Evidence map›Paper›PMID 36685900›Full record

ArticleFrontiers in genetics2022

Functional impact of multi-omic interactions in breast cancer subtypes.

Soledad Ochoa, Enrique Hernández-Lemus

Abstract read
In one paragraph

Article in Frontiers in genetics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing 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

7 citing papers in PubMed.

  1. Article
  2. Article
  3. Potential Drug Synergy Through the ERBB2 Pathway in HER2+ Breast Tumors.International journal of molecular sciences · 2024
    Article
  4. Article
  5. Article
  6. Article
  7. 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

2 authors.

Soledad OchoaComputational Genomics Division, National Institute of Genomic Medicine, Mexico City, Mexico.
Enrique Hernández-LemusComputational Genomics Division, National Institute of Genomic Medicine, Mexico City, Mexico.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multi-omic approaches are expected to deliver a broader molecular view of cancer. However, the promised mechanistic explanations have not quite settled yet. Here, we propose a theoretical and computational analysis framework to semi-automatically produce network models of the regulatory constraints influencing a biological function. This way, we identified functions significantly enriched on the analyzed omics and described associated features, for each of the four breast cancer molecular subtypes. For instance, we identified functions sustaining over-representation of invasion-related processes in the basal subtype and DNA modification processes in the normal tissue. We found limited overlap on the omics-associated functions between subtypes; however, a startling feature intersection within subtype functions also emerged. The examples presented highlight new, potentially regulatory features, with sound biological reasons to expect a connection with the functions. Multi-omic regulatory networks thus constitute reliable models of the way omics are connected, demonstrating a capability for systematic generation of mechanistic hypothesis.

Indexed as

breast cancerDNA methylationHIFmulti-omicsnetwork biologyRASSOX9WNT

Identifiers

PMID36685900
PMCPMC9850112

What OpenQuestion holds

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LicenceCC BY
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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.