Animal studyindependent cross-checkabstract checked I-CAN-109 standard review

Stress hormones help drive cancer wasting in mice

Cancer- and endotoxin-induced cachexia require intact glucocorticoid signaling in skeletal muscle.

Overview

Braun TP et al.. FASEB J 2013 · PMID 23733748 · DOI 10.1096/fj.13-230375

Mice lacking glucocorticoid receptors in muscle lost 77% less muscle when they had tumours.

Does the study support the specific claim? Partly · Methodological quality: moderate

Original publication

Plain-language summary

Study explained simply
What did the researchers want to find out?

Test role of glucocorticoids in cachexia.

How was the study done?

Knockout mouse experiments.

How many people, animals or samples were studied?

Mice.

What was actually found?

Glucocorticoid signalling needed for much of the wasting.

How large was the observed effect?

77% less atrophy.

What do the results mean in everyday life?

Hormones are part of how cancer causes wasting.

What are the study's limitations?

Mouse data.

What does it say about Elawady's specific claim?

Partly supports the hormonal idea, not the conclusion.

Do the results apply to Germany and Europe?

Low.

What can explicitly not be concluded from this study?

Effects in humans.

Scientific in-depth review

1. Full reference

Authors
Braun TP et al.
Journal
FASEB J
Year
2013
Identifier
PMID 23733748 DOI 10.1096/fj.13-230375
Verification
verified – PubMed efetch 2026-10-26 + Crossref
Retracted
no
Corrections
none
Extent checked
abstract only
Conflicts of interest and funding

NIH and CIHR grants (PubMed record)

2. Research question

Do inflammation-induced and cancer-induced muscle atrophy require glucocorticoid signalling in muscle?

3. Study design and population

Study design
Animal study – Animal experimental study (conditional knockout mice)
Population

Mice (muscle-specific glucocorticoid receptor knockout) with LPS or tumour

Country

USA

Period

Published 2013

Sample size

not stated in abstract

Inclusion and exclusion criteria

not stated

4. Methods and endpoints

Exposure / intervention

Deletion of glucocorticoid receptor in muscle

Comparator

Control mice

Endpoints

Skeletal muscle atrophy

Statistical methods

not stated in abstract

5. Actual results

Results

Muscle-specific glucocorticoid receptor deletion gave 71% protection against LPS-induced atrophy; knockout mice had 77% less muscle atrophy in response to tumour growth.

Absolute risks

not applicable

Authors' conclusion

Glucocorticoids are a major determinant of inflammation-induced atrophy and play a critical role in cancer cachexia.

6. Strengths

  • Genetic causal design

7. Weaknesses

  • Mouse model
  • Does not address cause of death in humans

8. Risk of bias

Orienting tool
none applicable
Type of assessment
simplified assessment (abstract only)
Full formal assessment
no
Overall risk of bias
not assessable
Rationale

Animal study.

9. Assessment of the statistical interpretation

Large effect sizes in mice; transferability to humans uncertain.

10. Relevance to the specific claim

Supports a hormonal (glucocorticoid) mechanism within cancer wasting - a kernel of Elawady's 'cortisone' remark - while showing the process is triggered by the tumour.

11. Independent contrary findings

In this model the tumour drives the glucocorticoid response; it does not show that hormones rather than cancer cause death.

12. Transferability to Germany and Europe

Not applicable (animal).

13. Overall methodological judgement

Mechanistic support for the hormonal part; does not support the conclusion.

Multidimensional assessment
Multidimensional assessment
Authenticity of the sourceverified
Methodological qualitymoderate
Risk of biasnot assessable
Precision of resultsnot applicable
Directnessvery indirect
Reproducibilityunknown
Consistency with the overall evidenceconsistent
Regional transferabilitylow
Adequacy of the interpretation (by the archive)not applicable

14. Open questions

Human relevance.

15. Linked fact checks