DeCure's autonomous Cancer AI scientist is researching a drug-repurposing hypothesis for teratocarcinoma — screening already-approved drugs against its 1-gene Open Targets disease module to publish open-access research. Research is fast; the path to publication is funded in milestone stages.
Disease moduleTeratocarcinoma maps to a 1-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 teratocarcinoma 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
DAB adaptor protein 2 (DAB2) — DAB2 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 apo structuredrag to rotate · scroll to zoom
RCSB Protein Data Bank · entry 6O5O · 1.75 Å · ligand none (apo structure). Experimental structure, not a prediction.
What the evidence adds up to
A 1980 review notes that murine teratocarcinomas serve as models for human disease, containing differentiated tissues from all three germ layers plus the malignant embryonal carcinoma component. A teratoma is defined as a benign tumour lacking embryonal carcinoma.
A 1982 case report describes a 21-year-old man with mediastinal teratocarcinoma who had elevated serum alpha-fetoprotein (AFP), human chorionic gonadotropin (HCG), and carcinoembryonic antigen (CEA). After modified VAC chemotherapy (vincristine, dactinomycin, cyclophosphamide), serum AFP and HCG fell significantly, but serum CEA rose gradually to 6.5 ng/ml. Tumour tissue obtained at surgery and autopsy contained high levels of AFP (17,353.8 ng/g wet weight), beta-HCG (125.05 ng/g), and CEA (11.37 ng/g). Immunoperoxidase staining localised all three antigens to immature glandular tissue within the teratoma component.
A 2004 gene expression study used Affymetrix U74A microarrays to compare mouse embryonic stem (ES) cell cultures and tumours with the teratocarcinoma cell line SCC-PSA1 and its tumours in nude mice. Sixty-eight genes differed significantly between ES cell culture and the teratocarcinoma line, and 51 between ES cell tumours and teratocarcinomas (P < 0.00005). Twenty genes were common to both comparisons. Comparing ES cell culture to ES cell tumour identified 22 upregulated and 42 downregulated genes (P < 0.0001); comparing the teratocarcinoma cell line to its tumour identified 34 upregulated and 25 downregulated genes (P < 0.001). Only 10 genes overlapped between these two lists. GenMapp analysis pointed to the cell cycle pathway as actively involved in teratocarcinoma induction. The authors conclude that many key developmental genes may play a role in the transformation of ES cells into teratocarcinoma cells.
What remains missing is any controlled clinical trial of a repurposed drug in human teratocarcinoma. The 1982 case is a single patient, the 2004 study is purely preclinical in mice, and the 1980 review offers no therapeutic intervention. No drug beyond the standard VAC regimen appears in these abstracts. Patient stratification by marker profile or gene expression signature has not been tested prospectively. Funding for a systematic drug screen in teratocarcinoma models or for a multi-centre trial in the rare human disease is absent.
Evidence
Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.
Cancer · 1982 · 19 citations
Alpha-fetoprotein (AFP), human chorionic gonadotropin (HCG), and carcinoembryonic antigen (CEA) demonstrated in the immature glands of mediastinal teratocarcinoma. A case report
AbstractA 21-year-old man with mediastinal teratocarcinoma showed high levels of serum tumor markers: alpha-fetoprotein (AFP), human chorionic gonadotropin (HCG), and carcinoembryonic antigen (CEA). After modified VAC chemotherapy (vincristine, dactinomycin, and cyclophosphamide), AFP and HCG levels in the serum were reduced significantly, while serum CEA increased gradually to the level of 6.5 ng/ml. Histopathologic study of the tumor obtained by surgical resection and autopsy revealed teratocarcinoma (a combination of embryonal carcinoma and teratoma). By the indirect immunoperoxidase technique, the antigens AFP, HCG, and CEA were stained in the immature glandular tissues of teratoma. By serial section of the tumor, the antigens tested were found in the same gland of the tumor. In addition, the tumor contained high levels of AFP (17353.8 ng/g.wt.), beta-HCG (beta-HCG) (125.05 ng/g.wt.), and CEA (11.37 ng/g.wt.).
Gene Expression Profiling of Mouse Teratocarcinomas Uncovers Epigenetic Changes Associated with the Transformation of Mouse Embryonic Stem Cells
AbstractThe molecular mechanisms of the development of teratocarcinomas from stem cells are largely unknown. To determine which genes are associated with the transformation of these cells, we have performed oligonucleotide microarray analysis, using Affymetrix U74A GeneChips, on both cell cultures and tumors in nude mice. We identified 68 genes that significantly differed in expression between the ES cell culture and the teratocarcinoma cell line, SCC-PSA1, and 51 genes with statistically different expression patterns between the ES cell tumors and the teratocarcinomas (P < .00005). We found that there were 20 genes that had common expression patterns in both groups. We also examined the role of the transition from in vitro to in vivo by comparing ES cell culture to ES cell tumor, and teratocarcinoma cell line to teratocarcinomas. We identified 22 genes that were upregulated in the ES cell tumors and 42 that had a decreased expression in the tumor (P < .0001). In comparing SCC-PSA1 to its tumor, we identified 34 upregulated genes and 25 downregulated genes (P < .001). There were only 10 genes in common from these two lists. GenMapp search revealed that several pathways, especially the cell cycle pathway, are actively involved in the induction of teratocarcinomas. Our results indicate that many key development genes may play a key role in the transformation of ES cells into teratocarcinoma cells.
AbstractTeratocarcinomas of mice, like other murine tumors, have been used as models of their counterparts in man. Like human teratocarcinomas they contain differentiated tissues representing each of the primary germ layers, as well as embryonal carcinoma, a highly malignant tissue so-named because it resembles embryonic epithelium of the human embryo. A teratoma is a benign tumor containing derivatives of the three germ layers but devoid of embryonal carcinoma (Dixon and Moore, 1953).
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.
