Evidence map›Paper›PMID 39123348›Full record

ReviewCancers2024

Defensins: Exploring Their Opposing Roles in Colorectal Cancer Progression.

Hussein Sabit, Timothy M Pawlik, Shaimaa Abdel-Ghany, Borros Arneth

Abstract readReview
In one paragraph

Review in Cancers, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

4 citing papers in PubMed.

  1. Emerging antimicrobial peptides in gastrointestinal disorders: Dual role in immunity and therapy.World journal of gastrointestinal pharmacology and therapeutics · 2026
    Review
  2. Article
  3. Article
  4. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors.

Hussein SabitDepartment of Medical Biotechnology, College of Biotechnology, Misr University for Science and Technology, Giza P.O. Box 77, Egypt.ORCID 0000-0001-9021-8334
Timothy M PawlikDepartment of Surgery, The Ohio State University, Wexner Medical Center, 250 Cunz Hall, 1841 Neil Ave. Columbus, OH 43210, USA.ORCID 0000-0002-7994-9870
Shaimaa Abdel-GhanyDepartment of Environmental Biotechnology, College of Biotechnology, Misr University for Science and Technology, Giza P.O. Box 77, Egypt.
Borros ArnethInstitute of Laboratory Medicine and Pathobiochemistry, Molecular Diagnostics, Hospital of the Universities of Giessen and Marburg (UKGM), Justus Liebig University Giessen, Feulgenstr. 12, 35392 Giessen, Germany.ORCID 0000-0002-9793-0970

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Colorectal cancer (CRC) represents a significant global healthcare burden, with a particularly concerning rising incidence among younger adults. This trend may highlight potential links between diet, gut microbiome, and CRC risk. Novel therapeutic options have been increasingly based on the understanding of molecular mechanisms and pathways. The PI3K/AKT/mTOR pathway, a crucial cell growth regulator, offers a promising target for CRC therapy. mTOR, a key component within this pathway, controls cell growth, survival, and metabolism. Understanding the specific roles of defensins, particularly human β-Defensin 1 (HBD-1), in CRC is crucial. HBD-1 exhibits potent antimicrobial activity and may influence CRC development. Deciphering defensin expression patterns in CRC holds the promise of improved understanding of tumorigenesis, which may pave the way for improved diagnostics and therapies. This article reviews recent advances in understanding regarding how HBD-1 influences CRC initiation and progression, highlighting the molecular mechanisms by which it impacts CRC. Further, we describe the interaction between defensins and mTOR pathway in CRC.

Indexed as

colon cancercolorectal cancerCRCdefensinsgut microbiotamTOR

Identifiers

PMID39123348
PMCPMC11311076

What OpenQuestion holds

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LicenceCC BY
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Registered trials

None linked

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.