DeCure for Liver inflammatory myofibroblastic tumor
DeCure's autonomous Cancer AI scientist is researching a drug-repurposing hypothesis for liver inflammatory myofibroblastic tumor — screening already-approved drugs against its 8-gene Open Targets disease module to publish open-access research. Research is fast; the path to publication is funded in milestone stages.
Disease moduleLiver inflammatory myofibroblastic tumor maps to a 8-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 liver inflammatory myofibroblastic tumor 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
clathrin heavy chain (CLTC) — CLTC 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 4-nitrophenyldrag to rotate · scroll to zoom
RCSB Protein Data Bank · entry 6E4L · 1.6 Å · ligand 5-bromo-N-(4-nitrophenyl)thiophene-2-sulfonamide (HRS). Experimental structure, not a prediction.
What the evidence adds up to
A 2004 case report describes a 7-year-old boy with a hilar inflammatory myofibroblastic tumour causing obstructive jaundice, portal vein phlebitis and occlusion. Attempted resection with portal vein reconstruction and bilioenteric drainage failed, and he required urgent orthotopic liver transplantation. The authors note that hilar lesions are locally aggressive, in contrast to more peripheral liver IMTs.
A 2021 retrospective review of seven children treated between 2006 and 2019 found that outcomes were good, with six of seven stable or in remission irrespective of treatment. Age range at presentation was 4 months to 15 years. Surgical resection where possible is the treatment of choice, and chemotherapy acted as first-line treatment when required. The only negative prognostic factor identified was local spread at presentation. A 2022 review states that hepatic IMTs are mostly benign and can regress spontaneously, but some patients develop relapses with conservative treatment, so many authors recommend surgery. A 2025 case report describes a 6-year-old girl with multicentric abdominal IMT whose massive tumour was treated with initial chemotherapy, producing a dramatic response in symptoms and size, which then allowed complete surgical resection with negligible postoperative morbidity. The authors conclude that initial chemotherapy for multicentric or locally advanced IMTs facilitates complete surgical resection.
A 2022 murine study on radiofrequency ablation of intrahepatic tumours found that activated myofibroblasts drive post-ablation tumour growth via the HGF/c-MET/STAT3 axis. Multi-day atorvastatin, a selective fibroblast inhibitor, reduced cellular and proliferative indices to baseline in micrometastatic models and completely inhibited accelerated growth of macrometastasis and negated increased intrahepatic burden in those models. This is preclinical work in mice, not human IMT patients.
What is still missing: prospective trials comparing chemotherapy regimens for unresectable or multicentric IMT, standardised criteria for when to operate versus when to observe or treat medically, and any human data on atorvastatin for IMT. The evidence base remains small retrospective series and single case reports.
Evidence
Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.
Pediatric Transplantation · 2004 · 23 citations
Liver transplantation for a hilar inflammatory myofibroblastic tumor
AbstractA 7-yr-old boy presented with obstructive jaundice secondary to an inflammatory myofibroblastic tumor centered on the hepatic hilum and extending into the liver. The tumor was further complicated by portal vein phlebitis and occlusion. Attempted resection of the tumor with portal vein reconstruction and bilioenteric drainage was unsuccessful and he required urgent orthotopic liver transplantation. In contrast to more peripheral inflammatory myofibroblastic tumors in the liver, hilar lesions are locally aggressive, causing occlusive portal phlebitis and biliary obstruction. Successful management may include the need for liver transplantation.
Journal of Pediatric Gastroenterology and Nutrition · 2021 · 5 citations
Paediatric Gastrointestinal, Hepatic and Pancreatic Inflammatory Myofibroblastic Tumours, A Single Centre Experience
AbstractABSTRACT: Inflammatory myofibroblastic tumours (IMTs) are rare soft tissue tumours. Reports of gastrointestinal tract, liver and pancreas tumours are limited. The objective of this study is to identify presenting features, contributing prognostic / etiological factors and any variability in outcomes in the context of different historical treatments. We retrospectively reviewed the records of seven children treated at our hospital between 2006 and 2019 and assessed the demographic, presentation, treatment, immunohistochemistry, and outcomes of their tumours. Age range at presentation was 4 months-15 years with a male predominance. Presentations were typically due to local mass effect or incidental discovery. Systemic symptoms were rare. Outcomes were good with six out of seven stable or in remission irrespective of treatment. Surgical resection where possible is the treatment of choice. Medical therapy had good outcomes with chemotherapy acting as first line treatment when required. The only negative prognostic factor identified was local spread at the time of presentation.
