ArticleGenes & diseases2014
LKB1 Tumor Suppressor: Therapeutic Opportunities Knock when LKB1 Is Inactivated.
Article in Genes & diseases, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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
31 citing papers in PubMed, 45 citations in OpenAlex.
- Genetic Medicine Approaches for Tumor Suppressor Loss: Therapeutic Replacement with Self-Amplifying RNA.Pharmaceutical research · 2026Review
- Ligand-Based Pharmacophore Mapping and Virtual Screening for the Search of Biguanide-Like Molecules With Antidiabetic Potentials Targeting Liver Kinase B1.Biochemistry research international · 2026Article
- Suppression of LKB1-mutant lung adenocarcinoma by natural killer cells from females.Journal of the National Cancer Institute · 2025Article
- Uncovering the rewired IAP-JAK regulatory axis as an immune-dependent vulnerability of LKB1-mutant lung cancer.Nature communications · 2025Article
- TGF-β1-mediated intercellular signaling fuels cooperative cellular invasion.Cell reports · 2025Article
- Metabolic Signaling in the Tumor Microenvironment.Cancers · 2025Review
- Quantification of AICAR and study of metabolic markers after administration.RSC advances · 2024Article
- Phase Ib/II Study of Lacnotuzumab in Combination with Spartalizumab in Patients with Advanced Malignancies.Journal of immunotherapy and precision oncology · 2024Article
- Metabolic heterogeneity in early-stage lung adenocarcinoma revealed by RNA-seq and scRNA-seq.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023Article
- Article
- Niche-Dependent Regulation of Lkb1 in the Proliferation of Lung Epithelial Progenitor Cells.International journal of molecular sciences · 2022Article
- Metformin resistant MDA-MB-468 cells exhibit EMT-like phenotype and increased migration capacity.Molecular biology reports · 2022Article
- Extracellular Vesicles Mediate Immune Responses to Tissue-Associated Self-Antigens: Role in Solid Organ Transplantations.Frontiers in immunology · 2022Review
- LKB1: Can We Target an Hidden Target? Focus on NSCLC.Frontiers in oncology · 2022Review
- LKB1 deficiency upregulates RELM-α to drive airway goblet cell metaplasia.Cellular and molecular life sciences : CMLS · 2021Article
- Leflunomide Suppresses the Growth of LKB1-Inactivated Tumors in the Immune-Competent Host and Attenuates Distant Cancer Metastasis.Molecular cancer therapeutics · 2021Article
- Activity of Birinapant, a SMAC Mimetic Compound, Alone or in Combination in NSCLCs With Different Mutations.Frontiers in oncology · 2020Article
- The Multifaceted Role of HSF1 in Tumorigenesis.Advances in experimental medicine and biology · 2020Review
- Haplotype-resolved and integrated genome analysis of the cancer cell line HepG2.Nucleic acids research · 2019Article
- LKB1 and YAP phosphorylation play important roles in Celastrol-induced β-catenin degradation in colorectal cancer.Therapeutic advances in medical oncology · 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
3 authors at 1 institution in 1 country.
Funding
Abstract
LKB1 is commonly thought of as a tumor suppressor gene because its hereditary mutation is responsible for a cancer syndrome, and somatic inactivation of LKB1 is found in non-small cell lung cancer, melanoma, and cervical cancers. However, unlike other tumor suppressors whose main function is to either suppress cell proliferation or promote cell death, one of the functions of LKB1-regulated AMPK signaling is to suppress cell proliferation in order to promote cell survival under energetic stress conditions. This unique, pro-survival function of LKB1 has led to the discovery of reagents, such as phenformin, that specifically exploit the vulnerability of LKB1-null cells in their defect in sensing energetic stress. Such targeted agents represent a novel treatment strategy because they induce cell killing when LKB1 is absent. This review article summarizes various vulnerabilities of LKB1-mutant cells that have been reported in the literature and discusses the potential of using existing or developing novel reagents to target cancer cells with defective LKB1.
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.