Evidence map›Paper›PMID 32772213›Full record

ReviewCancer metastasis reviews2020

Splice variants of RAS-translational significance.

Erzsébet Rásó

Abstract readReview
In one paragraph

Review in Cancer metastasis reviews, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing 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

15 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. YB-1 activating cascades as potential targets in KRAS-mutated tumors.Strahlentherapie und Onkologie : Organ der Deutschen Rontgengesellschaft ... [et al] · 2023
    Review
  8. Article
  9. Review
  10. Review
  11. The role of KRAS splice variants in cancer biology.Frontiers in cell and developmental biology · 2022
    Review
  12. Article
  13. Anticancer drug resistance: An update and perspective.Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy · 2021
    Review
  14. Review
  15. 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

1 author.

Erzsébet Rásó2nd Department of Pathology, Semmelweis University, Budapest, Hungary. rasoerzs@gmail.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

One of the mechanisms potentially explaining the discrepancy between the number of human genes and the functional complexity of organisms is generating alternative splice variants, an attribute of the vast majority of multi-exon genes. Members of the RAS family, such as NRAS, KRAS and HRAS, all of which are of significant importance in cancer biology, are no exception. The structural and functional differences of these splice variants, particularly if they contain the canonical (and therefore routinely targeted for diagnostic purposes) hot spot mutations, pose a significant challenge for targeted therapies. We must therefore consider whether these alternative splice variants constitute a minor component as originally thought and how therapies targeting the canonical isoforms affect these alternative splice variants and their overall functions.

Indexed as

Genes, rasProtein Processing, Post-TranslationalAlternative SplicingAmino Acid SequenceAnimalsBase SequenceHumansMutationNeoplasmsProto-Oncogene Proteins p21(ras)RNA, MessengerProto-Oncogene Proteins p21(ras)RNA, MessengerExpressionFunctionHRASKRASNRASSplicing

Identifiers

PMID32772213
PMCPMC7680328

What OpenQuestion holds

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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.