ReviewCancers2019
Smad7 and Colorectal Carcinogenesis: A Double-Edged Sword.
Review in Cancers, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 28 citations in OpenAlex.
- Murine toxicology assessment of avgn7.2, a novel gene therapeutic for inclusion body myositis and other muscle wasting diseases.Gene therapy · 2026Article
- Codon-optimized human Smad7 gene therapy enhances skeletal muscle mass and function in a murine model of Duchenne muscular dystrophy.Gene therapy · 2026Article
- Smad7 is a negative regulator of immunogenic cell death in colorectal cancer.Oncoimmunology · 2025Article
- TGF-β Modulated Pathways in Colorectal Cancer: New Potential Therapeutic Opportunities.International journal of molecular sciences · 2024Review
- Article
- Multifaceted role of microRNAs in gastric cancer stem cells: Mechanisms and potential biomarkers.World journal of gastrointestinal oncology · 2024Review
- The Role of the Transforming Growth Factor-β Signaling Pathway in Gastrointestinal Cancers.Biomolecules · 2023Review
- ALKBH1-mediated mMolecular oncology · 2023Article
- The role of SET domain containing lysine methyltransferase 7 in tumorigenesis and development.Cell cycle (Georgetown, Tex.) · 2023Review
- Regulation of transforming growth factor-β signaling as a therapeutic approach to treating colorectal cancer.World journal of gastroenterology · 2022Review
- Curcumol inhibits the growth of xenograft-tumors in mice and the biological activities of pancreatic cancer cells by regulating the miR-21-5p/SMAD7 axis.Cell cycle (Georgetown, Tex.) · 2022Article
- Expression and function of Smad7 in autoimmune and inflammatory diseases.Journal of molecular medicine (Berlin, Germany) · 2021Review
- Involvement of Smad7 in Inflammatory Diseases of the Gut and Colon Cancer.International journal of molecular sciences · 2021Review
- Association of Body Mass Index With Colorectal Cancer Risk by Genome-Wide Variants.Journal of the National Cancer Institute · 2021Article
- A Bibliometric Analysis Based on Web of Science: Current Perspectives and Potential Trends of SMAD7 in Oncology.Frontiers in cell and developmental biology · 2021Article
- Overexpression of Smad7 in hypothalamic POMC neurons disrupts glucose balance by attenuating central insulin signaling.Molecular metabolism · 2020Article
- A novel prognostic risk score model based on immune-related genes in patients with stage IV colorectal cancer.Bioscience reports · 2020Article
- Smad7 Controls Immunoregulatory PDL2/1-PD1 Signaling in Intestinal Inflammation and Autoimmunity.Cell reports · 2019Article
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
No grant is acknowledged in the PubMed record.
Abstract
Colorectal carcinogenesis is a complex process in which many immune and non-immune cells and a huge number of mediators are involved. Among these latter factors, Smad7, an inhibitor of the transforming growth factor (TGF)-β1 signaling that has been involved in the amplification of the inflammatory process sustaining chronic intestinal inflammation, is supposed to make a valid contribution to the growth and survival of colorectal cancer (CRC) cells. Smad7 is over-expressed by tumoral cells in both sporadic CRC and colitis-associated CRC, where it sustains neoplastic processes through activation of either TGFβ-dependent or non-dependent pathways. Consistently, genome-wide association studies have identified single nucleotide polymorphisms of the Smad7 gene associated with CRC and shown that either amplification or deletion of the Smad7 gene associates with a poor prognosis or better outcome, respectively. On the other hand, there is evidence that over-expression of Smad7 in immune cells infiltrating the inflamed gut of patients with inflammatory bowel disease can elicit anti-tumor responses, with the down-stream effect of attenuating CRC cell growth. Taken together, these observations suggest a double role of Smad7 in colorectal carcinogenesis, which probably depends on the cell subset and the biological context analyzed. In this review, we summarize the available evidences about the role of Smad7 in both sporadic and colitis-associated CRC.
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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.