ArticleMolecular and clinical oncology2022
Potential of
Article in Molecular and clinical oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed, 5 citations in OpenAlex.
No citing paper in PubMed yet.
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 at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Given its role in tumorigenesis and its correlation with various pathologic features of colorectal cancer (CRC), DEK is considered to have the potential to predict CRC prognosis. This review attempts to summarize current knowledge and evidence supporting the potential of DEK as a prognostic biomarker of CRC. We searched meta-analyses, systematic reviews, cohort studies, and cell line studies published in the last 10 years. A literature search was conducted in PubMed, Pubmed Central (PMC), Proquest, EBSCOHost, Scopus, and Cochrane Library using the keywords 'colorectal/colon/rectal cancer', 'DEK', 'biomarker', and 'prognosis'. Studies that were not published in English, without accessible full text, unrelated to clinical questions, or conducted with a design unsuitable for the eligibility criteria were excluded. Seven included studies reported the potential of DEK as a prognostic biomarker of CRC and its role in cancer cell proliferation, invasion, and metastasis. This role is achieved through the Wnt/β-catenin pathway, prevention of apoptosis through destabilization of p53, and bridging inflammation and tumorigenesis through the nuclear factor (NF)-κB pathway, causing chronic inflammation and activation of tumorigenic genes. DEK overexpression is also associated with CRC clinical and pathological features, such as tumor size, lymph node metastasis, serosal invasion, differentiation, tumor staging, and epithelial-mesenchymal transition. DEK overexpression was found to be associated with lower survival and recovery rates. Its prognostic value was comparable with other prognostic biomarkers of CRC, such as BRAF, topoisomerase-1, and CEA. A cohort study reported that DEK overexpression was associated with a better response to fluoropyrimidine-based chemotherapy, while a cell-line study indicated a correlation between DEK overexpression with a worse response to irinotecan-based chemotherapy. In conclusion, considering its correlation with CRC pathology, its association with worse CRC patient survival, and its possibility to forecast the therapeutic response of various chemotherapeutic regimens, DEK has the potential to be used as a CRC prognostic biomarker.
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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.