ReviewTrends in cancer2016
Differentiation and Inflammation: 'Best Enemies' in Gastrointestinal Carcinogenesis.
Review in Trends in cancer, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.
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
9 citing papers in PubMed, 1 synthesis or guideline pooled it, 17 citations in OpenAlex.
- Mechanisms of obesity- and diabetes mellitus-related pancreatic carcinogenesis: a comprehensive and systematic review.Signal transduction and targeted therapy · 2023Pooled it
- Inflammation-induced PELP1 expression promotes tumorigenesis by activating GM-CSF paracrine secretion in the tumor microenvironment.The Journal of biological chemistry · 2022Article
- Extrinsic KRAS Signaling Shapes the Pancreatic Microenvironment Through Fibroblast Reprogramming.Cellular and molecular gastroenterology and hepatology · 2022Article
- Article
- Prevention and Reversion of Pancreatic Tumorigenesis through a Differentiation-Based Mechanism.Developmental cell · 2019Article
- Role of mTORC1 in intestinal epithelial repair and tumorigenesis.Cellular and molecular life sciences : CMLS · 2019Review
- Long non-coding RNA LINC01503 promotes colorectal cancer cell proliferation and invasion by regulating miR-4492/FOXK1 signaling.Experimental and therapeutic medicine · 2018Article
- Endogenous Anti-Inflammatory Very-Long-Chain Dicarboxylic Acids: Potential Chemopreventive Lipids.Metabolites · 2018Article
- The developmental origin of brain tumours: a cellular and molecular framework.Development (Cambridge, England) · 2018Review
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 at 1 institution in 1 country.
Funding
Abstract
While recent studies demonstrate that cancer can arise from mutant stem cells, this hypothesis does not explain why tissues without defined stem cell populations are susceptible to inflammation-driven tumorigenesis. We propose that chronic inflammatory diseases, such as colitis and pancreatitis, predispose to gastrointestinal (GI) adenocarcinoma by reprogramming differentiated cells. Focusing on colon and pancreas, we discuss recently discovered connections between inflammation and loss of cell differentiation, and propose that dysregulation of cell fate may be a novel rate-limiting step of tumorigenesis. We review studies identifying differentiation mechanisms that limit tumor initiation and that, upon reactivation, can prevent or revert the cancer cell transformed phenotype. Together, these findings suggest that differentiation-targeted treatments hold promise as a therapeutic strategy in GI cancer.
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.