ArticleLeukemia2006
Jak3- and JNK-dependent vascular endothelial growth factor expression in cutaneous T-cell lymphoma.
Article in Leukemia, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 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
55 citing papers in PubMed, 114 citations in OpenAlex.
- Serum survivin and vascular endothelial growth factor in extranodal NK/T-cell lymphoma, nasal type: implications for a potential new prognostic indicator.Haematologica · 2015Trial
- R-CHOP with or without bevacizumab in patients with previously untreated diffuse large B-cell lymphoma: final MAIN study outcomes.Haematologica · 2014Trial
- JAK-STAT signaling pathway in cancer: from molecular mechanisms to clinical intervention.Molecular cancer · 2026Review
- Angiogenesis and lymphangiogenesis in primary cutaneous lymphomas: a narrative review.Clinical and experimental medicine · 2025Review
- Review
- NewCells · 2023Article
- Article
- Metastasis and MAPK Pathways.International journal of molecular sciences · 2022Review
- Predominant Role of mTOR Signaling in Skin Diseases with Therapeutic Potential.International journal of molecular sciences · 2022Review
- Safety and danger of biologic treatments in psoriasis in context of cutaneous T-cell lymphoma (CTCL).Postepy dermatologii i alergologii · 2021Review
- The JAK/STAT signaling pathway: from bench to clinic.Signal transduction and targeted therapy · 2021Review
- JAK3 Is Expressed in the Nucleus of Malignant T Cells in Cutaneous T Cell Lymphoma (CTCL).Cancers · 2021Article
- Immune Check Point Inhibitors in Primary Cutaneous T-Cell Lymphomas: Biologic Rationale, Clinical Results and Future Perspectives.Frontiers in oncology · 2021Review
- Ruxolitinib with resminostat exert synergistic antitumor effects in Cutaneous T-cell Lymphoma.PloS one · 2021Article
- Sperm associated antigen 9 promotes oncogenic KSHV-encoded interferon regulatory factor-induced cellular transformation and angiogenesis by activating the JNK/VEGFA pathway.PLoS pathogens · 2020Article
- Cellular Interactions and Inflammation in the Pathogenesis of Cutaneous T-Cell Lymphoma.Frontiers in cell and developmental biology · 2020Review
- Genome profiling revealed the activation of IL2RG/JAK3/STAT5 in peripheral T‑cell lymphoma expressing the ITK‑SYK fusion gene.International journal of oncology · 2019Article
- miR-337 suppresses cutaneous T-cell lymphoma via the STAT3 pathway.Cell cycle (Georgetown, Tex.) · 2019Article
- Elucidating the mechanism of action of domatinostat (4SC-202) in cutaneous T cell lymphoma cells.Journal of hematology & oncology · 2019Article
- Malignant T cells activate endothelial cells via IL-17 F.Blood cancer journal · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Biopsies from patients with cutaneous T-cell lymphoma (CTCL) exhibit stage-dependent increase in angiogenesis. However, the molecular mechanisms responsible for the increased angiogenesis are unknown. Here we show that malignant CTCL T cells spontaneously produce the potent angiogenic protein, vascular endothelial growth factor (VEGF). Dermal infiltrates of CTCL lesions show frequent and intense staining with anti-VEGF antibody, indicating a steady, high production of VEGF in vivo. Moreover, the VEGF production is associated with constitutive activity of Janus kinase 3 (Jak3) and the c-Jun N-terminal kinases (JNKs). Sp600125, an inhibitor of JNK activity and activator protein-1 (AP-1) binding to the VEGF promoter, downregulates the VEGF production without affecting Jak3 activity. Similarly, inhibitors of Jak3 inhibit the VEGF production without affecting JNK activity. Downregulation of Stat3 with small interfering RNA has no effect, whereas curcumin, an inhibitor of both Jak3 and the JNKs, almost completely blocks the VEGF production. In conclusion, we provide evidence of VEGF production in CTCL, which is promoted by aberrant activation of Jak3 and the JNKs. Inhibition of VEGF-inducing pathways or neutralization of VEGF itself could represent novel therapeutic modalities in CTCL.
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.