Evidence map›Paper›PMID 34748401›Full record

ArticleMolecular and cellular biology2022

Stress Responses as Master Keys to Epigenomic Changes in Transcriptome and Metabolome for Cancer Etiology and Therapeutics.

Atanu Mondal, Apoorva Bhattacharya, Vipin Singh, Shruti Pandita, Albino Bacolla, Raj K Pandita, John A Tainer, Kenneth S Ramos, Tej K Pandita, Chandrima Das

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.1field-weighted citation impact, top 60% 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

1 citing paper in PubMed, 2 citations in OpenAlex.

  1. Article
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

10 authors at 5 institutions in 2 countries.

Atanu Mondal *Biophysics and Structural Genomics Division, Saha Institute of Nuclear Physics, Kolkata, India.
Apoorva Bhattacharya *Biophysics and Structural Genomics Division, Saha Institute of Nuclear Physics, Kolkata, India.
Vipin Singh *Biophysics and Structural Genomics Division, Saha Institute of Nuclear Physics, Kolkata, India.
Shruti PanditaDivision of Hematology and Medical Oncology, St. Louis University, St. Louis, Missouri, USA.
Albino BacollaDepartment of Molecular and Cellular Oncology, University of Texas M.D. Anderson Cancer Center, Houston, Texas, USA.
Raj K PanditaDepartment of Molecular and Cellular Biology, Baylor College of Medicine, Houston, Texas, USA.
John A TainerDepartment of Molecular and Cellular Oncology, University of Texas M.D. Anderson Cancer Center, Houston, Texas, USA.
Kenneth S RamosCenter for Genomics and Precision Medicine, Texas A&M College of Medicine, Houston, Texas, USA.
Tej K PanditaDepartment of Molecular and Cellular Biology, Baylor College of Medicine, Houston, Texas, USA.ORCID 0000-0002-1399-808X
Chandrima DasBiophysics and Structural Genomics Division, Saha Institute of Nuclear Physics, Kolkata, India.
Saha Institute of Nuclear Physics · INTexas A&M Health Science Center · USThe University of Texas MD Anderson Cancer Center · USBaylor College of Medicine · USSaint Louis University · US

Funding

Transcription-Coupled & Replication-Associated Excision RepairP01CA092584 · NCI · UNIVERSITY OF CALIF-LAWRENC BERKELEY LAB · PI John A. Tainer · 2001 to 2026
$89.6M
User Training and OutreachP30GM124169 · NIGMS · UNIVERSITY OF CALIF-LAWRENC BERKELEY LAB · PI Gregory L Hura · 2017 to 2026
$28.6M
Mesoscale and Nanoscale Technologies Integrated by Structures for DNA Repair Complexes (MANTIS-DRC)R35CA220430 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI John A. Tainer · 2018 to 2026
$7.6M
NCI NIH HHS P01 CA092584NCI NIH HHS R35 CA220430NIGMS NIH HHS P30 GM124169
6 · The paper itself

Abstract

From initiation through progression, cancer cells are subjected to a magnitude of endogenous and exogenous stresses, which aid in their neoplastic transformation. Exposure to these classes of stress induces imbalance in cellular homeostasis and, in response, cancer cells employ informative adaptive mechanisms to rebalance biochemical processes that facilitate survival and maintain their existence. Different kinds of stress stimuli trigger epigenetic alterations in cancer cells, which leads to changes in their transcriptome and metabolome, ultimately resulting in suppression of growth inhibition or induction of apoptosis. Whether cancer cells show a protective response to stress or succumb to cell death depends on the type of stress and duration of exposure. A thorough understanding of epigenetic and molecular architecture of cancer cell stress response pathways can unveil a plethora of information required to develop novel anticancer therapeutics. The present view highlights current knowledge about alterations in epigenome and transcriptome of cancer cells as a consequence of exposure to different physicochemical stressful stimuli such as reactive oxygen species (ROS), hypoxia, radiation, hyperthermia, genotoxic agents, and nutrient deprivation. Currently, an anticancer treatment scenario involving the imposition of stress to target cancer cells is gaining traction to augment or even replace conventional therapeutic regimens. Therefore, a comprehensive understanding of stress response pathways is crucial for devising and implementing novel therapeutic strategies.

Indexed as

Cell Transformation, NeoplasticEpigenomicsHumansHypoxiaMetabolomeNeoplasmsOxidative StressReactive Oxygen SpeciesTranscriptomeReactive Oxygen SpeciesDNA damageepigenetic responsehyperthermiahypoxianutrient deprivationoxidative stress

Identifiers

PMID34748401
PMCPMC8773053
OpenAlexW3212685173

What OpenQuestion holds

Textmetadata
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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.