Evidence map›Paper›PMID 35011637›Full record

ReviewCells2021

Three-Dimensional Genome Organization in Breast and Gynecological Cancers: How Chromatin Folding Influences Tumorigenic Transcriptional Programs.

Stephanie I Nuñez-Olvera, Jonathan Puente-Rivera, Rosalio Ramos-Payán, Carlos Pérez-Plasencia, Yarely M Salinas-Vera, Lorena Aguilar-Arnal, César López-Camarillo

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.8field-weighted citation impact, top 33% 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

6 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. 3D genomic organization in cancers.Quantitative biology (Beijing, China) · 2023
    Review
  5. Article
  6. Review
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 5 institutions in 1 country.

Stephanie I Nuñez-OlveraDepartamento de Biología Celular y Fisiología, Instituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México, Mexico City 04510, Mexico.
Jonathan Puente-RiveraPosgrado en Ciencias Genómicas, Universidad Autónoma de la Ciudad de México, Mexico City 03100, Mexico.ORCID 0000-0001-6941-6248
Rosalio Ramos-PayánFacultad de Ciencias Químico Biológicas, Universidad Autónoma de Sinaloa, Culiacan City 80030, Mexico.ORCID 0000-0001-7500-7571
Carlos Pérez-PlasenciaLaboratorio de Genómica, Instituto Nacional de Cancerologia, Mexico City 14080, Mexico.
Yarely M Salinas-VeraDepartamento de Bioquímica, Centro de Investigación y Estudios Avanzados, Mexico City 07360, Mexico.
Lorena Aguilar-ArnalDepartamento de Biología Celular y Fisiología, Instituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México, Mexico City 04510, Mexico.ORCID 0000-0003-4473-4471
César López-CamarilloPosgrado en Ciencias Genómicas, Universidad Autónoma de la Ciudad de México, Mexico City 03100, Mexico.
Universidad Autónoma de la Ciudad de México · MXUniversidad Nacional Autónoma de México · MXCentro de Investigación en Materiales Avanzados · MXInstituto Nacional de Cancerología · MXUniversidad Autónoma de Sinaloa · MX

Funding

Consejo Nacional de Ciencia y Tecnología FORDECYT-PRONACES/51207/2020
6 · The paper itself

Abstract

A growing body of research on the transcriptome and cancer genome has demonstrated that many gynecological tumor-specific gene mutations are located in cis-regulatory elements. Through chromosomal looping, cis-regulatory elements interact which each other to control gene expression by bringing distant regulatory elements, such as enhancers and insulators, into close proximity with promoters. It is well known that chromatin connections may be disrupted in cancer cells, promoting transcriptional dysregulation and the expression of abnormal tumor suppressor genes and oncogenes. In this review, we examine the roles of alterations in 3D chromatin interactions. This includes changes in CTCF protein function, cancer-risk single nucleotide polymorphisms, viral integration, and hormonal response as part of the mechanisms that lead to the acquisition of enhancers or super-enhancers. The translocation of existing enhancers, as well as enhancer loss or acquisition of insulator elements that interact with gene promoters, is also revised. Remarkably, similar processes that modify 3D chromatin contacts in gene promoters may also influence the expression of non-coding RNAs, such as long non-coding RNAs (lncRNAs) and microRNAs (miRNAs), which have emerged as key regulators of gene expression in a variety of cancers, including gynecological malignancies.

Indexed as

Genome, HumanTranscription, GeneticAnimalsBreast NeoplasmsCarcinogenesisChromatinFemaleGenital Neoplasms, FemaleHumansChromatin3D genomebreast cancercis-regulatory elementsCTCFepigenetic regulationgynecological cancerstopology-associated domains

Identifiers

PMID35011637
PMCPMC8750285
OpenAlexW4200590287

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.