DeCure's autonomous Cancer AI scientist is researching a drug-repurposing hypothesis for male reproductive organ cancer — screening already-approved drugs against its 34-gene Open Targets disease module to publish open-access research. Research is fast; the path to publication is funded in milestone stages.
Disease moduleMale reproductive organ cancer maps to a 34-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 male reproductive organ cancer 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
SET and mariner transposase domain methyltransferase (SETMAR) — SETMAR 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 sahdrag to rotate · scroll to zoom
RCSB Protein Data Bank · entry 3BO5 · 1.59 Å · ligand S-ADENOSYL-L-HOMOCYSTEINE (SAH). Experimental structure, not a prediction.
What the evidence adds up to
The 2025 mouse study tested naringenin, a flavonoid, against cisplatin-induced testicular damage. In that experiment, naringenin treatment normalised total oxidant status, total antioxidant capacity, and the oxidative stress index in cisplatin-treated male mice, while reducing the pro-inflammatory cytokines TNF-α, IL-1β, and IL-6 and suppressing NF-κB activation. Naringenin also restored the Bax/Bcl-2 balance and suppressed p38 MAPK activation. Histological assessments showed improved seminiferous tubule morphology and spermatogenesis in the naringenin-plus-cisplatin group. These are mouse data only; no human trial is reported.
A 2019 analysis of cancer cell lines found that the correlation between the genes DDR1 and ZEB1 was sex-dependent in liver cancer cell lines but not in colon or lung cancer cell lines. In female-derived liver cancer lines a negative correlation was observed, whereas in male-derived lines it was not. Kaplan-Meier survival curves from public databases suggested a sex-biased difference in the correlation between DDR1 expression and overall survival in liver cancer patients. The study did not examine male reproductive organ cancers directly.
A 2023 review on male infertility and urological tumours was retracted. The remaining abstracts from 1996 and 2014 are general reviews that describe the negative impact of genitourinary cancer treatments — orchiectomy, prostatectomy, radiotherapy, chemotherapy, hormonal suppression — on male sexual function and fertility, and note that cryopreservation, GnRH analogues, and androgen replacement are available preservation strategies. No new drug intervention is tested in those reviews.
What is missing: human clinical data for naringenin in men receiving cisplatin; any trial that tests a drug specifically for male reproductive organ cancer in patients; prospective studies that stratify patients by sex or by DDR1/ZEB1 expression; and funding for translational work that moves the mouse naringenin findings into a phase 1 safety study.
Evidence
Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.
Oncology Letters · 2019 · 13 citations · open access
Sex‑biased differences in the correlation between epithelial‑to‑mesenchymal transition‑associated genes in cancer cell lines
AbstractThere is a wide disparity in the incidence, malignancy and mortality of different types of cancer between each sex. The sex-specificity of cancer seems to be dependent on the type of cancer. Cancer incidence and mortality have been demonstrated as sex-specific in a number of different types of cancer, such as liver cancer, whereas sex-specificity is not noticeable in certain other types of cancer, including colon and lung cancer. The present study aimed to elucidate the molecular basis for sex-biased gene expression in cancer. The mRNA expression of the epithelial-to-mesenchymal transition-associated genes was investigated, including E-cadherin (also termed CDH1), vimentin (VIM), discoidin domain receptor 1 (DDR1) and zinc finger E-box binding homeobox 1 (ZEB1) in female- and male-derived cancer cell lines by reverse transcription (RT)-PCR and the Broad-Novartis Cancer Cell Line Encyclopedia (CCLE) database analysis. A negative correlation was observed between DDR1 and ZEB1 only in the female-derived cancer cell lines via RT-PCR analysis. A negative correlation between DDR1 index (defined by the logarithmic value of DDR1 divided by ZEB1, based on the mRNA data from the RT-PCR analysis) and an invasive phenotype was observed in cancer cell lines in a sex-specific manner. Analysis of the CCLE database demonstrated that DDR1 and ZEB1, which are already known to be sex-biased, were negatively correlated in female-derived liver cancer cell lines, but not in male-derived liver cancer cell lines. In contrast, cell lines of colon and lung cancer did not reveal any sex-dependent difference in the correlation between DDR1 and ZEB1. Kaplan-Meier survival curves using the transcriptomic datasets such as Gene Expression Omnibus, European Genome-phenome Archiva and The Cancer Genome Atlas databases suggested a sex-biased difference in the correlation between DDR1 expression pattern and overall survival in patients with liver cancer. The results of the present study indicate that sex factors may affect the regulation of gene expression, contributing to the sex-biased progression of the different types of cancer, particularly liver cancer. Overall, these findings suggest that analyses of the correlation between DDR1 and ZEB1 may prove useful when investigating sex-biased cancers.
