ArticleJournal of the Endocrine Society2017
EGFR Induces E2F1-Mediated Corticotroph Tumorigenesis.
Article in Journal of the Endocrine Society, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.
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
33 citing papers in PubMed, 1 synthesis or guideline pooled it, 48 citations in OpenAlex.
- Targeted analysis of Ubiquitin-Specific Peptidase (USP8) in a population of Iranian people with Cushing's disease and a systematic review of the literature.BMC endocrine disorders · 2024Pooled it
- Molecular biology of pituitary neuroendocrine tumors.Journal of neuro-oncology · 2026Review
- Independent signaling pathways provide a fail-safe mechanism to prevent tumorigenesis.bioRxiv : the preprint server for biology · 2025Article
- SKA3 promotes lung adenocarcinoma progression via the EGFR/E2F1/SKA3/integrin β1 signaling loop.Molecular and cellular biochemistry · 2025Article
- Glucocorticoid Resistance Syndrome as a Hidden Cause of Nonneoplastic Hypercortisolism.Journal of the Endocrine Society · 2025Article
- Management of Cushing's disease in the initial phase~From detection to surgery~.Endocrine journal · 2025Review
- Genetic models of Cushing's disease : From cells, in vivo transgenic models to human pituitary organoids.Pituitary · 2025Review
- Advances in the role of membrane-bound transcription factors in carcinogenesis and therapy.Discover oncology · 2024Review
- Article
- Transcriptome of GH-producing pituitary neuroendocrine tumours and models are significantly affected by somatostatin analogues.Cancer cell international · 2023Article
- Review
- Molecular Derangements and the Diagnosis of ACTH-Dependent Cushing's Syndrome.Endocrine reviews · 2022Review
- Aberrant Nuclear Translocation of E2F1 and Its Association in Cushing's Disease.Endocrinology · 2022Article
- Genetic Basis of ACTH-Secreting Adenomas.International journal of molecular sciences · 2022Review
- Current and Emerging Medical Therapies in Pituitary Tumors.Journal of clinical medicine · 2022Review
- Impact of RSUME Actions on Biomolecular Modifications in Physio-Pathological Processes.Frontiers in endocrinology · 2022Review
- The Clinical and Pathological Characteristics of Refractory Pituitary Adenomas: A Single Center Experience.Frontiers in oncology · 2022Article
- Tumor Shrinkage by Metyrapone in Cushing Disease Exhibiting Glucocorticoid-Induced Positive Feedback.Journal of the Endocrine Society · 2021Article
- Targeting the TR4 nuclear receptor with antagonist bexarotene can suppress the proopiomelanocortin signalling in AtT-20 cells.Journal of cellular and molecular medicine · 2021Article
- Aggressive Cushing's Disease: Molecular Pathology and Its Therapeutic Approach.Frontiers in endocrinology · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
The epidermal growth factor receptor (EGFR), expressed in adrenocorticotrophic hormone (ACTH)-secreting pituitary adenomas causing Cushing disease, regulates ACTH production and corticotroph proliferation. To elucidate the utility of EGFR as a therapeutic target for Cushing disease, we generated transgenic (Tg) mice with corticotroph-specific human EGFR expression (corti-EGFR-Tg) using a newly constructed corticotroph-specific promoter. Pituitary-specific EGFR expression was observed by 2.5 months, and aggressive ACTH-secreting pituitary adenomas with features of Crooke's cells developed by 8 months with 65% penetrance observed. Features consistent with the Cushing phenotype included elevated plasma ACTH and corticosterone levels, increased body weight, glucose intolerance, and enlarged adrenal cortex. Gefitinib, an EGFR tyrosine kinase inhibitor, suppressed tumor POMC expression and downstream EGFR tumor signaling, and ACTH and corticosterone levels were attenuated by 80% and 78%, respectively. Both E2F1 and phosphorylated Ser-337 E2F1 were increased in corti-EGFR-Tg mice and also colocalized with human POMC (hPOMC) in human pituitary corticotroph tumor samples. EGFR inhibition reversed E2F1 activity
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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.