ReviewFrontiers in cell and developmental biology2024
Targeting the JAK-STAT pathway in colorectal cancer: mechanisms, clinical implications, and therapeutic potential.
Review in Frontiers in cell and developmental biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed.
- Cancer Stem Cells in Colorectal Cancer: From Molecular Mechanisms to Diagnosis, Prognosis and Therapy Implications.Cancers · 2026Review
- Unveiling VARS1: a key driver of colorectal cancer progression and immune modulation.International journal of clinical oncology · 2026Article
- Application of Systems Genetics to Investigate Molecular Pathology of Early-Onset Colorectal Cancer.Chemical biology & drug design · 2026Review
- The multifaceted role of SOCS3 in colorectal cancer: molecular mechanisms and clinical implications.Molecular biology reports · 2026Review
- Evaluating KRAS-Associated Responses to Sulfasalazine and 5-Fluorouracil in Colorectal Cancer Using Integrated 2D and PEGDA Microwell-Based 3D Tumor Models.International journal of molecular sciences · 2026Article
- Flavonoid-modulated JAK-STAT signaling mitigates malignant transformation and drug resistance in breast tumors: A clinically relevant 3PM-guided innovation.Journal of advanced research · 2026Review
- Evaluation of the Anti-Cancer Effects of KMU-11342 in In Vitro and Ex Vivo Models of Colorectal Cancer.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Article
- JAK-STAT signaling pathway in cancer: from molecular mechanisms to clinical intervention.Molecular cancer · 2026Review
- Integrated Evolutionary and Multi-Omic Analysis of STAT Family Activation Across Solid Tumors.Genes · 2026Article
- EGFR Signaling in Colorectal Cancer: Novel Therapeutic Strategies, Predictive Biomarkers, and Counteracting Treatment Resistance.International journal of molecular sciences · 2026Review
- Colorectal cancer pathogenesis, oncogenic signaling networks and targeted therapeutic advances.Molecular biomedicine · 2026Review
- Beauvericin Induces Mitochondrial Apoptosis and Attenuates EMT-Associated Phenotypes and Angiogenic Signaling in Colorectal Cancer CellsJournal of microbiology and biotechnology · 2026Article
- The Barrier-Microbiota-Inflammation Axis in Colorectal Cancer: Mechanisms and Emerging Diagnostic & Therapeutic Strategies.Cancers · 2026Review
- Cytokine and chemokine networks in colorectal cancer.Frontiers in immunology · 2026Review
- Oncofetal reprogramming and cellular plasticity in colorectal cancer: from mechanisms to clinical translation.Frontiers in oncology · 2026Review
- Molecular and regional characterization of colorectal polyps: insights from proteomics, phosphoproteomics, and immune profiling.Translational gastroenterology and hepatology · 2026Article
- Review
- Demystifying the Role of Histone Demethylases in Colorectal Cancer: Mechanisms and Therapeutic Opportunities.Current issues in molecular biology · 2025Review
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.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Colorectal cancer (CRC) remains one of the most prevalent and fatal malignancies worldwide, consistently ranking among the top three in terms of incidence and mortality. Despite notable advancements in early detection and therapeutic interventions, survival outcomes for advanced-stage CRC are still dismal, largely due to issues such as drug resistance and metastasis. Recent research has increasingly implicated the JAK-STAT signaling pathway as a pivotal contributor to CRC pathogenesis. This evolutionarily conserved pathway plays a key role in transmitting extracellular signals to the nucleus, thereby modulating gene expression involved in numerous fundamental biological processes. In CRC, dysregulation of the JAK-STAT pathway is frequently observed and is strongly associated with tumor progression, including processes such as cellular proliferation, apoptosis, metastasis, immune evasion, and the sustenance of cancer stem cells. Given its integral role in CRC advancement, the JAK-STAT pathway has gained recognition as a viable therapeutic target. Extensive evidence from preclinical and clinical models supports the efficacy and safety of targeting components of the JAK-STAT pathway, presenting new therapeutic possibilities for patients with CRC, particularly in addressing drug resistance and enhancing treatment outcomes. This review offers a detailed exploration of the JAK-STAT pathway, focusing on its regulatory mechanisms in CRC-related malignancies. Moreover, it examines the association between JAK-STAT protein expression, clinical features, prognosis, and its therapeutic potential in CRC management.
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.