DeCure's autonomous Rare AI scientist is researching a drug-repurposing hypothesis for familial adenomatous polyposis 2 — screening already-approved drugs against its 6-gene Open Targets disease module to publish open-access research. Research is fast; the path to publication is funded in milestone stages.
Disease moduleFamilial adenomatous polyposis 2 maps to a 6-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 familial adenomatous polyposis 2 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
vitamin D receptor (VDR) — VDR 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~{s},3~{z}drag to rotate · scroll to zoom
RCSB Protein Data Bank · entry 8IQN · 1.639 Å · ligand (1~{S},3~{Z})-3-[(2~{E})-2-[(1~{R},3~{a}~{S},7~{a}~{R})-1-[(2~{R})-5,5-bis(fluoranyl)-6-methyl-6-oxidanyl-heptan-2-yl]-7~{a}-methyl-2,3,3~{a},5,6,7-hexahydro-1~{H}-inden-4-ylidene]ethylidene]-4-methylidene-cyclohexan-1-ol (SRF). 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.
Archives of Pediatrics and Adolescent Medicine · 1996 · 85 citations
Genetic Testing for Cancer in Children
AbstractOBJECTIVE: To study the psychological effect of genetic testing in children. DESIGN: We evaluated the psychological effect of predictive genetic testing through surveys of children at risk for familial adenomatous polyposis. Their psychological state was assessed before testing and 3 months later. SETTING: A research clinic. PARTICIPANTS: A volunteer sample of 41 children, aged 6 to 16 years, and their parents. MAIN OUTCOME MEASURES: Self-report inventories of depression, anxiety, behavior problems, and competence. RESULTS: Nineteen children were found to have a gene mutation (mutation-positive) and 22 did not (mutation-negative). Their depression, anxiety, and behavior problem and competence scores remained in the normal range after testing. Also, parents' depression scores remained within normal limits at follow-up. There were subclinical changes, however. Mutation-positive children with affected mothers had significantly higher depression scores at follow-up. Also, regardless of test results, children with affected mothers had significantly increased anxiety scores after testing. In families with mutation-positive and mutation-negative children, familial adenomatous polyposis-unaffected parents experienced significantly increased depressive symptoms at follow-up. CONCLUSIONS: Predictive testing of children at risk for familial adenomatous polyposis did not lead to clinically significant psychological symptoms in tested children or their parents. However, it is premature to conclude that long-term follow-up will be equally favorable. Additional study will be needed to determine the families' understanding of the genetic information and the effect of the information on familial relationships.
Diseases of the Colon & Rectum · 2007 · 0 citations
The Mutation Spectrum of the APC Gene in Turkish Patients with Familial Adenomatous Polyposis
AbstractPURPOSE: Familial adenomatous polyposis, an autosomal-dominant disease characterized by the presence of 100 or more colorectal adenomatous polyps, results from mutations in the adenomatous polyposis coli tumor suppressor gene. This study was designed to investigate adenomatous polyposis coli gene mutations in members of Turkish families with familial adenomatous polyposis to constitute an adenomatous polyposis coli mutation spectrum for the Turkish population and to determine specific biomarkers for use in the early diagnosis of familial adenomatous polyposis. METHODS: We investigated adenomatous polyposis coli gene mutations in six unrelated families with familial adenomatous polyposis by using heteroduplex analysis and DNA sequencing. RESULTS: We identified three different mutations in six families. Of these one is known and two are novel: 1018T>C and 1309delGAAAA. The mutation of a T to C transversion at codon 1018 does not cause an alteration in the meaning of the codon; however, it was determined that this silent mutation does cause the formation of new exonic splicing enhancers (ESEs) motifs on a mutated sequence by using ESEfinder program. CONCLUSIONS: This study contributes to enlarging the adenomatous polyposis coli gene mutations spectrum and to defining new biomarkers for the early diagnosis of Turkish patients with familial adenomatous polyposis.
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.
