ArticleThe Journal of clinical endocrinology and metabolism2011
The Akt-specific inhibitor MK2206 selectively inhibits thyroid cancer cells harboring mutations that can activate the PI3K/Akt pathway.
Article in The Journal of clinical endocrinology and metabolism, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers, 1 of them a synthesis that pooled it.
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Who cites it
66 citing papers in PubMed, 1 synthesis or guideline pooled it, 105 citations in OpenAlex.
- Genetic mutations in the treatment of anaplastic thyroid cancer: a systematic review.BMC surgery · 2013Pooled it
- Preclinical and early clinical evaluation of the oral AKT inhibitor, MK-2206, for the treatment of acute myelogenous leukemia.Clinical cancer research : an official journal of the American Association for Cancer Research · 2014Trial
- Recent Advances in Neoadjuvant Treatment of Anaplastic Thyroid Carcinoma: A Narrative Review.Current treatment options in oncology · 2026Review
- Cancer Stemness and Dedifferentiation in Anaplastic Thyroid Carcinoma: Insights into a Multigenic, Microenvironmental Network and the Role of CD44.Biomedicines · 2026Review
- Cooperative CCL2/CCR2 and HGF/MET signaling enhances breast cancer growth and invasion associated with metabolic reprogramming.Cancer biology & therapy · 2025Article
- Targeting the CCL5/CCR5 axis in tumor-stromal crosstalk to overcome cisplatin resistance in neuroendocrine prostate cancer.Journal of experimental & clinical cancer research : CR · 2025Article
- Nf2/FGFR1/AKT axis directs cranial neural crest-derived skull morphogenesis via collagen synthesis and trafficking.JCI insight · 2025Article
- PTEN Regulates Myofibroblast Activation in Valvular Interstitial Cells Based on Subcellular Localization.Advanced biology · 2025Article
- OPN3-mediated positive regulation of angiogenesis in HUVECs through VEGFR2 interaction.Communications biology · 2025Article
- PTEN mutations impair CSF dynamics and cortical networks by dysregulating periventricular neural progenitors.Nature neuroscience · 2025Article
- Genomic alterations in thyroid cancer: biological and clinical insights.Nature reviews. Endocrinology · 2024Review
- Mechanistic Insights of Thyroid Cancer Progression.Endocrinology · 2023Review
- Additional Oncogenic Alterations in RAS-Driven Differentiated Thyroid Cancers Associate with Worse Clinicopathologic Outcomes.Clinical cancer research : an official journal of the American Association for Cancer Research · 2023Article
- A Predictive Model of Adaptive Resistance to BRAF/MEK Inhibitors in Melanoma.International journal of molecular sciences · 2023Article
- Genetic Characterization of Ovarian Tumor Tissues from Patients with Epithelial Ovarian Cancer in a Philippine Tertiary Hospital: A Descriptive Study.Asian Pacific journal of cancer prevention : APJCP · 2023Article
- Suppression of FAM83D Inhibits Glioma Proliferation, Invasion and Migration by Regulating the AKT/mTOR Signaling Pathway.Translational oncology · 2022Article
- Targeting NOX4 disrupts the resistance of papillary thyroid carcinoma to chemotherapeutic drugs and lenvatinib.Cell death discovery · 2022Article
- Article
- Nuclear interaction of Arp2/3 complex and BRAFAmerican journal of cancer research · 2022Article
- Role of PI3K/Akt/mTOR pathway in mediating endocrine resistance: concept to clinic.Exploration of targeted anti-tumor therapy · 2022Review
6 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
contextThe phosphoinositide 3-kinase (PI3K)/Akt pathway is widely postulated to be an effective therapeutic target in thyroid cancer.
objectiveThe aim of the study was to test the therapeutic potential of the novel Akt inhibitor MK2206 for thyroid cancer.
designWe examined the effects of MK2206 on thyroid cancer cells with respect to the genotypes of the PI3K/Akt pathway.
resultsProliferation of thyroid cancer cells OCUT1, K1, FTC133, C643, Hth7, and TPC1, which harbored PIK3CA, PTEN, Ras, or RET/PTC mutations that could activate the PI3K/Akt pathway, was potently inhibited by MK2206 with IC(50) values mostly below or around 0.5 μm. In contrast, no potent inhibition by MK2206 was seen in most of the Hth74, KAT18, SW1736, WRO, and TAD2 cells that did not harbor mutations in the PI3K/Akt pathway. The inhibition efficacy was also genetic-selective. Specifically, the average inhibition efficacies were 59.2 ± 11.3 vs. 36.4 ± 8.8% (P = 0.005) at 1 μm MK2206 and 64.4 ± 11.5 vs. 38.5 ± 18.9% (P = 0.02) at 3 μm MK2206 for cells with mutations vs. cells without. The SW1736 cell, lacking mutations in the PI3K/Akt pathway, had minimal response to MK2206, but transfection with exogenous PIK3CA mutants, PIK3CA H1047R and E545K, significantly increased its sensitivity to MK2206. MK2206 also completely overcame the feedback activation of Akt from temsirolimus-induced mammalian target of rapamycin suppression, and the two inhibitors synergistically inhibited thyroid cancer cell growth.
conclusionsOur study demonstrates a genetic selectivity of MK2206 in inhibiting thyroid cancer cells by targeting the PI3K/Akt pathway, supporting a clinical trial in thyroid cancer.
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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.