Evidence map›Paper›PMID 38167159›Full record

ReviewCell communication and signaling : CCS2024

Interplay of oxidative stress, cellular communication and signaling pathways in cancer.

Muhammad Javed Iqbal, Ayesha Kabeer, Zaighum Abbas, Hamid Anees Siddiqui, Daniela Calina, Javad Sharifi-Rad, William C Cho

Open access · goldAbstract readVideo-Audio MediaReview
In one paragraph

Review in Cell communication and signaling : CCS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 218 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
218citing papers in PubMed, 3 pooled it
73.2field-weighted citation impact, top 1% 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

218 citing papers in PubMed, 3 syntheses or guidelines pooled it, 313 citations in OpenAlex.

  1. Pooled it
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  3. Cellular and Molecular Pathophysiology of Gestational Diabetes.International journal of molecular sciences · 2024
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  17. Sex-specific associations of the bilirubin-to-albumin ratio with lung cancer risk: evidence from Cox regression and causal survival forest analysis.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
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158 more citing papers are in PubMed but not listed here.

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

7 authors at 4 institutions in 4 countries.

Muhammad Javed IqbalDepartment of Biotechnology, University of Sialkot, Sialkot, Punjab, Pakistan.
Ayesha KabeerDepartment of Biotechnology, University of Sialkot, Sialkot, Punjab, Pakistan.
Zaighum AbbasDepartment of Biotechnology, University of Sialkot, Sialkot, Punjab, Pakistan.
Hamid Anees SiddiquiDepartment of Biotechnology, University of Sialkot, Sialkot, Punjab, Pakistan.
Daniela CalinaDepartment of Clinical Pharmacy, University of Medicine and Pharmacy of Craiova, 200349, Craiova, Romania. calinadaniela@gmail.com.
Javad Sharifi-RadFacultad de Medicina, Universidad del Azuay, Cuenca, Ecuador. javad.sharifirad@gmail.com.
William C ChoDepartment of Clinical Oncology, Queen Elizabeth Hospital, Kowloon, Hong Kong. chocs@ha.org.hk.
University of SialkotHospital Authority · CNUniversidad del Azuay · ECUniversity of Medicine and Pharmacy of Craiova · RO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer remains a significant global public health concern, with increasing incidence and mortality rates worldwide. Oxidative stress, characterized by the production of reactive oxygen species (ROS) within cells, plays a critical role in the development of cancer by affecting genomic stability and signaling pathways within the cellular microenvironment. Elevated levels of ROS disrupt cellular homeostasis and contribute to the loss of normal cellular functions, which are associated with the initiation and progression of various types of cancer. In this review, we have focused on elucidating the downstream signaling pathways that are influenced by oxidative stress and contribute to carcinogenesis. These pathways include p53, Keap1-NRF2, RB1, p21, APC, tumor suppressor genes, and cell type transitions. Dysregulation of these pathways can lead to uncontrolled cell growth, impaired DNA repair mechanisms, and evasion of cell death, all of which are hallmark features of cancer development. Therapeutic strategies aimed at targeting oxidative stress have emerged as a critical area of investigation for molecular biologists. The objective is to limit the response time of various types of cancer, including liver, breast, prostate, ovarian, and lung cancers. By modulating the redox balance and restoring cellular homeostasis, it may be possible to mitigate the damaging effects of oxidative stress and enhance the efficacy of cancer treatments. The development of targeted therapies and interventions that specifically address the impact of oxidative stress on cancer initiation and progression holds great promise in improving patient outcomes. These approaches may include antioxidant-based treatments, redox-modulating agents, and interventions that restore normal cellular function and signaling pathways affected by oxidative stress. In summary, understanding the role of oxidative stress in carcinogenesis and targeting this process through therapeutic interventions are of utmost importance in combating various types of cancer. Further research is needed to unravel the complex mechanisms underlying oxidative stress-related pathways and to develop effective strategies that can be translated into clinical applications for the management and treatment of cancer. Video Abstract.

Indexed as

NeoplasmsNF-E2-Related Factor 2CarcinogenesisHumansKelch-Like ECH-Associated Protein 1Oxidation-ReductionOxidative StressReactive Oxygen SpeciesSignal TransductionTumor MicroenvironmentKelch-Like ECH-Associated Protein 1NF-E2-Related Factor 2Reactive Oxygen SpeciesCancerCarcinogenesis mechanismsOxidative stressReactive oxygen species

Identifiers

PMID38167159
PMCPMC10763046
OpenAlexW4390499110

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.