Evidence map›Paper›PMID 34439272›Full record

ArticleCancers2021

Genomic Mapping of Splicing-Related Genes Identify Amplifications in

María Del Mar Noblejas-López, Igor López-Cade, Jesús Fuentes-Antrás, Gonzalo Fernández-Hinojal, Ada Esteban-Sánchez, Aránzazu Manzano, José Ángel García-Sáenz, Pedro Pérez-Segura, Miguel De La Hoya, Atanasio Pandiella and 3 more

Abstract read
In one paragraph

Article in Cancers, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
–field-weighted citation impact
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

9 citing papers in PubMed.

  1. Article
  2. UnveilingBiomedicines · 2024
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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

13 authors.

María Del Mar Noblejas-LópezTranslational Oncology Laboratory, Translational Research Unit, Albacete University Hospital, 02008 Albacete, Spain.ORCID 0000-0001-9250-9688
Igor López-CadeMolecular Oncology Laboratory, Hospital Clínico San Carlos (HCSC), Instituto de Investigación Sanitaria San Carlos (IdISSC), 28040 Madrid, Spain.ORCID 0000-0001-8069-1507
Jesús Fuentes-AntrásExperimental Therapeutics Unit, Hospital Clínico San Carlos (HCSC), Instituto de Investigación Sanitaria San Carlos (IdISSC), 28040 Madrid, Spain.
Gonzalo Fernández-HinojalExperimental Therapeutics Unit, Hospital Clínico San Carlos (HCSC), Instituto de Investigación Sanitaria San Carlos (IdISSC), 28040 Madrid, Spain.
Ada Esteban-SánchezMolecular Oncology Laboratory, Hospital Clínico San Carlos (HCSC), Instituto de Investigación Sanitaria San Carlos (IdISSC), 28040 Madrid, Spain.ORCID 0000-0002-1850-590X
Aránzazu ManzanoExperimental Therapeutics Unit, Hospital Clínico San Carlos (HCSC), Instituto de Investigación Sanitaria San Carlos (IdISSC), 28040 Madrid, Spain.
José Ángel García-SáenzMedical Oncology Department, Hospital Clínico San Carlos (HCSC), Instituto de Investigación Sanitaria San Carlos (IdISSC), 28040 Madrid, Spain.
Pedro Pérez-SeguraMedical Oncology Department, Hospital Clínico San Carlos (HCSC), Instituto de Investigación Sanitaria San Carlos (IdISSC), 28040 Madrid, Spain.
Miguel De La HoyaMolecular Oncology Laboratory, Hospital Clínico San Carlos (HCSC), Instituto de Investigación Sanitaria San Carlos (IdISSC), 28040 Madrid, Spain.
Atanasio PandiellaInstituto de Biología Molecular y Celular del Cáncer (IBMCC-CIC), Instituto de Investigación Biomédica de Salamanca (IBSAL), Consejo Superior de Investigaciones Científicas (CSIC) and CIBERONC, 37007 Salamanca, Spain.
Balázs GyőrffyDepartment of Bioinformatics, Semmelweis University, H-1094 Budapest, Hungary.ORCID 0000-0002-5772-3766
Vanesa García-BarberánMolecular Oncology Laboratory, Hospital Clínico San Carlos (HCSC), Instituto de Investigación Sanitaria San Carlos (IdISSC), 28040 Madrid, Spain.ORCID 0000-0002-2531-0203
Alberto OcañaTranslational Oncology Laboratory, Translational Research Unit, Albacete University Hospital, 02008 Albacete, Spain.ORCID 0000-0002-1067-9630

Funding

ACEPAIN NACRIS Cancer Foundation NADiputación de Albacete NAInstituto de Salud Carlos III PI18/01020Instituto de Salud Carlos III PI19/00808Ministry for Innovation and Technology 2018-1.3.1-VKE-2018-00032Ministry for Innovation and Technology 2018-2.1.17-TET-KR-00001Ministry for Innovation and Technology 2020-1.1.6-JÖVŐ-2021-00013Ministry for Innovation and Technology 2020-4.1.1.-TKP2020Spanish Ministry of Education FPU18/01319
6 · The paper itself

Abstract

Alternative splicing is an essential biological process, which increases the diversity and complexity of the human transcriptome. In our study, 304 splicing pathway-related genes were evaluated in tumors from breast cancer patients (TCGA dataset). A high number of alterations were detected, including mutations and copy number alterations (CNAs), although mutations were less frequently present compared with CNAs. In the four molecular subtypes, 14 common splice genes showed high level amplification in >5% of patients. Certain genes were only amplified in specific breast cancer subtypes. Most altered genes in each molecular subtype clustered to a few chromosomal regions. In the Luminal subtype, amplifications of

Indexed as

BET inhibitorsluminal breast cancersplicing pathway

Identifiers

PMID34439272
PMCPMC8391113

What OpenQuestion holds

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Registered trials

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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.