ReviewCellular and molecular life sciences : CMLS2021
Adamantinomatous craniopharyngioma as a model to understand paracrine and senescence-induced tumourigenesis.
Review in Cellular and molecular life sciences : CMLS, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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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.
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Who cites it
20 citing papers in PubMed, 56 citations in OpenAlex.
- Aprepitant, a Neurokinin-1 Receptor Antagonist, as a Disruptive Drug for the Treatment of Pediatric Cancer.Journal of clinical medicine · 2026Review
- A Patient-Derived Organoid Biobank of Adamantinomatous Craniopharyngioma as a Platform for Drug Discovery.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Antibody-drug conjugates for primary brain tumors.Frontiers in oncology · 2026Review
- Pharmacological Treatment for Adamantinomatous Craniopharyngioma.Current oncology reports · 2025Review
- Cellular senescence in cancer: Unveiling dual roles, tumor microenvironment dynamics and therapeutic innovations (Review).Oncology letters · 2025Review
- FAP as a prognostic biomarker and radiomics-based predictor of angiogenesis-associated recurrence in Adamantinomatous craniopharyngioma.Pituitary · 2025Article
- Molecular subtypes of adamantinomatous craniopharyngiomas.Neuro-oncology · 2025Review
- New insights in cellular senescence: The pituitary model.Journal of neuroendocrinology · 2025Review
- (B)On(e)-cohistones and the epigenetic alterations at the root of bone cancer.Cell death and differentiation · 2025Review
- The SASP factor IL-6 sustains cell-autonomous senescent cells via a cGAS-STING-NFκB intracrine senescent noncanonical pathway.Aging cell · 2024Article
- Targeting Cell Senescence and Senolytics: Novel Interventions for Age-Related Endocrine Dysfunction.Endocrine reviews · 2024Review
- Single-cell and spatial sequencing identifies senescent and germinal tumor cells in adamantinomatous craniopharyngiomas.Cell & bioscience · 2024Article
- Unraveling the complexity of the senescence-associated secretory phenotype in adamantinomatous craniopharyngioma using multimodal machine learning analysis.Neuro-oncology · 2024Article
- The significance ofFrontiers in immunology · 2024Review
- Single-cell RNA sequencing highlights intratumor heterogeneity and intercellular network featured in adamantinomatous craniopharyngioma.Science advances · 2023Article
- Inhibition of integrated stress response protects against lipid-induced senescence in hypothalamic neural stem cells in adamantinomatous craniopharyngioma.Neuro-oncology · 2023Article
- Is "cellular senescence" a misnomer?GeroScience · 2022Review
- Adamantinomatous craniopharyngioma cyst fluid can trigger inflammatory activation of microglia to damage the hypothalamic neurons by inducing the production of β-amyloid.Journal of neuroinflammation · 2022Article
- Hypothalamic syndrome.Nature reviews. Disease primers · 2022Review
- Update on management of craniopharyngiomas.Journal of neuro-oncology · 2022Review
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
Abstract
Cellular senescence is a process that can prevent tumour development in a cell autonomous manner by imposing a stable cell cycle arrest after oncogene activation. Paradoxically, senescence can also promote tumour growth cell non-autonomously by creating a permissive tumour microenvironment that fuels tumour initiation, progression to malignancy and metastasis. In a pituitary tumour known as adamantinomatous craniopharyngioma (ACP), cells that carry oncogenic β-catenin mutations and overactivate the WNT signalling pathway form cell clusters that become senescent and activate a senescence-associated secretory phenotype (SASP). Research in mouse models of ACP has provided insights into the function of the senescent cell clusters and revealed a critical role for SASP-mediated activities in paracrine tumour initiation. In this review, we first discuss this research on ACP and subsequently explore the theme of paracrine tumourigenesis in other tumour models available in the literature. Evidence is accumulating supporting the notion that paracrine signalling brought about by senescent cells may underlie tumourigenesis across different tumours and cancer models.
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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.