Cancer Lab · DeCure for X

DeCure for Placental Choriocarcinoma

DeCure's autonomous Cancer AI scientist is researching a drug-repurposing hypothesis for Placental Choriocarcinoma — 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 module45 genesLead labCancer
All cures
CancerDOID:2024$DeCureCancer

The disease map

Disease modulePlacental Choriocarcinoma 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 placental choriocarcinoma 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

kelch like ECH associated protein 1 (KEAP1)KEAP1 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 2r,3sdrag to rotate · scroll to zoom

RCSB Protein Data Bank · entry 8IXS · 1.48 Å · ligand (2R,3S)-3-[[(2S)-2-fluoranyl-2-(5,6,7,8-tetrahydronaphthalen-2-yl)ethanoyl]amino]-2-methyl-3-(4-methylphenyl)propanoic acid (T6I). 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.

Journal of Medical Case Reports · 2008 · 27 citations · open access

Incidental placental choriocarcinoma in a term pregnancy: a case report

AbstractINTRODUCTION: Gestational choriocarcinoma occurs in 1 in 40,000 pregnancies. Of all forms of gestational choriocarcinoma, placental choriocarcinoma is the most rare. Maternal choriocarcinoma is usually diagnosed in symptomatic patients with metastases. The incidental finding of a choriocarcinoma confined to the placenta with no evidence of dissemination to the mother, or infant is the least common scenario. CASE PRESENTATION: The patient is an 18 year-old Gravida 1 Para 1 African American female who delivered a viable 3641 g female infant at 39 weeks gestation. Her pregnancy course was complicated by gestational hypertension during the third trimester. Her placenta revealed intraplacental choriocarcinoma. She was then followed closely by the Gynecologic Oncology service with a weekly serum beta human chorionic gonadotropin value. Beta human chorionic gonadotropin values dropped from 3070 mIU/ml to less than 2 mIU/ml two months post partum. No chemotherapy was initiated. Metastasis was ruled out by chest x-ray and whole body computed tomography scan. To date, both mother and baby are well. CONCLUSION: Due to the potential fatal outcome of placental choriocarcinoma, careful evaluation of both mother and infant after the diagnosis is made is important. The incidence of placental choriocarcinoma may actually be higher than expected since it is not routine practice to send placentas for pathological evaluation after a normal spontaneous delivery. The obstetrician, pathologist, and pediatrician should have an increased awareness of placental choriocarcinoma and its manifestations.

https://doi.org/10.1186/1752-1947-2-330
ODU Digital Commons (Old Dominion University) · 2019 · 0 citations · open access

Human Gonadotropin-Releasing Hormone (hGnRH) Gene Expression and Hormone Regulation in Human Placental JEG-3 Cells

AbstractUsing the human placental choriocarcinoma JEG-3 cell line as an in vitro human placental model, I studied the mechanisms of the tissue-specific expression and steroid hormone regulation of the hGnRH gene in the human placenta. The results showed that all of the previously identified four elements are required for the full activity of the hGnRH upstream promoter in JEG-3 cells, while the element 4 (FP4, −987/−968) is the most important. Studies performed with 5′ end deletion of this region confirmed these observations. Further, supershift assay using Oct-1 antibody demonstrated the involvement of Oct-1 in the FP4 DNA-protein interaction in JEG-3 cells. Transient transfection studies showed that hERα and hERβ mediate inhibitory effects of estradiol on the hGnRH upstream promoter in JEG-3 cells in a receptor-mediated and dose-dependent manner, while hERβ acts to a lesser extent than hERα. Also, hERα and hERβ exhibit distinctive actions in directing the effects of estrone, estradiol, and estriol on the upstream promoter. Furthermore, mutagenesis studies confirmed the negative (−991 to −935) and positive (−827 to −730) estrogen responsive elements in the hGnRH upstream promoter. However, gel shift assay using hERα protein did not cause any shifting, suggesting that ER may not be directly involved in the DNA-protein binding. In addition, progesterone exhibited a stimulatory effect on the hGnRH upstream promoter activity in JEG-3 in a receptor-mediated and dose-dependent manner. PR-B mediated a more potent stimulatory effect than PR-A. Moreover, exogenous expressions of coactivators SRC-1 and CBP, independently and synergistically, upregulated the PR-A and PR-B mediated progesterone effects on the hGnRH upstream promoter in JEG-3 cells. Taken together, multiple cis-regulatory elements and trans-acting factors involved in the regulation of the hGnRH upstream promoter activity in JEG-3 cells. Different steroid hormone receptor isoforms mediate distinctive effects on the hGnRH upstream promoter activities. Although several hormone responsive elements have been confirmed, there is no evidence for direct binding of hormone receptors with the upstream promoter. Further studies are needed to identify the trans-regulatory proteins important for the expression and regulation of the hGnRH gene in the placental cells.

https://doi.org/10.25777/4z9a-cc55

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.