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The Study

Unmutated RRAS2 emerges as a key oncogene in post-partum-associated triple negative breast cancer

In simple terms

This study is like trying to say a toy causes a room to be messy, but we don’t know if the toy was randomly placed or just happened to be there. We can’t say it caused the mess—we just see it’s there.

58%

Analysis score

58/ 90

Maximum 90 for a randomized controlled trial.

Where the score came from

Reporting0
Methodology54
Publication100
Statistical77
Study type (basis of the score)
Randomized Controlled Trial
Level 1b - Individual RCT
What’s the bottom line?

Scientists found that a gene called RRAS2, when too active, can turn normal breast cells into cancer — but only if the woman has been pregnant.

Where does this study sit?

Reviews of RCTs (Meta-analyses)

Max 100

Randomized Trials

Max 90

Reviews of Cohort Studies

Max 85

Cohort Studies

Max 72

Reviews of Case-Control Studies

Max 63

Case-Control Studies

Max 58

Cross-Sectional & Case Series

Max 50

Expert Opinion

Max 5
StrongerWeaker
Randomized Trials
Level 1b
58

58 / 100

Quality score

Participants are randomly assigned to treatment or control groups, minimizing bias. The gold standard for testing whether an intervention causes an effect.

Cannot establish causation

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Key takeaways

Summary

Based on the study abstract and findings.

  1. 1Yes — this gene overexpression is linked to the most aggressive breast cancer type and worse survival, and it’s more common in women who recently had children.
  2. 2In mice, 100% of pregnant females with extra RRAS2 got breast cancer.
  3. 3In women, 68% of breast cancers had too much RRAS2, especially in young moms with triple-negative cancer.

Score breakdown, methodology, conflicts of interest, evidence analysis & raw study data

Publication

Journal

Molecular Cancer

Year

2024

Authors

C. Cifuentes, Clara L. Oeste, Isabel Fernández-Pisonero, Alejandro M Hortal, C. García-Macías, Jeanne Hochart, R. Rubira, L. Horndler, Carlos Horndler, Xosé R. Bustelo, Balbino Alarcón

Open Access
13 citations
Analysis v5
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