Evidence map›Paper›PMID 33163298›Full record

ReviewCureus2020

Comparing the Role of the p53 Gene and Telomerase Enzyme in 'Accelerated Aging Due to Cancer': A Literature Review.

Paramvijay Singh Dhalla, Arunima Kaul, Jian Garcia, Anusha Bapatla, Raheela Khalid, Ana S Armenta-Quiroga, Safeera Khan

Open access · diamondAbstract readReview
In one paragraph

Review in Cureus, 2020. 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 51% 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, 1 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

7 authors at 1 institution in 1 country.

Paramvijay Singh DhallaMedicine, California Institute of Behavioral Neurosciences & Psychology, Fairfield, USA.
Arunima KaulInternal Medicine, California Institute of Behavioral Neurosciences & Psychology, Fairfield, USA.
Jian GarciaInternal Medicine, California Institute of Behavioral Neurosciences & Psychology, Fairfield, USA.
Anusha BapatlaInternal Medicine, California Institute of Behavioral Neurosciences & Psychology, Fairfield, USA.
Raheela KhalidInternal Medicine, California Institute of Behavioral Neurosciences & Psychology, Fairfield, USA.
Ana S Armenta-QuirogaInternal Medicine, California Institute of Behavioral Neurosciences & Psychology, Fairfield, USA.
Safeera KhanInternal Medicine, California Institute of Behavioral Neurosciences & Psychology, Fairfield, USA.
California Institute of Behavioral Neurosciences and Psychology (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aging is defined as progressive physiological alterations in an organism that lead to senescence. In response to stress, when proliferative-competent cells undergo permanent, irreversible growth arrest (like replicative dividing limit, oncogene activation, oxidative stress, or deoxyribonucleic acid (DNA) damage), it is termed as cellular senescence. Biomarkers p53, telomerase, and other inflammatory cytokines have a vital link with senescence, and directed use of these markers might be useful in manipulating cancer and the aging process. We included studies related to topics ' accelerated aging due to cancer', telomerase's relation to Aging and Cancer, p53's relation to Aging and Cancer, Atherosclerosis and Cancer from Search databases like PubMed and Google Scholar. We relied on peer-reviewed articles and included literature from the last 10 years written in the English language. Degenerative diseases in humans are usually linked to atherosclerosis, and atherosclerosis is associated with short leukocyte telomere length. Cancer itself and its treatment are linked with accelerated aging by causing progressive shortening of telomeres during cell replication, resulting in cell death. Gene p53 is known to have a dual effect that works as a tumor suppressor and has pro-aging side effects. In experimental studies, when p53 overcomes multiple regulatory mechanisms controlling its activity, then only the pro-aging side effects of p53 manifested. This might be a potential key for treating cancer without causing the side-effects of aging. In this review, we aim to explain and summarize the interdependent nature of p53, telomeres, and other conventional mechanisms of aging and cancer like inflammation, oxidative stress, uncontrolled proliferation, angiogenesis, micro ribonucleic acids (RNAs), and apoptosis, with a more synergistic approach that can help in developing new therapeutics and play a potential role in shaping modern human lifespan and revolutionize cancer treatment.

Indexed as

agingatherosclerosiscancermetforminp16ink4ap53progeriasaspstatintelomerase

Identifiers

PMID33163298
PMCPMC7641464
OpenAlexW3091231502

What OpenQuestion 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 OpenQuestion graph.