Evidence map›Paper›PMID 24587674›Full record

ReviewWorld journal of gastroenterology2014

Clock genes: their role in colorectal cancer.

Theodoros Karantanos, George Theodoropoulos, Dimitrios Pektasides, Maria Gazouli

Open access · bronzeAbstract readReview
In one paragraph

Review in World journal of gastroenterology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
3.1field-weighted citation impact, top 8% of its field
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

43 citing papers in PubMed, 80 citations in OpenAlex.

  1. Trial
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  8. Circadian rhythm disruption and endocrine-related tumors.World journal of clinical oncology · 2024
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  19. Circadian Clock Disruption Suppresses PDL1Cellular and molecular gastroenterology and hepatology · 2021
    Article
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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 at 1 institution in 1 country.

Theodoros KarantanosTheodoros Karantanos, George Theodoropoulos, First Department of Propaedeutic Surgery, School of Medicine, University of Athens, 11725 Athens, Greece.
George TheodoropoulosTheodoros Karantanos, George Theodoropoulos, First Department of Propaedeutic Surgery, School of Medicine, University of Athens, 11725 Athens, Greece.
Dimitrios PektasidesTheodoros Karantanos, George Theodoropoulos, First Department of Propaedeutic Surgery, School of Medicine, University of Athens, 11725 Athens, Greece.
Maria GazouliTheodoros Karantanos, George Theodoropoulos, First Department of Propaedeutic Surgery, School of Medicine, University of Athens, 11725 Athens, Greece.
Athens State University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Clock genes create a complicated molecular time-keeping system consisting of multiple positive and negative feedback loops at transcriptional and translational levels. This circadian system coordinates and regulates multiple cellular procedures implicated in cancer development such as metabolism, cell cycle and DNA damage response. Recent data support that molecules such as CLOCK1, BMAL1 and PER and CRY proteins have various effects on c-Myc/p21 and Wnt/β-catenin pathways and influence multiple steps of DNA damage response playing a critical role in the preservation of genomic integrity in normal and cancer cells. Notably, all these events have already been related to the development and progression of colorectal cancer (CRC). Recent data highlight critical correlations between clock genes' expression and pathogenesis, progression, aggressiveness and prognosis of CRC. Increased expression of positive regulators of this circadian system such as BMAL1 has been related to decrease overall survival while decreased expression of negative regulators such as PER2 and PER3 is connected with poorer differentiation, increased aggressiveness and worse prognosis. The implications of these molecules in DNA repair systems explain their involvement in the development of CRC but at the same time provide us with novel targets for modern therapeutic approaches for patients with advanced CRC.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsbeta CateninCell CycleCell Cycle ProteinsCell DifferentiationCircadian RhythmCLOCK ProteinsColorectal NeoplasmsCyclin-Dependent Kinase Inhibitor p21Disease ProgressionDNA DamageGene ExpressionHumansNuclear ProteinsPeriod Circadian Proteinsbeta CateninCDKN1A protein, humanCell Cycle ProteinsCLOCK ProteinsCyclin-Dependent Kinase Inhibitor p21Nuclear ProteinsPER2 protein, humanPeriod Circadian ProteinsProtein-Tyrosine KinasesProto-Oncogene Proteins c-mycTranscription FactorsWEE1 protein, humanClock genesColorectal cancerDevelopmentPrognosis

Identifiers

PMID24587674
PMCPMC3934468
OpenAlexW2006553178

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.