ArticleScience translational medicine2016
Targeted BMI1 inhibition impairs tumor growth in lung adenocarcinomas with low CEBPα expression.
Article in Science translational medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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
32 citing papers in PubMed, 52 citations in OpenAlex.
- Dual actionability of BMI1 activation and mitotic vulnerability defines adaptive Osimertinib resistance in EGFR-mutant NSCLC.Cell death & disease · 2026Article
- Progress and prospects of the combination of BMI1-targeted therapy and immunotherapy in cervical cancer.American journal of cancer research · 2025Review
- A comprehensive analysis of CEBPA on prognosis and function in uterine corpus endometrial carcinoma.Scientific reports · 2024Article
- Unveiling the Effects of the COVID-19 Pandemic on Lung Cancer Surgery.Medicina (Kaunas, Lithuania) · 2024Article
- Tumor Microenvironment Landscapes Supporting EGFR-mutant NSCLC Are Modulated at the Single-cell Interaction Level by Unesbulin Treatment.Cancer research communications · 2024Article
- Signaling pathways in cancer metabolism: mechanisms and therapeutic targets.Signal transduction and targeted therapy · 2023Review
- Targeting cancer stemness mediated by BMI1 and MCL1 for non-small cell lung cancer treatment.Journal of cellular and molecular medicine · 2022Article
- LKB1 drives stasis and C/EBP-mediated reprogramming to an alveolar type II fate in lung cancer.Nature communications · 2022Article
- Identification of a targetable KRAS-mutant epithelial population in non-small cell lung cancer.Communications biology · 2021Article
- The Role of Polycomb Group Protein BMI1 in DNA Repair and Genomic Stability.International journal of molecular sciences · 2021Review
- Article
- Extended lifespan of bronchial epithelial cells maintains normal cellular phenotype and transcriptome integrity.ERJ open research · 2021Article
- Article
- H2A Monoubiquitination Links Glucose Availability to Epigenetic Regulation of the Endoplasmic Reticulum Stress Response and Cancer Cell Death.Cancer research · 2020Article
- A novel BMI-1 inhibitor QW24 for the treatment of stem-like colorectal cancer.Journal of experimental & clinical cancer research : CR · 2019Article
- The Polycomb Repressor Complex 1 Drives Double-Negative Prostate Cancer Metastasis by Coordinating Stemness and Immune Suppression.Cancer cell · 2019Article
- Effects of C/EBPα overexpression on alveolar epithelial type II cell proliferation, apoptosis and surfactant protein-C expression after exposure to hyperoxia.BMC pulmonary medicine · 2019Article
- Acute myeloid leukemia driven by the CALM-AF10 fusion gene is dependent on BMI1.Experimental hematology · 2019Article
- Article
- BMI1 is a therapeutic target in recurrent medulloblastoma.Oncogene · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
32 authors at 10 institutions in 4 countries.
Funding
Abstract
Lung cancer is the most common cause of cancer deaths. The expression of the transcription factor C/EBPα (CCAAT/enhancer binding protein α) is frequently lost in non-small cell lung cancer, but the mechanisms by which C/EBPα suppresses tumor formation are not fully understood. In addition, no pharmacological therapy is available to specifically target C/EBPα expression. We discovered a subset of pulmonary adenocarcinoma patients in whom negative/low C/EBPα expression and positive expression of the oncogenic protein BMI1 (B lymphoma Mo-MLV insertion region 1 homolog) have prognostic value. We also generated a lung-specific mouse model of C/EBPα deletion that develops lung adenocarcinomas, which are prevented by Bmi1 haploinsufficiency. BMI1 activity is required for both tumor initiation and maintenance in the C/EBPα-null background, and pharmacological inhibition of BMI1 exhibits antitumor effects in both murine and human adenocarcinoma lines. Overall, we show that C/EBPα is a tumor suppressor in lung cancer and that BMI1 is required for the oncogenic process downstream of C/EBPα loss. Therefore, anti-BMI1 pharmacological inhibition may offer a therapeutic benefit for lung cancer patients with low expression of C/EBPα and high BMI1.
Indexed as
Identifiers
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.