DeCure for Autoimmune lymphoproliferative syndrome type 2A
DeCure's autonomous Immuno AI scientist is researching a drug-repurposing hypothesis for autoimmune lymphoproliferative syndrome type 2A — 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 moduleAutoimmune lymphoproliferative syndrome type 2A 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 autoimmune lymphoproliferative syndrome type 2a 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.
What the evidence adds up to
Autoimmune lymphoproliferative syndrome type 2A is a childhood disorder of abnormal lymphocyte homeostasis. Deficient Fas-mediated apoptosis caused by a mutation of the Caspase-10 gene is an important factor in its pathogenesis. A 2001 review noted that in one subpopulation of ALPS patients no mutations had been identified at that time, and argued that this group, then called ALPS type III, could be more common than believed because the variability of clinical presentation and absence of a known genetic defect made diagnosis difficult. A 2005 case report described a patient whose clinical features were consistent with ALPS but stated that a precise diagnosis required more laboratory evaluations.
Two abstracts from 2018 and 2002 concern lymphoproliferative disorders in different contexts. The 2018 report described two patients with long-standing autoimmune diseases on immunosuppressants who developed aggressive lymphoproliferative disorders; sustained regression occurred with simple discontinuation of the immunosuppressive agents. The 2002 clinico-pathologic conference described an 18-month-old boy with severe combined immunodeficiency who died after developing post-transplant lymphoproliferative disorder following a bone marrow transplant. Neither abstract involves ALPS type 2A or any drug treatment for it.
No abstract in this set reports any drug tested in autoimmune lymphoproliferative syndrome type 2A, any survival or response rate, or any sample of patients with that specific mutation. What is missing is any clinical trial, any drug candidate, any patient stratification by Caspase-10 genotype, and any funding for research directed at this precise disorder.
Evidence
Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.
Leukemia & lymphoma/Leukemia and lymphoma · 2001 · 30 citations
Autoimmune Lymphoproliferative Syndrome Type III: An Indefinite Disorder
AbstractAutoimmune Lymphoproliferative Syndrome (ALPS) is a childhood disorder characterized by chronic nonmalignant lymphoproliferation and autoimmunity. Although the pathogenesis is not fully understood, deficient Fas mediated apoptosis appears to be an important factor. This deficiency can be caused by a mutation of the APT1 gene (ALPS type Ia), of the FasL gene (ALPS type Ib), or of the Caspase-10 gene (ALPS type II). In one sub population of patients, no mutations have been identified as yet (ALPS type III). According to published data, the latter group is much smaller than the group of patients with ALPS type Ia. However, because of the variability of the clinical presentation and the absence of a known genetic defect, this disease is difficult to diagnose, the more so as few data have been reported on these patients. Thus, ALPS type III could be more common than believed until now. In this review we provide evidence for this hypothesis.
Autoimmune lymphoproliferative syndrome: meticulous care for diagnosis.
AbstractAutoimmune lymphoproliferative syndrome (ALPS) is a prototypic disorder of abnormal lymphocyte homeostasis. In the September 2005 issue of The Iranian Journal of Allergy, Asthma and Immunology, a patient with clinical features consistent with ALPS was described. Although the clinical presentation was in favor of ALPS, a precise diagnosis needed more laboratory evaluations.
BMJ Case Reports · 2018 · 2 citations · open access
Treatment of advanced stage methotrexate-associated lymphoproliferative disorders (MTX-LPDs) with methotrexate discontinuation
AbstractWe present two cases of patient's with long-standing autoimmune diseases being treated with immunosuppressants that developed aggressive lymphoproliferative disorders. Immunosuppressants have a well-known association with disorders. Sustained regression of these lymphoproliferative disorders occurred with simple discontinuation of these immunosuppressive agents.
Fetal and Pediatric Pathology · 2002 · 0 citations
CLINICO-PATHOLOGIC CONFERENCE: 18-MONTH-OLD BOY WITH FEVER AND SEVERE RESPIRATORY INFECTION
AbstractAn 18-month-old boy with severe combined immunodeficiency (SCID) due to an IL2-y-receptor defect had a successful engraftment following a related mismatched allogeneic bone transplant. He subsequently developed post-transplant lymphoproliferative disorder, with severe respiratory infection which resulted in death. The case presentation is followed by a discussion with differential diagnosis of the clinical findings, and then by a discussion of the pathology found and the implications of this diagnosis.
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.
