DeCure's autonomous Cancer AI scientist is researching a drug-repurposing hypothesis for astrocytoma — screening already-approved drugs against its 45-gene Open Targets disease module to publish open-access research. Research is fast; the path to publication is funded in milestone stages.
Disease moduleAstrocytoma maps to a 45-gene Open Targets module — the target space DeCure's AI scientist screens approved drugs against.
DeCure.ai methodSignature reversal (LINCS) plus network proximity (STRING) rank already-approved drugs likely to perturb this module — the same engine that produces DeCure.ai's repurposing hypotheses.
Repurposing thesisScreening approved medicines against this disease module, then publishing the evidence for the strongest candidate. Known pharmacology and human exposure data make the first question sharper — they do not establish safety or efficacy in a new indication.
Research record
01
ResearchComing soon
Candidate research + dossier — target rationale, drug-repurposing thesis and evidence pack.proof: Published dossier + on-chain hash
02
ValidationComing soon
In-vitro biological validation at a contract research org (CRO).proof: CRO contract + in-vitro report
03
Peer review & paperComing soon
Peer-reviewed paper published open-access (preprint + journal).proof: DOI + open-access link + on-chain hash
Current lead
No approved-drug candidate for astrocytoma is corroborated in the literature DeepSearch retrieved. Some conditions are managed with non-pharmacological care — a device, surgery or physical therapy — rather than a medicine; that may be the case here, or the literature we found may simply be too sparse yet to support a drug-repurposing angle.
Molecular view
fibroblast growth factor receptor 4 (FGFR4) — FGFR4 is one of the genes genetically linked to this disease in Open Targets — shown as context, not as a drug target we're pursuing: no approved-drug candidate for this disease is yet corroborated in the literature we found.
Loading structure…
helix sheet 1~{r}drag to rotate · scroll to zoom
RCSB Protein Data Bank · entry 8KH8 · 1.49 Å · ligand 1-[4-[(1~{R})-1-[3,5-bis(chloranyl)pyridin-4-yl]ethoxy]-5-cyano-pyridin-2-yl]-3-[6-methanoyl-5-[(4-methyl-2-oxidanylidene-piperazin-1-yl)methyl]-3-(2-morpholin-4-ylethoxy)pyridin-2-yl]urea (VVW). Experimental structure, not a prediction.
Evidence
Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.
OncoTargets and Therapy · 2019 · 8 citations · open access
<p>Biological Functions of TNKS1 and Its Relationship with Wnt/β-Catenin Pathway in Astrocytoma</p>
AbstractBACKGROUND: Tankyrase1 (TNKS1), which often shows abnormal expression in many malignant tumor cells, plays an important role in tumor progression. In our previous study, we found that TNKS1 is also closely related to pathologic grade in human astrocytoma and its expression level is positively correlated with the Wnt/β-catenin pathway. This study is aimed to further elucidate the biological functions of TNKS1 as well as its relationship with the Wnt/β-catenin pathway. METHODS: TNSK1 overexpression and knockdown vectors were constructed and transfected into glioblastoma cell lines U251 MG and U87, respectively. Viability, apoptosis, cell cycle and cell invasiveness in the treated cells were investigated. RESULTS: In comparison with untreated cells, U251 and U87 cells overexpressing TNSK1 showed significantly increased cell viability and decreased apoptosis, while the TNKS1 knockdown U251 and U87 cells had reduced cell invasive ability and increased apoptosis, respectively. In addition, immunoprecipitation study showed that TNKS1 could be detected by β-catenin antibody after pull-down, indicating that TNKS1 directly interacts with β-catenin, further indicating that TNKS1 could be regarded as a positive regulator of the Wnt/β-catenin pathway in astrocytoma. Moreover, knockdown of TNKS1 in U251 and U87 cells also leads to suppressed Wnt/β-catenin signaling, and subsequent decrease of cell growth and proliferation, reduced invasion ability and increased apoptosis. CONCLUSION: Our findings suggest that TNKS1 might be a potential new therapeutic target for human astrocytoma in gene therapy.
AbstractAstrocytoma of the brain in adults is invariably a fatal disease. The majority of cases present with inoperable, high-grade III or IV tumours. The place of radiotherapy in the management of such cases is of limited value. However, prolonged remission, and even occasional cures, have been reported (Sheline, 1977). Recurrence of high-grade astrocytoma long after surgery and/or radiotherapy is a rare event in clinical practice. Radical surgery has no place in such cases. Chemotherapy has also been tried with occasional transient success (Levin et al, 1980). Re-irradiation of selected cases has been tried in the past with occasional short remission in some patients (Dritschillo et al, 1981). We present the treatment result of a 36-year-old woman with recurrent Grade III astrocytoma, 9 years after initial biopsy and radiotherapy, who was given a second course of radiotherapy and chemotherapy.
Disease module: DeepOracle (Open Targets). Structures: RDKit from PubChem SMILES. Literature: retrieved by DeepSearch across 234,678,978 indexed works (targeted per-candidate search), resolved on OpenAlex.
DeCure is a research and publication project, not medical advice and not a treatment. "DeCure for X" describes a research goal, not a claim that a cure exists. Backing a cure is a contribution to fund the research — it is not an investment, and confers no yield, royalty, equity or IP ownership. Papers are published open-access by the DeCure.ai DAO.
