ReviewIn vivo (Athens, Greece)
K-
Review in In vivo (Athens, Greece). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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
12 citing papers in PubMed, 29 citations in OpenAlex.
- The Wnt/β-catenin-P2-HNF4α feedback loop facilitates colorectal tumorigenesis and malignancy.Journal of translational medicine · 2025Article
- Genomic landscape of pathogenic mutations in Pakistani population with late-stage colorectal cancer.Pakistan journal of medical sciences · 2025Article
- DNA signature and occult blood in stool led to diagnosis of an early-onset metastatic rectal cancer in a young pregnant woman: a case report.Journal of gastrointestinal oncology · 2024Article
- New Perspectives in Colorectal Cancers Treatment, the Role of MicroRNAs.Current drug targets · 2024Review
- Fucoxanthin Inhibits Development of Sigmoid Colorectal Cancer in a PDX Model With Alterations of Growth, Adhesion, and Cell Cycle Signals.Cancer genomics & proteomics · 2023Article
- Is serum thymidine kinase 1 a prognostic biomarker in primary tumor location of colorectal carcinomas?Discover oncology · 2023Article
- BMP4 and PHLDA1 are plausible drug-targetable candidate genes for KRAS G12A-, G12D-, and G12V-driven colorectal cancer.Molecular and cellular biochemistry · 2021Article
- The Landscape of Alterations in DNA Damage Response Pathways in Colorectal Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2021Article
- Fucoxanthin and Colorectal Cancer Prevention.Cancers · 2021Review
- Clinicopathological characteristics and mutational profile of KRAS and NRAS in Tunisian patients with sporadic colorectal cancerTurkish journal of medical sciences · 2021Article
- Dual Role of Reactive Oxygen Species and their Application in Cancer Therapy.Journal of Cancer · 2021Review
- The Clinical Relevance of Frequent Germline Genetic Variants Detected by Targeted Sequencing in Patients With Rectal Adenocarcinoma (READ).Cancer genomics & proteomicsArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
K-ras oncogene is a key factor in colorectal cancer. Based on published and our data we propose that K-ras could be the oncogene responsible for the inactivation of the tumor-suppressor gene APC, currently considered as the initial step in colorectal tumorigenesis. K-ras fulfills the criteria of the oncogene-induced DNA damage model, as it can provoke well-established causes for inactivating tumor-suppressors, i.e. DNA double-strand breaks (causing allele deletion) and ROS production (responsible for point mutation). The model we propose is a variation of the currently existing model and hypothesizes that, in a subgroup of colorectal carcinomas, K-ras mutation may precede APC inactivation, representing the earliest driving force and, probably, an early biomarker of colorectal carcinogenesis. This observation is clinically useful, since it may modify the preventive colorectal cancer strategy, restricting numerically patients undergoing colonoscopies to those bearing K-ras mutation in their colorectum, either in benign polyps or the normal accompanying mucosa.
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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.