Ganesan, N. | Search bioRxiv

bioRxiv2026

CancerStop.dev: An Interactive Web Platform Integrating Prognostic Data, Clinical Trials, and Genomic Resources for Patient Empowerment

Patients facing cancer diagnoses must navigate fragmented information spanning prognosis, clinical research opportunities, and genomics-informed therapy. CancerStop.dev is a React-based web platform that consolidates trusted public resources into a single patient-centered interface to support informed decision-making. The platforms built-in ComboReg module presents interactive relative survival estimates up to 10 years after diagnosis by modeling (combined regression) age-at-diagnosis and stage-at-diagnosis using publicly available data from the SEER Program. Users can adjust an age slider and view stage-specific curves, enabling individualized and comprehensible visualizations of survivorship trends. A Clinical Trials module links directly to ClinicalTrials.gov, providing context-aware queries and free-form keyword filtering (e.g., mutations, investigational agents) to surface ongoing studies. The Genes & More module connects to NCBI ClinVar for variant-level insights, facilitating precision medicine exploration when genetic testing results are available. An Approved Drugs module routes to the National Cancer Institute resources listing FDA-approved agents relevant to specific cancers, aiding therapy literacy. A curated search tool (PresciQure) complements these features by streamlining access to the biomedical literature, package inserts of FDA-approved drugs, and related oncology resources. The platform is non-prescriptive, emphasizes transparency regarding data provenance and limitations, and is positioned to incorporate additional cancer types, demographic stratifications, and multi-omic resources. CancerStop.dev aims to empower patients, caregivers, and clinicians with timely, integrated, and navigable information, thereby strengthening their advocacy and encouraging participation in research and precision care. SignificanceCancerStop.dev integrates prognosis, clinical trials, and genomic insights into a single, user-friendly platform, enabling patient and care teams to make faster, better-informed decisions.

cancer biology↗

bioRxiv2023

Effect of AM114 on apoptosis and proinflammatory cytokines in IL-1-beta treated human THP-1 derived macrophages

BackgroundChalcones and their derivatives are precursors of flavonoids and isoflavonoids abundantly present in edible plants. It displays a wide range of pharmacological activities, such as anticancer, antiinflammatory, antibacterial and antioxidant. AM-114 (3,5-Bis-[benzylidene-4-boronic acid]-1-methylpiperidin-4-one), a boronic-chalcone derivative exhibits potent anticancer activity through inhibition of the proteasome on human colon cancer cell line. However, the cytotoxic and anti-inflammatory effects of AM114 on THP-1 derived macrophages remain to be studied. Aim of the studyInflammation is a complex reaction managed by a variety of immune cells such as monocytes and macrophages. In response to inflammatory stimuli, the macrophages secrete increased proinflammatory cytokines, chemokines such as interleukin-6 (IL-6) and interleukin-8(IL-8). The proteasome complex is essential for several cellular processes including protein degradation, cellular differentiation and antigen presentation. In this study, human monocyte cell line THP-1 stimulated with interleukin-1-beta (IL-1-beta) was used as a model to investigate the in vitro effects of AM114, a proteasome inhibitor (PI), on apoptosis and release of proinflammatory cytokines. Materials and methodsThe effect of AM114, with or without IL-1-beta stimulated THP-1derived macrophages, was assessed by comparing with aspirin. The cell viability was determined by MTT assay. The qualitative measurement of apoptosis was determined by acridine orange/ ethidium bromide (AO/EtBr), Hoechst 33342 staining and rhodamine 123 assays. The quantitative measurement of apoptosis was carried out to determine the caspase-3 activity by spectrofluorimetric method and DNA fragmentation by agarose gel electrophoresis. The release of proinflammatory cytokines and chemokines such as IL-6 and IL-8 was also measured by enzyme linked immunosorbent assay (ELISA) method. The ANOVA was used to compare the different groups. ResultsIn the present study the IC50 concentration of AM114 and Aspirin on THP-1 cells were determined as 3.6 micromolar and 3900 micromolar respectively. The THP-1 derived macrophages treated with IL-1-beta showed insufficient apoptosis and increased release of proinflammatory cytokines. However the treatment of AM114, on stimulated THP-1 derived macrophages showed pronounced apoptotic features. The caspase-3 activity was increased 1.9 fold in AM114 with IL-1-beta treated THP-1 derived macrophages as compared to the unstimulated THP-1 derived macrophages pretreated with AM114. An increase of 3.2 fold in caspase-3 activity was observed in stimulated THP-1 derived macrophages pretreated with AM114 in comparison with stimulated THP-1 derived macrophages pretreated with aspirin. A significant increase of 5.0 and 3.0 fold DNA damage were observed in stimulated THP-1 derived macrophages treated with AM114 and aspirin as compared to unstimulated cells. Moreover AM114 treated cells showed significant decrease (p value less than 0.001) in the release of IL-6 and IL-8 on stimulated THP-1 derived macrophages. ConclusionThe results on the induction of apoptosis and suppression of proinflammatory cytokines suggest that AM114 is more effective than aspirin in stimulated THP-1 derived macrophages.

cell biology↗