Myofibroblasts: A key promoter of tumorigenesis following radiofrequency tumor ablation
AbstractRadiofrequency ablation (RFA) of intrahepatic tumors induces distant tumor growth through activation of interleukin 6/signal transducer and activator of transcription 3 (STAT3)/hepatocyte growth factor (HGF)/tyrosine-protein kinase Met (c-MET) pathway. Yet, the predominant cellular source still needs to be identified as specific roles of the many types of periablational infiltrating immune cells requires further clarification. Here we report the key role of activated myofibroblasts in RFA-induced tumorigenesis and successful pharmacologic blockade. Murine models simulating RF tumorigenic effects on a macrometastatic tumor and intrahepatic micrometastatic deposits after liver ablation and a macrometastatic tumor after kidney ablation were used. Immune assays of ablated normal parenchyma demonstrated significantly increased numbers of activated myofibroblasts in the periablational rim, as well as increased HGF levels, recruitment other cellular infiltrates; macrophages, dendritic cells and natural killer cells, HGF dependent growth factors; fibroblast growth factor-19 (FGF-19) and receptor of Vascular Endothelial Growth Factor-1 (VEGFR-1), and proliferative indices; Ki-67 and CD34 for microvascular density. Furthermore, macrometastatic models demonstrated accelerated distant tumor growth at 7d post-RFA while micrometastatic models demonstrated increased intrahepatic deposit size and number at 14 and 21 days post-RFA. Multi-day atorvastatin, a selective fibroblast inhibitor, inhibited RFA-induced HGF and downstream growth factors, cellular markers and proliferative indices. Specifically, atorvastatin treatment reduced cellular and proliferative indices to baseline levels in the micrometastatic models, however only partially in macrometastatic models. Furthermore, adjuvant atorvastatin completely inhibited accelerated growth of macrometastasis and negated increased micrometastatic intrahepatic burden. Thus, activated myofibroblasts drive RF-induced tumorigenesis at a cellular level via induction of the HGF/c-MET/STAT3 axis, and can be successfully pharmacologically suppressed.
Research and Practical Medicine Journal · 2022 · 1 citations · open access
Inflammatory myofibroblastic liver tumor
AbstractInflammatory myofibroblastic tumors (inflammatory myofibroblastic tumors) IMT in the clinical practice of an oncologist are very rare diagnostic findings. Currently, the bulk of scientific publications about IMT are devoted to reviews of clinical cases. If initially IMT were considered as pseudo-tumors, now they are classified as intermediate fibroblastic/myofibroblastic tumors according to the WHO histological classification. Management of patients with hepatic IMT are debatable today. Hepatic IMT are mostly benign lesions and characterized by spontaneous regression without any treatment. However, sometimes therapeutic and surgical treatment of these lesions is necessary. Many authors recommend surgical treatment, as with conservative treatment, some patients develop relapses. This rare observation demonstrates our experience of liver resection for inflammatory myofibroblastic liver tumor in 76 year-old patient.
Journal of Gastrointestinal Cancer · 2025 · 1 citations · open access
Can Chemotherapy Facilitate Less Morbid Surgery in Multicentric Intra-abdominal Inflammatory Myofibroblastic Tumor?
AbstractBACKGROUND: Inflammatory myofibroblastic tumor is a rare benign neoplasm affecting young adults and children. Although often considered benign, its locally aggressive nature and tendency to recur make its management immensely challenging, particularly without robust evidence to guide treatment. Surgical excision offers the best hope for a cure; however, this can lead to significant morbidity and may not always be possible, especially for multicentric diseases. CASE PRESENTATION: We report a multicentric abdominal inflammatory myofibroblastic tumor in a 6-year-old girl who presented with massive abdominal distention. The sheer size of the mass, coupled with multicentric presentation and absent mobility on clinical examination, would have led to a very morbid surgical exploration. This patient was treated with initial chemotherapy, which led to a dramatic response in both symptoms and size of masses, facilitating a complete surgical resection with negligible postoperative morbidity. CONCLUSIONS: Although surgery is the preferred treatment for a resectable disease, initial chemotherapy for multicentric or locally advanced inflammatory myofibroblastic tumors facilitates complete surgical resection.
Inflammatory myofibroblastoma mimicking cavernous hemangioma in the liver
AbstractA 37-year-old female patient was admitted to the hospital with a large liver mass, diagnosed as hepatic inflammatory myofibroblastic tumour (HIMT), characterized by unique radiographic features and predominantly occurring in adults. HIMT consists of myofibroblast spindle cells infiltrated by plasma cells and/or lymphocytes, with an unclear aetiology linked to factors like infection and immune response. Treatment typically involves surgical resection, with chemotherapy or targeted therapy options for cases of incomplete resection or metastasis, emphasizing the need for precise diagnosis and tailored treatment strategies.
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.