Urologia Journal · 2023 · 5 citations · open access
RETRACTED: Male infertility and urological tumors: Pathogenesis and therapeutical implications
AbstractMost genitourinary tract cancers have a negative impact on male fertility. Although testicular cancers have the worst impact, other tumors such as prostate, bladder, and penis are diagnosed early and treated in relatively younger patients in which couple fertility can be an important concern. The purpose of this review is to highlight both the pathogenetic mechanisms of damage to male fertility in the context of the main urological cancers and the methods of preserving male fertility in an oncological setting, in light of the most recent scientific evidence. A systematic review of available literature was carried out on the main scientific search engines, such as PubMed, Clinicaltrials.Gov, and Google scholar. Three hundred twenty-five relevant articles on this subject were identified, 98 of which were selected being the most relevant to the purpose of this review. There is a strong evidence in literature that all of the genitourinary oncological therapies have a deep negative impact on male fertility: orchiectomy, partial orchiectomy, retroperitoneal lymphadenectomy (RPLND), radical cystectomy, prostatectomy, penectomy, as well as radiotherapy, chemotherapy, and hormonal androgen suppression. Preservation of fertility is possible and includes cryopreservation, hormonal manipulation with GnRH analogs before chemotherapy, androgen replacement. Germ cell auto transplantation is an intriguing strategy with future perspectives. Careful evaluation of male fertility must be a key point before treating genitourinary tumors, taking into account patients' age and couples' perspectives. Informed consent should provide adequate information to the patient about the current state of his fertility and about the balance between risks and benefits in oncological terms. Standard approaches to genitourinary tumors should include a multidisciplinary team with urologists, oncologists, radiotherapists, psycho-sexologists, andrologists, gynecologists, and reproductive endocrinologists.
AbstractCancer is a common medical problem. The disease itself and its treatment has many complex effects on male sexual function, hormonal status and fertility and these effects can easily be underestimated by the health care professional. The patient and his partner may feel that discussing such problems is not only embarrassing but inappropriate in the presence of a serious and potentially life threatening medical condition. This paper reviews potential problems related to male sexual health following the diagnosis and treatment of a malignancy. There are general details about the psychological impact and specific details of the repercussions from cancer treatment for a range of malignancies. The sexual consequences for men with cancer of the testis and prostate are discussed in some detail. The appendix lists resources and information for sufferers and their families.
British Journal of Healthcare Assistants · 2014 · 2 citations
Men's health series 3: two male-specific cancers
AbstractMen are as likely as women to develop a whole range of cancers. This article will define what is meant by the term ‘cancer’, present a number of basic statistics relating to cancer and will then highlight two specific male cancers: cancer of the prostate gland and testicular cancer. The causes, effects and treatments of these two specific cancers will be presented.
Protective effect of Naringenin on cisplatin-testicular damage through the oxidation and p38 MAPK inflammatory pathway
AbstractOBJECTIVE: Cisplatin (CIS), a platinum-based chemotherapeutic, is highly effective in cancer treatment but often leads to severe adverse effects, including testicular damage and infertility. The oxidative stress and inflammation induced by CIS result in disrupted spermatogenesis, decreased testosterone levels, and testicular apoptosis, primarily mediated by elevated reactive oxygen species (ROS), pro-inflammatory cytokines, and activation of pathways like NF-κB and p38 MAPK. This study explores the protective role of naringenin (NG), a flavonoid with antioxidant, anti-inflammatory, and anti-apoptotic properties, in mitigating CIS-induced testicular damage in a murine model. METHODS: Male mice were divided into control, CIS, NG, NG + CIS treated groups. Key outcomes included serum testosterone levels, oxidative stress markers, inflammatory mediators, Bax/Bcl-2 expression, histopathological evaluations, and morphometric analyses. RESULTS: NG treatment attenuated CIS-induced oxidative stress by normalizing total oxidant status (TOS), total antioxidant capacity (TAC), and oxidative stress index (OSI) levels while reducing pro-inflammatory cytokines (TNF-α, IL-1β, IL-6) and NF-κB activation. NG also modulated apoptotic pathways by restoring the balance of Bax/Bcl-2 and suppressing p38 MAPK activation. Histological assessments revealed improved seminiferous tubule morphology and spermatogenesis in the NG+CIS group. CONCLUSIONS: NG effectively counteracts CIS-induced testicular toxicity, highlighting its therapeutic potential in preserving male fertility during chemotherapy by mitigating oxidative, inflammatory, and apoptotic damage.
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.
