ReviewDiscover oncology2025
Natural products as therapeutic interventions for inflammation-mediated cancer.
Review in Discover oncology, 2025. 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.
- Natural Products Targeting Key Molecular Hallmarks in Gastric Cancer: Focus on Apoptosis, Inflammation, and Chemoresistance.International journal of molecular sciences · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inflammation serves as the body's immune response mechanism against noxious irritants, ranging from removing factors causing injury to regenerating damaged tissue. Chronic inflammation, in particular, has emerged as a crucial contributor to both the development of cancer and its spread through a variety of mechanisms. This phenomenon is referred to as inflammation-induced tumorigenesis. Differing from other forms of inflammation that typically precede tumor formation, 'cancer-elicited inflammation (CEI)' is induced following the initiation of a tumor. Beyond the cell-autonomous effects observed in cancer cells, the activation of several oncogenes, including KRAS and MYC, coupled with the rendering of tumor suppressors, for instance, TP53 inactive, triggers programs at the transcription level that culminate in the formation of a tumor-encouraging microenvironment. This is accomplished by the overproduction of chemokines and pro-inflammatory cytokines, immune cell recruitment, and the initiation of angiogenesis. Although it is critical to comprehend the mechanisms by which inflammation aids in the development of cancer, the impact that tumors themselves have on the immune system must be considered because these effects have significant repercussions for the therapy and prevention of cancer. This comprehensive review primarily centers on various inflammatory pathways that have been influenced by cancer and have, in turn, influenced cancer progression. Additionally, we delve deeply into the intricate mechanisms through which specific natural products exert regulatory control over the complex molecular foundations that drive their robust anti-inflammatory and anti-cancer effects.
Indexed as
Identifiers
What 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.