DeCure's autonomous Rare AI scientist is researching a drug-repurposing hypothesis for Familial adenomatous polyposis — screening already-approved drugs against its 36-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 maps to a 36-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 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
transthyretin (TTR) — TTR 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 2,4-dimethylphenyldrag to rotate · scroll to zoom
RCSB Protein Data Bank · entry 8C86 · 1.1 Å · ligand (2,4-dimethylphenyl)(4-hydroxy-3-methoxy-5-nitrophenyl)methanone (TQ0). Experimental structure, not a prediction.
What the evidence adds up to
In a prospective endoscopic follow-up of 50 patients with familial adenomatous polyposis in northern Italy, duodenal adenomas were found in 19 patients (38 percent) at the first endoscopy and in 43 (86 percent) by the end of the study. The mean Spigelman score, which grades precancerous duodenal lesions, increased significantly over the follow-up period. No duodenal cancer was detected. Eleven patients developed stage IV (severe) precancerous duodenal lesions and were treated with endoscopic or surgical resection. Among those with stage IV disease, 2 of 25 patients who had undergone proctocolectomy with ileoanal anastomosis reached that stage, compared with 8 of 15 patients who had colectomy with ileorectal anastomosis (p=0.0024). The authors concluded that the natural history of precancerous duodenal lesions in FAP may be related to the type of colorectal surgery performed.
A separate case report describes a 57-year-old man with a submucosally invasive well-differentiated rectal adenocarcinoma and approximately 100 adenomatous polyps confined to the rectum and sigmoid colon. There was no family history of colorectal disease and no extracolonic manifestations. Screening for an APC germline mutation using protein truncation test and single-stranded conformation polymorphism found no mutation. The authors suggested this might represent a novel entity of adenomatous polyposis with a peculiar distribution, possibly caused by a genetic alteration other than APC mutation.
A 1990 book review of a volume titled Familial Adenomatous Polyposis is also listed but provides no original data.
What remains missing is any prospective trial testing a drug to reduce polyp burden or prevent cancer in FAP. The evidence above is limited to surgical outcomes and a single unusual case. No randomised controlled trial, no biomarker-stratified patient selection, and no funding for a repurposing study are described.
Evidence
Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.
Diseases of the Colon & Rectum · 2006 · 7 citations · open access
Impact of Surgery on the Development of Duodenal Cancer in Patients with Familial Adenomatous Polyposis
AbstractPURPOSE: Precancerous duodenal lesions in patients with familial adenomatous polyposis can be detected with duodenoscopy and treatment may prevent the development of cancer. We proposed to determine the frequency, natural history, cumulative risk, and risk factors of the precancerous duodenal lesions in a series of patients diagnosed in northern Italy. METHODS: A prospective, endoscopic, follow-up protocol was performed in 50 patients examined by gastroduodenoscopy at two years of interval or less. The presence and severity of precancerous lesions of the duodenal mucosa were evaluated by Spigelman score. Twenty-five patients (50 percent) had proctocolectomy and ileoanal anastomosis, 15 (30 percent) had colectomy and ileorectal anastomosis, and 5 (10 percent) had proctocolectomy and definitive ileostomy from 0 to 3 years before the admission to the surveillance program. All patients showed more than a thousand adenomas in the colorectal mucosa. No patients with attenuated polyposis were found. RESULTS: At the first endoscopy, duodenal adenomas could be detected in 19 of 50 patients (38 percent), whereas at the end of the follow-up, 43 (86 percent) had duodenal lesions. The final mean Spigelman score increased during the follow-up period (P<0.001 respect to baseline values). No duodenal cancer could be detected. Eleven patients had or developed severe precancerous duodenal lesions (Stage IV) treated with endoscopic or surgical resection. The distribution of patients with Stage IV according to the surgery of the colon was: 2 of 25 treated with ileoanal anastomosis and 8 of 15 with ileorectal anastomosis (P=0.0024, Fisher's exact test). CONCLUSIONS: Patients with familial adenomatous polyposis are at risk of significant neoplasia. The natural history of precancerous lesions might be related to surgical treatment of colorectal neoplasms.
JNCI Journal of the National Cancer Institute · 1990 · 0 citations
BOOK REVIEWS
AbstractJournal Article BOOK REVIEWS Get access Familial Adenomatous Polyposis . Lemuel Herrera , ed. New York : Alan R. Liss, Inc. , 1989 , 430 pp. $129.50. HANS E. KAISER HANS E. KAISER Department of Pathology, University of Maryland, School of Medicine 10 S. Pine St. Baltimore, MD 21201 Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 82, Issue 17, 5 September 1990, Page 1430, https://doi.org/10.1093/jnci/82.17.1430 Published: 05 September 1990
Diseases of the Colon & Rectum · 2000 · 0 citations
Rectosigmoidal adenomatous polyposis: A novel entity of polyposis?
AbstractPURPOSE: We report a patient with rectosigmoidal adenomatous polyposis. METHODS: A 57-year-old male presented with a submucosally invasive well-differentiated adenocarcinoma in the rectum and approximately 100 adenomatous polyps with an extremely unusual distribution limited exclusively to the rectum and sigmoid colon. RESULTS: There was no family history of colorectal disease or any related disorders. No extracolonic manifestations were found. Because this case was considered to be a discriminative phenotype of familial adenomatous polyposis, DNA from a peripheral sample of whole blood was screened for APC germline mutation by a combination of protein truncation test and single stranded conformation polymorphism, but no mutation was found. CONCLUSION: This patient may have a novel entity of adenomatous polyposis with a peculiar distribution. It may be caused by some genetic alteration other than APC mutation.
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.
