ReviewCurrent oncology reports2026
THBS2 as a Key Regulator in Gastrointestinal Tumors: from Molecular Mechanisms to Clinical Applications.
Review in Current oncology reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Down-regulation of THBS2 inhibits the malignant progression of Burkitt lymphoma by blocking the PI3K/AKT/c-MYC pathway.Frontiers in oncology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
purpose of reviewThrombospondin-2 (THBS2), an extracellular matrix (ECM) regulator, plays a multifaceted role in tumorigenesis. This review systematically summarizes recent advances regarding THBS2 in gastrointestinal tumors (including gastric, colorectal, pancreatic, and liver cancers) and evaluates its potential as a key player in the tumor microenvironment (TME), immune regulation, and clinical diagnostics and therapeutics. RECENT
findingsTHBS2 promotes tumor proliferation and migration by activating the MAPK/PI3K/AKT pathway via integrins. It remodels the t TME through a TGF-β1-THBS2 feedback loop involving cancer-associated fibroblasts (CAFs). Furthermore, THBS2 facilitates metastasis and immune evasion by modulating ECM structure and cytoskeletal dynamics. Emerging therapeutic strategies aim to block THBS2 interactions with CD36/CD47 to enhance anti-PD-1 immunotherapy, disrupt the TGF-β-THBS2 signaling axis, or combine with matrix metalloproteinase (MMP) inhibitors to suppress fibrosis and tumor dissemination. THBS2 acts as a critical regulator in the pathogenesis and progression of digestive tract tumors. Translating THBS2 into clinical practice requires addressing its context-dependent dual nature, tumor heterogeneity, and potential off-target resistance.
Indexed as
Identifiers
41642416What Socratic 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 Socratic graph.