Evidence map›Paper›PMID 36441404›Full record

ReviewApplied biochemistry and biotechnology2023

Regulatory Components of Oxidative Stress and Inflammation and Their Complex Interplay in Carcinogenesis.

Loganathan Chandramani Priya Dharshini, Rajan Radha Rasmi, Chinnadurai Kathirvelan, Kalavathi Murugan Kumar, K M Saradhadevi, Kunnathur Murugesan Sakthivel

Abstract readReview
PubMed Publisher
In one paragraph

Review in Applied biochemistry and biotechnology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
4.5field-weighted citation impact, top 4% 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

42 citing papers in PubMed, 56 citations in OpenAlex.

  1. Genetic signatures of lung cancer: association and biomarker potential of EGFR, KRAS, and HER2 polymorphisms.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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  9. PrPEnvironmental science & technology · 2026
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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

6 authors at 4 institutions in 1 country.

Loganathan Chandramani Priya DharshiniDepartment of Biotechnology, PSG College of Arts and Science, Civil Aerodrome Post, Coimbatore, 641 014, Tamil Nadu, India.
Rajan Radha RasmiDepartment of Biotechnology, PSG College of Arts and Science, Civil Aerodrome Post, Coimbatore, 641 014, Tamil Nadu, India.
Chinnadurai KathirvelanDepartment of Animal Nutrition, Veterinary College and Research Institute, Tamil Nadu Veterinary and Animal Sciences University (TANUVAS), Namakkal, 637 002, Tamil Nadu, India.
Kalavathi Murugan KumarSchool of Lifescience, Department of Bioinformatics, Pondicherry University, Pondicherry, 605014, India.
K M SaradhadeviDepartment of Biochemistry, Bharathiar University, Coimbatore, 641046, Tamil Nadu, India.
Kunnathur Murugesan SakthivelDepartment of Biochemistry, PSG College of Arts and Science, Civil Aerodrome Post, Coimbatore, 641 014, Tamil Nadu, India. sakthikm@gmail.com.
Bharathiar University · INPondicherry University · INPSG INSTITUTE OF TECHNOLOGY AND APPLIED RESEARCH · INTamil Nadu Veterinary and Animal Sciences University · IN

Funding

DHR No:12014/11/2018- HR/E-office:3151264PSGCAS Seed Grant Ref No.PSGCAS/SGS/2019-2020/Biochem/020
6 · The paper itself

Abstract

Cancer progression is closely linked to oxidative stress (OS) inflammation. OS is caused by an imbalance between the amount of reactive oxygen species produced and antioxidants present in the body. Excess ROS either oxidizes biomolecules or activates the signaling cascade, resulting in inflammation. Immune cells secrete cytokines and chemokines when inflammation is activated. These signaling molecules attract a wide range of immune cells to the site of infection or oxidative stress. Similarly, increased ROS production by immune cells at the inflamed site causes oxidative stress in the affected area. A review on the role of oxidative stress and inflammation in cancer-related literature was conducted to obtain data. All of the information gathered was focused on the current state of oxidative stress and inflammation in various cancers. After gathering all relevant information, a narrative review was created to provide a detailed note on oxidative stress and inflammation in cancer. Proliferation, differentiation, angiogenesis, migration, invasion, metabolic changes, and evasion of programmed cell death are all aided by OS and inflammation in cancer. Imbalance between reactive oxygen species (ROS) and antioxidants lead to oxidative stress that damages macromolecules (nucleic acids, lipids and proteins). It causes breakdown of the biological signaling cascade. Prolonged oxidative stress causes inflammation by activating transcription factors (NF-κB, p53, HIF-1α, PPAR-γ, Nrf2, AP-1) that alter the expression of many other genes and proteins, including growth factors, tumor-suppressor genes, oncogenes, and pro-inflammatory cytokines, resulting in cancer cell survival. The present review article examines the complex relationship between OS and inflammation in certain types of cancer (colorectal, breast, lung, bladder, and gastric cancer).

Indexed as

AntioxidantsNeoplasmsCarcinogenesisCytokinesHumansInflammationOxidative StressReactive Oxygen SpeciesAntioxidantsCytokinesReactive Oxygen SpeciesCancerCytokinesInflammationOxidative stressTranscription factors

Identifiers

PMID36441404
OpenAlexW4310029919

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.