ReviewCancer drug resistance (Alhambra, Calif.)2022
Tousled-like kinase 1: a novel factor with multifaceted role in mCRPC progression and development of therapy resistance.
Review in Cancer drug resistance (Alhambra, Calif.), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 24 citations in OpenAlex.
- Diagnostic and prognostic value of lncSPATA8-AS1 in prostate cancer and its regulatory effect on tumor progression.Cancer biology & therapy · 2026Article
- Multi-ancestry transcriptome-wide association studies uncover insights into breast cancer genetics and biology.Nature communications · 2026Article
- Platycodin D Overcomes Cisplatin Resistance in Gastric Cancer by Inducing Ferroptosis through TLK1-Dependent UHRF2/DNMT3A/ALOX15 Pathway.Chinese journal of integrative medicine · 2026Article
- NEK Family Kinases: Structure, Function, and Role in Disease.Biomolecules · 2025Review
- Article
- Autophosphorylation of the Tousled-like kinases TLK1 and TLK2 regulates recruitment to damaged chromatin via PCNA interaction.Nucleic acids research · 2025Article
- Tousled-like kinase loss confers PARP inhibitor resistance in BRCA1-mutated cancers by impeding non-homologous end joining repair.Molecular medicine (Cambridge, Mass.) · 2025Article
- The TLK-ASF1 histone chaperone pathway plays a critical role in IL-1β-mediated AML progression.Blood · 2024Article
- Autophosphorylation of the Tousled-like kinases TLK1 and TLK2 regulates recruitment to damaged chromatin via PCNA interaction.bioRxiv : the preprint server for biology · 2024Article
- TLK1-mediated RAD54 phosphorylation spatio-temporally regulates Homologous Recombination Repair.Nucleic acids research · 2023Article
- Untousling the Role of Tousled-like Kinase 1 in DNA Damage Repair.International journal of molecular sciences · 2023Review
- Targeting Prostate Cancer, the 'Tousled Way'.International journal of molecular sciences · 2023Review
- NEK1-Mediated Phosphorylation of YAP1 Is Key to Prostate Cancer Progression.Biomedicines · 2023Article
- The TLK1-MK5 Axis Regulates Motility, Invasion, and Metastasis of Prostate Cancer Cells.Cancers · 2022Article
- Interplay of Developmental Hippo-Notch Signaling Pathways with the DNA Damage Response in Prostate Cancer.Cells · 2022Review
- New insights for drug resistance in metastatic castration-resistant prostate cancer.Cancer drug resistance (Alhambra, Calif.) · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Standard treatment for advanced Prostate Cancer (PCa) consists of androgen deprivation therapy (ADT), but ultimately fails, resulting in the incurable phase of the disease: metastatic castration-resistant prostate cancer (mCRPC). Targeting PCa cells before their progression to mCRPC would greatly improve the outcome, if strategies could be devised selectively targeting androgen receptor (AR)-dependent and/or independent compensatory pathways which promote mCRPC development. Combination therapy by targeting the DNA damage response (DDR) along with ADT has been limited by general toxicity, and a goal of clinical trials is how to target the DDR more specifically. In recent years, our lab has identified a key role for the DDR kinase, TLK1, in mediating key aspects of adaptation to ADT, first by promoting a cell cycle arrest (through the TLK1>NEK1>ATR>Chk1 kinase cascade) under the unfavorable growth conditions (androgen deprivation), and then by reprogramming the PCa cells to adapt to androgen-independent growth via the NEK1>YAP/AR>CRPC conversion. In addition, TLK1 plays a key anti-apoptotic role via the NEK1>VDAC1 regulation on the intrinsic mitochondrial apoptotic pathway when the DDR is activated. Finally, TLK1 was recently identified as having an important role in motility and metastasis via regulation of the kinases MK5/PRAK and AKT (indirectly via AKTIP).
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.