrence and survival with positive MRD strongly associated with poor outcomes and negative MRD indicates sustained remission. However, MRD detection faces significant limitations, such as tumor heterogeneity, inconstant ctDNA levels, technical issues of false-negative results, and limited clinical accessibility. Therefore, this review presents current evidence regarding the molecular detection of MRD in gynecologic malignancies and assesses its prognostic and predictive relevance. Ultimately, MRD continuous integration into clinical practice offers a promising modality to enable early relapse detection, more precise therapeutic decision-making, and the improvement of personalized medicine access to gynecologic cancers worldwide.

Cervical cancer remains one of the most lethal cancers affecting women, with infection by high-risk Human Papillomavirus (HR-HPV), especially HPV-16, recognized as a primary cause. Phyllanthus urinaria, a plant that grows in Indonesia, has demonstrated notable both antiviral and anticancer properties. This study aimed to investigate the potential of P. urinaria as both an antiviral and anti-cervical cancer agent. The HPV-16 E6 protein was modeled using homology modelling, with model accuracy verified through torsional angle assessment and identification of conserved regions. Molecular docking was performed to examine E6–p53 interactions. Fraction of n-hexane compounds of P. urinaria were further evaluated for their interaction with E6 by molecular docking and molecular dynamics simulation. Additionally, in vitro cytotoxicity assays were conducted using HaCaT (normal keratinocyte) and HeLa (cervical cancer) cell lines. Compounds from P. urinaria were found to interact with E6 within conserved regions and these interactions were more stable conformationally than those observed for p53. In vitro assay demonstrated that P. urinaria exhibited moderate cytotoxicity against HeLa cells but had limited toxicity toward HaCaT cells. The n-hexane fraction of P. urinaria leaves exhibits anti-cervical cancer activity by inhibiting HPV-16 E6 and eliminating cervical cancer cells.

Background: Hemorrhagic wounds pose significant clinical challenges, with approximately 20% associated with surgical site infections and an increased mortality risk. Despite growing interest in natural product-based medicines, the molecular targets and bioactive phytochemicals of Musa acuminata peel relevant to hemorrhagic wound healing are insufficiently established. Methods: This study employed an integrative in silico approach to identify bioactive phytochemicals from the ethyl acetate extract of Musa acuminata peel as potential wound healing agents. Liquid chromatography-high resolution mass spectrometry (LC-HRMS) profiling was performed for phytochemical characterization, followed by drug-likeness and toxicity screening via OSIRIS DataWarrior. Network pharmacology, molecular docking, molecular dynamics (MD), binding free energy calculation, pharmacokinetic properties prediction, and density functional theory (DFT) analysis were subsequently conducted. Results: LC–HRMS profiling identified 211 compounds across 21 chemical classes, of which 18 met drug-likeness criteria. Network pharmacology revealed five key protein targets. Molecular docking demonstrated that Compound 16 (−9.34 kcal/mol) and Compound 17 (−9.26 kcal/mol) exhibited stronger binding affinity toward VEGFR2 than Axitinib (−9.15 kcal/mol), with key interactions at glutamic acid-917 (GLU917) and cysteine-919 (CYS919). MD simulations over 100 ns confirmed complex stability, with BP16 showing superior binding stability and favorable MM/PBSA free energy. Pharmacokinetics and DFT analysis further supported BP16 as the most promising lead compound, exhibiting favorable pharmacokinetic properties, low predicted toxicity, and enhanced electronic stability. Conclusions: BP16 and BP17 are identified as potential VEGFR2-targeting candidates, providing a rational mechanistic foundation for future experimental validation as natural hemorrhagic wound healing therapeutics.