ArticleNature communications2017
Stem cell senescence drives age-attenuated induction of pituitary tumours in mouse models of paediatric craniopharyngioma.
Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.
What it found
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Who cites it
74 citing papers in PubMed, 133 citations in OpenAlex.
- Apc-deficient pituitary stem cells drive adamantinomatous craniopharyngioma through senescence-associated inflammation.EMBO molecular medicine · 2026Article
- Predicting early recurrence of craniopharyngioma using multi-omics radiomic modeling: a retrospective cohort study.Neurosurgical review · 2026Article
- Oncogene inactivation-induced senescence facilitates tumor relapse.Nature communications · 2026Article
- Laser microdissection-based multi-omics integration unveils the pathological atlas and tumor differentiation network of adamantinomatous craniopharyngioma.Acta neuropathologica communications · 2026Article
- Epigenetic dynamics of cellular senescence: From mechanistic insights to precision senotherapy.Chinese medical journal · 2026Review
- Consensus Pituitary Atlas, a scalable resource for annotation, novel marker discovery, and analyses in mouse pituitary gland research.Cell reports · 2026Article
- The role of stem cells in pituitary tumour formation.Endocrine-related cancer · 2026Review
- Cellular senescence in gastric cancer: a novel prognostic stratification and immune predictor.BMC medical genomics · 2026Article
- A Patient-Derived Organoid Biobank of Adamantinomatous Craniopharyngioma as a Platform for Drug Discovery.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Interrogation of the cellular hierarchies reveals neoplastic evolution and therapeutic vulnerability in craniopharyngioma.Neuro-oncology · 2026Article
- Navitoclax acts synergistically with irradiation to induce apoptosis in preclinical models of H3K27M-altered diffuse midline glioma.Scientific reports · 2025Article
- Transfer of Aging: Implications for Pediatric Solid Organ Transplantation.Pediatric transplantation · 2025Review
- Pharmacological Treatment for Adamantinomatous Craniopharyngioma.Current oncology reports · 2025Review
- Balancing senescence and apoptosis: therapeutic insights into aging and cancer.Molecular and cellular biochemistry · 2025Review
- Molecular subtypes of adamantinomatous craniopharyngiomas.Neuro-oncology · 2025Review
- New insights in cellular senescence: The pituitary model.Journal of neuroendocrinology · 2025Review
- Current clinical trials for craniopharyngiomas: what's on the horizon?Journal of neuro-oncology · 2025Review
- Finger-like protrusions in adamantinomatous craniopharyngiomas: implications for recurrence and prognosis following complete tumor resection and predictive factors.Neurosurgical review · 2025Article
- Senescence as a therapeutic target in cancer and age-related diseases.Nature reviews. Drug discovery · 2025Review
- Differential proteomic profiles of exosomes in pediatric and adult adamantinomatous craniopharyngioma cyst fluid.Molecular biology reports · 2024Article
14 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
19 authors at 8 institutions in 4 countries.
Funding
Abstract
Senescent cells may promote tumour progression through the activation of a senescence-associated secretory phenotype (SASP), whether these cells are capable of initiating tumourigenesis in vivo is not known. Expression of oncogenic β-catenin in Sox2+ young adult pituitary stem cells leads to formation of clusters of stem cells and induction of tumours resembling human adamantinomatous craniopharyngioma (ACP), derived from Sox2- cells in a paracrine manner. Here, we uncover the mechanisms underlying this paracrine tumourigenesis. We show that expression of oncogenic β-catenin in Hesx1+ embryonic precursors also results in stem cell clusters and paracrine tumours. We reveal that human and mouse clusters are analogous and share a common signature of senescence and SASP. Finally, we show that mice with reduced senescence and SASP responses exhibit decreased tumour-inducing potential. Together, we provide evidence that senescence and a stem cell-associated SASP drive cell transformation and tumour initiation in vivo in an age-dependent fashion.
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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.