ArticleCancer research2019
Drak/STK17A Drives Neoplastic Glial Proliferation through Modulation of MRLC Signaling.
Article in Cancer research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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
15 citing papers in PubMed, 25 citations in OpenAlex.
- Genotype-Informed Whole-Animal Kinome Screening Reveals Shared Kinase Vulnerabilities Across Driver Contexts in PDAC.Cancer science · 2026Article
- Alterations of the tumor microenvironment (TME) by exploratory gene expression analysis in recurrent glioblastoma following apatinib in combination with temozolomide.Biochemistry and biophysics reports · 2026Article
- STK17A (DRAK1) at the crossroads of apoptosis, immunity, and cancer: Emerging roles and therapeutic opportunities.Theranostics · 2026Review
- Article
- Review
- The role of ANLN in malignant tumors: pathogenesis, treatment resistance and targeted strategies.Frontiers in cell and developmental biology · 2025Review
- Potent, Selective, and Orally Bioavailable Quinazoline-Based STK17A/B Dual Inhibitors.ACS medicinal chemistry letters · 2024Article
- MRLC controls apoptotic cell death and functions to regulate epidermal development during planarian regeneration and homeostasis.Cell proliferation · 2024Article
- Multi-Omics Analysis and Verification of the Oncogenic Value of CCT8 in Pan-Cancers.Journal of inflammation research · 2023Article
- A protocol to useSTAR protocols · 2022Article
- Synaptic components are required for glioblastoma progression in Drosophila.PLoS genetics · 2022Article
- Degradation of DRAK1 by CUL3/SPOP E3 Ubiquitin ligase promotes tumor growth of paclitaxel-resistant cervical cancer cells.Cell death & disease · 2022Article
- The Crossroads between RAS and RHO Signaling Pathways in Cellular Transformation, Motility and Contraction.Genes · 2021Review
- Tailless/TLX reverts intermediate neural progenitors to stem cells driving tumourigenesis via repression ofeLife · 2020Article
- RNase L Induces Expression of A Novel Serine/Threonine Protein Kinase, DRAK1, to Promote Apoptosis.International journal of molecular sciences · 2019Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Glioblastoma (GBM) and lower grade gliomas (LGG) are the most common primary malignant brain tumors and are resistant to current therapies. Genomic analyses reveal that signature genetic lesions in GBM and LGG include copy gain and amplification of chromosome 7, amplification, mutation, and overexpression of receptor tyrosine kinases (RTK) such as EGFR, and activating mutations in components of the PI3K pathway. In
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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.