A grade PMID 42321916
View analysis →Finding therapies hidden in 39,000 pediatric cancer papers.
Neurocompute scores pediatric oncology literature, surfaces overlooked therapeutic signals, and turns fragmented childhood cancer research into a living discovery terminal.
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A grade PMID 42690647
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All ranked pediatric cancer papers
In a retrospective cohort of 69 childhood cancer survivors with preserved follow-up LVEF, ventricular-arterial coupling was associated with anthracycline exposure and cardiotoxicity risk but did not differ overall between survivors and healthy controls or outperform LVEF.
The study provides evidence that VAC may complement echocardiographic surveillance in higher-risk childhood cancer survivors; it remains an inference, requiring prospective validation, that VAC-guided monitoring could enable earlier cardioprotective intervention or improve outcomes.
In a retrospective matched case-control study of 64 children with brain tumors or non-traumatic intracranial hemorrhage, implementation of a multidisciplinary emergency activation protocol was associated with shorter consultation-to-operating-room times and, in urgent hemorrhage cases, faster initial imaging.
The reported evidence supports improved workflow timing after protocol activation; it is reasonable but unproven to hypothesize that reducing these delays could improve neurologic or oncologic outcomes, because morbidity, survival, safety, and other patient-centered outcomes were not reported.
In a prospective observational cohort of 32 children receiving 106 high-dose methotrexate cycles for high-risk acute lymphoblastic leukemia, 48-hour single-point monitoring identified adequate clearance in 74.5% of cycles and elevated levels were associated with several toxicities.
The study provides preliminary evidence that a single 48-hour methotrexate measurement can guide discharge and trigger intensified hydration and leucovorin rescue in a preselected pediatric population; it is inferred, but not established, that this strategy could preserve safety while reducing monitoring burden and cost in resource-limited settings.
In a retrospective case series of five patients with anti-NMDAR encephalitis after first-line treatment failure, intravenous efgartigimod was associated with reduced disability scores and serum IgG, CSF antibody negativity in four patients, improvement in MRI or EEG abnormalities, and no reported serious adverse effects.
The reported clinical and biomarker changes support investigating FcRn inhibition as salvage therapy for refractory anti-NMDAR encephalitis; it is inferred, but not established by this uncontrolled series, that depletion of pathogenic IgG caused the neurological improvement or that the approach would benefit pediatric-oncology patients.
The study reports that neuroblastoma and patient-derived glioblastoma cells exhibit adhesion-associated morphologies in a 3D spherical cavity platform, with N-cadherin blockade disrupting spheroids and enhancing DOX cytotoxicity in malignant phenotypes.
The reported 3D associations and ADH-1 experiments support N-cadherin as an adhesion-related vulnerability; it remains an inference, not clinical evidence, that N-cadherin inhibition combined with chemotherapy could improve treatment selection or responses in aggressive neuroblastoma or glioblastoma.
This scoping review reports that hypothalamic obesity is more prevalent and rises more sharply after treatment in pediatric than adult craniopharyngioma, summarizes candidate biological pathways, and finds mixed, limited evidence for GLP-1 receptor agonists and bariatric surgery.
Evidence summarized in the review suggests that GLP-1 receptor agonism and selected bariatric procedures may reduce weight in some craniopharyngioma survivors with hypothalamic obesity; it remains an inference that mechanism- and age-tailored selection would improve pediatric cardiometabolic outcomes because randomized weight endpoints were negative and direct pediatric-versus-adult comparisons are absent.
The study reports that PAX3::FOXO1-directed PROTACs degraded up to 70% of endogenous fusion protein in fusion-positive rhabdomyosarcoma cell lines, altered its gene-expression signature, induced myogenic differentiation, synergized with vincristine, and reduced anchorage-independent growth by more than 80%.
The supplied in-vitro evidence supports targeted, proteasome-dependent degradation of PAX3::FOXO1 and associated differentiation and growth impairment; it is reasonable but still inferential to hypothesize that optimized clinical-grade degraders could suppress fusion-positive rhabdomyosarcoma or enhance vincristine activity in patients.
The study reports that BAIAP2 is overexpressed in medulloblastoma, that its knockdown reduces medulloblastoma-cell proliferation and migration, and that the BAIAP2-binding compound NSC678917 produces similar cellular effects.
The supplied evidence identifies BAIAP2 as a candidate medulloblastoma dependency and NSC678917 as a BAIAP2-binding preclinical hit; it is reasonable—but not yet demonstrated—to hypothesize that pharmacologic disruption of the BAIAP2 pathway could limit tumor growth or dissemination in vivo.
This single-institution retrospective cohort of 10 patients with desmoid-type fibromatosis reports a 60% overall response rate, sustained disease control in several cases, and no grade 3–4 adverse events with a strategy using celecoxib followed by methotrexate-vinblastine for progression.
The observed outcomes suggest that celecoxib may provide a tolerable initial disease-control option and that methotrexate-vinblastine may salvage some progressing cases; however, the inference that this sequence should be a primary treatment strategy requires confirmation in larger, age-specific prospective comparisons.
In samples from 61 adults with AML, multiparametric flow cytometry showed generally high CD84 expression across disease stages, leukemic subpopulations, and major molecular subtypes, while measured expression differed substantially between antibody clones.
The reported persistence and breadth of CD84 expression support target availability in adult AML; it is reasonable but still inferential to hypothesize that CD84-directed therapies, including CAR T cells, could cover heterogeneous or relapsed AML populations, because this study provides no therapeutic efficacy, safety, or pediatric validation.
This review summarizes recent PPGL guidance, emphasizing genotype-tailored care, specialized pediatric protocols, revised histopathology, advanced targeted therapies, and predictive tools.
The supplied record supports genotype-first management as an organizing clinical strategy for PPGL; it is plausible, but not demonstrated here, that matching surveillance, surgery, or targeted therapy to hereditary genotype could improve outcomes or reduce unnecessary treatment in pediatric patients.
In a single-center retrospective series of 14 adults with progressive or surgically unfavorable pilocytic astrocytoma, proton radiotherapy was associated with frequent radiographic regression, estimated 5-year overall survival of 100%, estimated 5-year progression-free survival of 83.3%, and predominantly low-grade toxicity, although radiation-induced contrast enhancement occurred in three patients.
The reported human observational evidence suggests that proton radiotherapy may provide durable local disease control with acceptable toxicity in selected adults with difficult-to-resect pilocytic astrocytoma; it is an inference—not established by this uncontrolled series—that proton dose distribution could offer a clinically meaningful late-toxicity advantage over other radiotherapy approaches or that these findings apply to pediatric patients.