Evidence map›Paper›PMID 32708340›Full record

ArticleGenes2020

TCGA Pan-Cancer Genomic Analysis of Alternative Lengthening of Telomeres (ALT) Related Genes.

Isaac Armendáriz-Castillo, Andrés López-Cortés, Jennyfer García-Cárdenas, Patricia Guevara-Ramírez, Paola E Leone, Andy Pérez-Villa, Verónica Yumiceba, Ana K Zambrano, Santiago Guerrero, César Paz-Y-Miño

Open access · goldAbstract read
In one paragraph

Article in Genes, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

14 citing papers in PubMed, 12 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

10 authors at 1 institution in 1 country.

Isaac Armendáriz-CastilloCentro de Investigación Genética y Genómica, Facultad de Ciencias de la Salud Eugenio Espejo, Universidad UTE, 170129 Quito, Ecuador.ORCID 0000-0003-2636-2707
Andrés López-CortésCentro de Investigación Genética y Genómica, Facultad de Ciencias de la Salud Eugenio Espejo, Universidad UTE, 170129 Quito, Ecuador.ORCID 0000-0003-1503-1929
Jennyfer García-CárdenasCentro de Investigación Genética y Genómica, Facultad de Ciencias de la Salud Eugenio Espejo, Universidad UTE, 170129 Quito, Ecuador.ORCID 0000-0001-9035-7668
Patricia Guevara-RamírezCentro de Investigación Genética y Genómica, Facultad de Ciencias de la Salud Eugenio Espejo, Universidad UTE, 170129 Quito, Ecuador.
Paola E LeoneCentro de Investigación Genética y Genómica, Facultad de Ciencias de la Salud Eugenio Espejo, Universidad UTE, 170129 Quito, Ecuador.ORCID 0000-0003-3351-2275
Andy Pérez-VillaCentro de Investigación Genética y Genómica, Facultad de Ciencias de la Salud Eugenio Espejo, Universidad UTE, 170129 Quito, Ecuador.ORCID 0000-0001-6758-4299
Verónica YumicebaCentro de Investigación Genética y Genómica, Facultad de Ciencias de la Salud Eugenio Espejo, Universidad UTE, 170129 Quito, Ecuador.ORCID 0000-0001-6998-7913
Ana K ZambranoCentro de Investigación Genética y Genómica, Facultad de Ciencias de la Salud Eugenio Espejo, Universidad UTE, 170129 Quito, Ecuador.ORCID 0000-0003-4102-3965
Santiago GuerreroCentro de Investigación Genética y Genómica, Facultad de Ciencias de la Salud Eugenio Espejo, Universidad UTE, 170129 Quito, Ecuador.
César Paz-Y-MiñoCentro de Investigación Genética y Genómica, Facultad de Ciencias de la Salud Eugenio Espejo, Universidad UTE, 170129 Quito, Ecuador.ORCID 0000-0002-6693-7344
Universidad UTE · EC

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Telomere maintenance mechanisms (TMM) are used by cancer cells to avoid apoptosis, 85-90% reactivate telomerase, while 10-15% use the alternative lengthening of telomeres (ALT). Due to anti-telomerase-based treatments, some tumors switch from a telomerase-dependent mechanism to ALT; in fact, the co-existence between both mechanisms has been observed in some cancers. Although different elements in the ALT pathway are uncovered, some molecular mechanisms are still poorly understood. Therefore, with the aim to identify potential molecular markers for the study of ALT, we combined in silico approaches in a 411 telomere maintenance gene set. As a consequence, we conducted a genomic analysis of these genes in 31 Pan-Cancer Atlas studies from The Cancer Genome Atlas and found 325,936 genomic alterations; from which, we identified 20 genes highly mutated in the cancer studies. Finally, we made a protein-protein interaction network and enrichment analysis to observe the main pathways of these genes and discuss their role in ALT-related processes, like homologous recombination and homology directed repair. Overall, due to the lack of understanding of the molecular mechanisms of ALT cancers, we proposed a group of genes, which after ex vivo validations, could represent new potential therapeutic markers in the study of ALT.

Indexed as

Telomere HomeostasisGenetic Predisposition to DiseaseHumansNeoplasmsProtein Interaction MapsTelomere-Binding ProteinsTelomere-Binding ProteinsALTcancerin silicotelomeres

Identifiers

PMID32708340
PMCPMC7397314
OpenAlexW3044473343

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.