Evidence map›Paper›PMID 35565323›Full record

ReviewCancers2022

Alternative Lengthening of Telomeres and Mediated Telomere Synthesis.

Kailong Hou, Yuyang Yu, Duda Li, Yanduo Zhang, Ke Zhang, Jinkai Tong, Kunxian Yang, Shuting Jia

Open access · goldAbstract readReview
In one paragraph

Review in Cancers, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.2field-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

16 citing papers in PubMed, 19 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

8 authors at 2 institutions in 1 country.

Kailong HouFaculty of Life Science and Technology, Kunming University of Science and Technology, 727 Jing Ming Nan Road, Kunming 650500, China.ORCID 0000-0003-2587-7581
Yuyang YuLaboratory of Molecular Genetics of Aging and Tumor, Medical School, Kunming University of Science and Technology, 727 Jing Ming Nan Road, Kunming 650500, China.
Duda LiLaboratory of Molecular Genetics of Aging and Tumor, Medical School, Kunming University of Science and Technology, 727 Jing Ming Nan Road, Kunming 650500, China.ORCID 0000-0001-8224-5367
Yanduo ZhangLaboratory of Molecular Genetics of Aging and Tumor, Medical School, Kunming University of Science and Technology, 727 Jing Ming Nan Road, Kunming 650500, China.
Ke ZhangLaboratory of Molecular Genetics of Aging and Tumor, Medical School, Kunming University of Science and Technology, 727 Jing Ming Nan Road, Kunming 650500, China.
Jinkai TongLaboratory of Molecular Genetics of Aging and Tumor, Medical School, Kunming University of Science and Technology, 727 Jing Ming Nan Road, Kunming 650500, China.
Kunxian YangFirst People's Hospital of Yunnan Province, 157 Jinbi Road, Kunming 650032, China.
Shuting JiaLaboratory of Molecular Genetics of Aging and Tumor, Medical School, Kunming University of Science and Technology, 727 Jing Ming Nan Road, Kunming 650500, China.ORCID 0000-0003-0452-260X
Kunming University of Science and Technology · CNFirst People's Hospital of Yunnan Province · CN

Funding

Yunnan Fundamental Research Project 202201AS070074Yunnan "Ten Thousand Talents Plan" Young Top Talent Project YNWRQNBJ-2019-240
6 · The paper itself

Abstract

Telomeres are DNA-protein complexes that protect eukaryotic chromosome ends from being erroneously repaired by the DNA damage repair system, and the length of telomeres indicates the replicative potential of the cell. Telomeres shorten during each division of the cell, resulting in telomeric damage and replicative senescence. Tumor cells tend to ensure cell proliferation potential and genomic stability by activating telomere maintenance mechanisms (TMMs) for telomere lengthening. The alternative lengthening of telomeres (ALT) pathway is the most frequently activated TMM in tumors of mesenchymal and neuroepithelial origin, and ALT also frequently occurs during experimental cellular immortalization of mesenchymal cells. ALT is a process that relies on homologous recombination (HR) to elongate telomeres. However, some processes in the ALT mechanism remain poorly understood. Here, we review the most recent understanding of ALT mechanisms and processes, which may help us to better understand how the ALT pathway is activated in cancer cells and determine the potential therapeutic targets in ALT pathway-stabilized tumors.

Indexed as

alternative lengthening of telomereshomologous recombinationtelomere maintenance mechanisms

Identifiers

PMID35565323
PMCPMC9105334
OpenAlexW4225146345

What Socratic 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 Socratic graph.