ReviewCancers2019
Neurokinin-1 Receptor Antagonists against Hepatoblastoma.
Review in Cancers, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
19 citing papers in PubMed, 34 citations in OpenAlex.
- Insights into the mechanisms of angiogenesis in hepatoblastoma.Frontiers in cell and developmental biology · 2025Review
- Dual regulation of gastrointestinal tumor progression by the IFN-γ/STAT1 pathway and prospects for targeted therapy.Frontiers in oncology · 2025Review
- Advances in the research and application of neurokinin-1 receptor antagonists.Journal of Zhejiang University. Science. B · 2024Review
- Association of Neurokinin-1 Receptor Signaling Pathways with Cancer.Current medicinal chemistry · 2024Review
- Summary of biological research on hepatoblastoma: a scoping review.Frontiers in pediatrics · 2024Article
- The Repurposing of Non-Peptide Neurokinin-1 Receptor Antagonists as Antitumor Drugs: An Urgent Challenge for Aprepitant.International journal of molecular sciences · 2023Review
- Aprepitant inhibits the development and metastasis of gallbladder cancer via ROS and MAPK activation.BMC cancer · 2023Article
- IFN-γ-STAT1-mediated NK2R expression is involved in the induction of antitumor effector CD8Cancer science · 2023Article
- Substance P-Friend or Foe.Journal of clinical medicine · 2022Article
- The Prognostic Potential of Neurokinin 1 Receptor in Breast Cancer and Its Relationship with Ki-67 Index.International journal of breast cancer · 2022Article
- Identification of Key Pathways Involved in White Strain ofFrontiers in pharmacology · 2022Article
- Transcriptome analysis revealed the role of mTOR and MAPK signaling pathways in the white strain ofFrontiers in pharmacology · 2022Article
- The Neurokinin-1 Receptor Is a Target in Pediatric Rhabdoid Tumors.Current oncology (Toronto, Ont.) · 2021Article
- Expression of Neurokinin B Receptor in the Gingival Squamous Cell Carcinoma Bone Microenvironment.Diagnostics (Basel, Switzerland) · 2021Article
- Neuropeptide Substance P Enhances Inflammation-Mediated Tumor Signaling Pathways and Migration and Proliferation of Head and Neck Cancers.Indian journal of surgical oncology · 2021Article
- Review
- Molecular Mechanisms of Hepatoblastoma.Seminars in liver disease · 2021Article
- Emerging Role and Mechanism of circRNAs in Pediatric Malignant Solid Tumors.Frontiers in genetics · 2021Review
- The Neurokinin-1 Receptor Antagonist Aprepitant: An Intelligent Bullet against Cancer?Cancers · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatoblastoma (HB) is the most common malignant liver tumor that occurs during childhood. The prognosis of children with HB is favorable when a complete surgical resection of the tumor is possible, but for high-risk patients, the prognosis is much worse. New anti-HB strategies must be urgently developed. The undecapeptide substance P (SP) after binding to the neurokinin-1 receptor (NK-1R), regulates cancer cell proliferation, exerts an antiapoptotic effect, induces cell migration for invasion/metastasis, and triggers endothelial cell proliferation for neoangiogenesis. HB samples and cell lines overexpress NK-1R (the truncated form) and SP elicits HB cell proliferation. One of these strategies could be the use of non-peptide NK-1R antagonists. These antagonists exert, in a concentration-dependent manner, an antiproliferative action against HB cells (inhibit cell proliferation and induce the death of HB cells by apoptosis). NK-1R antagonists exerted a dual effect in HB: Decreased both tumor volume and angiogenic activity. Thus, the SP/NK-1R system is an important target in the HB treatment and NK-1R antagonists could act as specific drugs against HB cells. In this review, we update and discuss the use of NK-1R antagonists in the treatment of HB.
Indexed as
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.