ArticleCancer discovery2020
Exploiting the Therapeutic Interaction of WNT Pathway Activation and Asparaginase for Colorectal Cancer Therapy.
Article in Cancer discovery, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.
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
39 citing papers in PubMed, 1 synthesis or guideline pooled it, 59 citations in OpenAlex.
- Patient-Derived Xenograft Models in Cervical Cancer: A Systematic Review.International journal of molecular sciences · 2021Pooled it
- Metabolic reprogramming in colorectal cancer: Mechanisms and therapeutic insights.Genes & diseases · 2027Review
- Review
- Amino Acids as Targets for Immunotherapy against Solid Tumors.Cell biochemistry and biophysics · 2026Review
- The lncRNA DAMER selectively guides mNature cell biology · 2026Article
- Reduced PRC2 function causes asparaginase resistance in T-ALL by decreasing WNT pathway activity.Blood advances · 2026Article
- DNA and RNA-based next-generation sequencing for companion diagnostic rearrangement detection in solid tumors.The oncologist · 2026Article
- Autophagy: mechanisms, roles in human diseases, and therapeutic perspectives.Frontiers in cell and developmental biology · 2026Review
- Amino acids metabolism: a potential target for cancer treatment.Molecular cancer · 2025Review
- Modulation of the tumor microenvironment by the ubiquitin-proteasome system in colorectal cancer.Journal of translational medicine · 2025Review
- Enhancing stability of enzymes for industrial applications: molecular insights and emerging approaches.World journal of microbiology & biotechnology · 2025Review
- SOD2 is a regulator of proteasomal degradation promoting an adaptive cellular starvation response.Cell reports · 2025Article
- Targeting Asparagine Metabolism in Solid Tumors.Nutrients · 2025Review
- Epigenetic and Oncogenic Inhibitors Cooperatively Drive Differentiation and Kill KRAS-Mutant Colorectal Cancers.Cancer discovery · 2024Article
- Article
- Metabolism of asparagine in the physiological state and cancer.Cell communication and signaling : CCS · 2024Review
- Consistency between Primary Uterine Corpus Malignancies and Their Corresponding Patient-Derived Xenograft Models.International journal of molecular sciences · 2024Article
- HSPA8 Activates Wnt/β-Catenin Signaling to Facilitate BRAF V600E Colorectal Cancer Progression by CMA-Mediated CAV1 Degradation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- High expression of NOLC1 as an independent prognostic factor for survival in patients with colorectal cancer.Journal of cancer research and clinical oncology · 2023Article
- Targeting cancer metabolic pathways for improving chemotherapy and immunotherapy.Cancer letters · 2023Review
Corrections and comments
- Commented on by
Authors and funding
17 authors at 5 institutions in 2 countries.
Funding
Abstract
Colorectal cancer is driven by mutations that activate canonical WNT/β-catenin signaling, but inhibiting WNT has significant on-target toxicity, and there are no approved therapies targeting dominant oncogenic drivers. We recently found that activating a β-catenin-independent branch of WNT signaling that inhibits GSK3-dependent protein degradation induces asparaginase sensitivity in drug-resistant leukemias. To test predictions from our model, we turned to colorectal cancer because these cancers can have WNT-activating mutations that function either upstream (i.e., R-spondin fusions) or downstream (
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.