ReviewFrontiers in oncology2026
The role of notch signaling in tumor angiogenesis in hematological malignancies.
Review in Frontiers in oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The evolutionarily conserved Notch signaling pathway is a contact-dependent communication mechanism regulating cell fate, tissue patterning, and cellular metabolism. Beyond canonical NICD-RBPJ transcription, Notch engages in non-canonical crosstalk with networks like Wnt and NF-κB. In tumor angiogenesis, the endothelial Foxc1/2-DLL4-Notch1 axis coordinates tip/stalk cell plasticity, while restricting glycolytic flux via PFKFB3 downregulation to promote vessel maturation. Consequently, pathway inhibition triggers non-productive hypersprouting and vascular collapse, whereas Notch activation strategies offer potential for therapeutic vessel normalization. Crucially, Notch acts as a driving oncogene in B-cell malignancies, promoting survival and chemoresistance. In mantle cell lymphoma (MCL), somatic mutations truncate the C-terminal PEST domain, preventing proteasomal degradation and inducing constitutive NICD hyperactivation-defining an aggressive, microenvironment-sustained clinical subset. Similar NOTCH1/2 aberrations drive clonal progression in marginal zone and MALT lymphomas, and indicate poor prognosis in Hepatitis C Virus-positive diffuse large B-cell lymphoma (DLBCL). Routine genomic screening for Notch alterations provides critical prognostic stratification, laying the basis for personalized, selective therapies in refractory hematological diseases.
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.