ArticleClinical cancer research : an official journal of the American Association for Cancer Research2011
Targeting the BMK1 MAP kinase pathway in cancer therapy.
Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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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.
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Who cites it
24 citing papers in PubMed, 30 citations in OpenAlex.
- A different MAPK, ERK5 plays a critical role in cell specification and differentiation.Biochemistry and biophysics reports · 2026Review
- The Polynomial Progression Subtype Inference Algorithm.Research square · 2025Article
- The significance of ERK5 catalytic-independent functions in disease pathways.Frontiers in cell and developmental biology · 2023Review
- Review
- Clinical, genetic and pharmacological data support targeting the MEK5/ERK5 module in lung cancer.NPJ precision oncology · 2021Article
- Impact of ERK5 on the Hallmarks of Cancer.International journal of molecular sciences · 2019Review
- MEK5 promotes lung adenocarcinoma.The European respiratory journal · 2019Article
- Article
- Reduction-oxidation pathways involved in cancer development: a systematic review of literature reviews.Oncotarget · 2017Review
- DCLK1 is correlated with MET and ERK5 expression, and associated with prognosis in malignant pleural mesothelioma.International journal of oncology · 2017Article
- Oncogenic signaling of MEK5-ERK5.Cancer letters · 2017Review
- Targeting BMK1 Impairs the Drug Resistance to Combined Inhibition of BRAF and MEK1/2 in Melanoma.Scientific reports · 2017Article
- MEK5/ERK5 signaling inhibition increases colon cancer cell sensitivity to 5-fluorouracil through a p53-dependent mechanism.Oncotarget · 2016Article
- Tumor cells with KRAS or BRAF mutations or ERK5/MAPK7 amplification are not addicted to ERK5 activity for cell proliferation.Cell cycle (Georgetown, Tex.) · 2016Article
- Article
- Extracellular signal-regulated kinase 5 promotes acute cellular and systemic inflammation.Science signaling · 2015Article
- MEK5-ERK5 pathway associates with poor survival of breast cancer patients after systemic treatments.Oncoscience · 2015Article
- Article
- Extracellular signal-regulated kinase 5 and cyclic AMP response element binding protein are novel pathways inhibited by vandetanib (ZD6474) and doxorubicin in mesotheliomas.American journal of respiratory cell and molecular biology · 2014Article
- Kinome profiling reveals breast cancer heterogeneity and identifies targeted therapeutic opportunities for triple negative breast cancer.Oncotarget · 2014Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The big mitogen activated protein kinase 1 (BMK1) pathway is the most recently discovered and least-studied mammalian mitogen-activated protein (MAP) kinase cascade, ubiquitously expressed in all types of cancer cells tested so far. Mitogens and oncogenic signals strongly activate this cellular MAP kinase pathway, thereby passing down proliferative, survival, chemoresistance, invasive, and angiogenic signals in tumor cells. Recently, several pharmacologic small molecule inhibitors of this pathway have been developed. Among them, the BMK1 inhibitor XMD8-92 blocks cellular BMK1 activation and significantly suppresses tumor growth in lung and cervical tumor models and is well tolerated in animals. On the other hand, MEK5 inhibitors, BIX02188, BIX02189, and compound 6, suppress cellular MEK5 activity, but no data exist to date on their effectiveness in animals.
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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.