Evidence map›Paper›PMID 36860927›Full record

ReviewJournal of Cancer2023

Potential clinical treatment prospects behind the molecular mechanism of alternative lengthening of telomeres (ALT).

Haolu Sun, Guijuan Chen, Baochang Guo, Shushu Lv, Guojun Yuan

Open access · goldAbstract readReview
In one paragraph

Review in Journal of Cancer, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

8 citing papers in PubMed, 9 citations in OpenAlex.

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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

5 authors at 4 institutions in 1 country.

Haolu SunDepartment of Pathophysiology, School of Basic Medical Sciences, Anhui Medical University, Hefei, 230011, China.
Guijuan ChenSchool of Environment and Chemical Engineering, Anhui Vocational and Technical College, Hefei, 230011, China.
Baochang GuoRehabilitation Department of Traditional Chinese Medicine, 969 Hospital of the Joint Support Force of the Chinese People's Liberation Army, Hohhot, 010000, China.
Shushu LvDepartment of Pathology, The First Affiliated Hospital of Huzhou University, Huzhou 313000, China.
Guojun YuanSchool of Environment and Chemical Engineering, Anhui Vocational and Technical College, Hefei, 230011, China.
Anhui Business College · CN181st Hospital of Chinese People's Liberation Army · CNAnhui Medical University · CNHuzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Normal somatic cells inevitably experience replicative stress and senescence during proliferation. Somatic cell carcinogenesis can be prevented in part by limiting the reproduction of damaged or old cells and removing them from the cell cycle [1, 2]. However, Cancer cells must overcome the issues of replication pressure and senescence as well as preserve telomere length in order to achieve immortality, in contrast to normal somatic cells [1, 2]. Although telomerase accounts for the bulk of telomere lengthening methods in human cancer cells, there is a non-negligible portion of telomere lengthening pathways that depend on alternative lengthening of telomeres (ALT) [3]. For the selection of novel possible therapeutic targets for ALT-related disorders, a thorough understanding of the molecular biology of these diseases is crucial [4]. The roles of ALT, typical ALT tumor cell traits, the pathophysiology and molecular mechanisms of ALT tumor disorders, such as adrenocortical carcinoma (ACC), are all summarized in this work. Additionally, this research compiles as many of its hypothetically viable but unproven treatment targets as it can (ALT-associated PML bodies (APB), etc.). This review is intended to contribute as much as possible to the development of research, while also trying to provide a partial information for prospective investigations on ALT pathways and associated diseases.

Indexed as

ALTdiseasesmolecular mechanismTelomerasetherapeutic targets

Identifiers

PMID36860927
PMCPMC9969575
OpenAlexW4318827679

What OpenQuestion holds

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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.