Evidence map›Paper›PMID 36271573›Full record

ReviewBiomedicine & pharmacotherapy = Biomedecine & pharmacotherapie2022

Natural products targeting the ATR-CHK1 signaling pathway in cancer therapy.

Salman Ahmed, Waqas Alam, Michael Aschner, Khalaf F Alsharif, Ashraf Albrakati, Luciano Saso, Haroon Khan

Open access · goldAbstract readReview
In one paragraph

Review in Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 11% 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

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.

  1. Pooled it
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  14. The journal of venomous animals and toxins including tropical diseases · 2025
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  16. PARP1 UFMylation ensures the stability of stalled replication forks.Proceedings of the National Academy of Sciences of the United States of America · 2024
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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

7 authors at 4 institutions in 3 countries.

Salman AhmedDepartment of Pharmacognosy, Faculty of Pharmacy and Pharmaceutical Sciences, University of Karachi, Karachi 75270, Pakistan.
Waqas AlamDepartment of Pharmacy, Abdul Wali Khan University Mardan, Mardan 23200, Pakistan.
Michael AschnerDepartment of Molecular Pharmacology, Albert Einstein College of Medicine, Forchheimer 209, 1300 Morris Park Avenue Bronx, NY 10461, USA.
Khalaf F AlsharifDepartment of Clinical Laboratory, College of Applied Medical Science, Taif University, P.O. Box 11099, Taif 21944, Saudi Arabia.
Ashraf AlbrakatiDepartment of Human Anatomy, College of Medicine, Taif University, P.O. Box 11099, Taif 21944, Saudi Arabia.
Luciano SasoDepartment of Physiology and Pharmacology "Vittorio Erspamer"Sapienza University, Rome 00185, Italy.
Haroon KhanDepartment of Pharmacy, Abdul Wali Khan University Mardan, Mardan 23200, Pakistan. Electronic address: hkdr2006@gmail.com.
Abdul Wali Khan University Mardan · PKTaif University · SAAlbert Einstein College of Medicine · USUniversity of Karachi · PK

Funding

Mechanisms of Methylmercury Induced Neuron ToxicityR01ES007331 · NIEHS · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI Michael Aschner, Aaron B Bowman · 1996 to 2026
$10.6M
NIEHS NIH HHS R01 ES007331
6 · The paper itself

Abstract

Cancer is one of the most severe medical conditions in the world, causing millions of deaths each year. Chemotherapy and radiotherapy are critical for treatment approaches, but both have numerous adverse health effects. Furthermore, the resistance of cancerous cells to anticancer medication leads to treatment failure. The rising burden of cancer requires novel efficacious treatment modalities. Natural remedies offer feasible alternative options against malignancy in contrast to available synthetic medication. Selective killing of cancer cells is privileged mainstream in cancer treatment, and targeted therapy represents the new tool with the potential to pursue this aim. The discovery of innovative therapies targeting essential components of DNA damage signaling and repair pathways such as ataxia telangiectasia mutated and Rad3 related Checkpoint kinase 1 (ATR-CHK1)has offered a possibility of significant therapeutic improvement in oncology. The activation and inhibition of this pathway account for chemopreventive and chemotherapeutic activity, respectively. Targeting this pathway can also aid to overcome the resistance of conventional chemo- or radiotherapy. This review enlightens the anticancer role of natural products by ATR-CHK1 activation and inhibition. Additionally, these compounds have been shown to have chemotherapeutic synergistic potential when used in combination with other anticancer drugs. Ideally, this review will trigger interest in natural products targeting ATR-CHK1 and their potential efficacy and safety as cancer lessening agents.

Indexed as

Biological ProductsNeoplasmsAtaxia Telangiectasia Mutated ProteinsCheckpoint Kinase 1DNA DamageHumansSignal TransductionAtaxia Telangiectasia Mutated ProteinsATR protein, humanBiological ProductsCheckpoint Kinase 1ATR-CHK1ChemopreventiveChemotherapeuticMDR cancerNatural products targeting ATR-CHK1

Identifiers

PMID36271573
PMCPMC9590097
OpenAlexW4303649600

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.