Evidence map›Paper›PMID 31134216›Full record

ArticleJCSM clinical reports

The Role of Systemic Inflammation in Cancer-Associated Muscle Wasting and Rationale for Exercise as a Therapeutic Intervention.

Calvin L Cole, Ian R Kleckner, Aminah Jatoi, Edward M Schwarz, Richard F Dunne

Open access · goldAbstract read
PubMed Full text at PMC
In one paragraph

Article in JCSM clinical reports. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed, 6 pooled it
4.1field-weighted citation impact, top 5% 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

55 citing papers in PubMed, 6 syntheses or guidelines pooled it, 78 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Pooled it
  6. Pooled it
  7. Trial
  8. Trial
  9. Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article
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

5 authors at 2 institutions in 1 country.

Calvin L ColeDepartment of Orthopaedics, Center for Musculoskeletal Research, University of Rochester Medical Center, Rochester, New York, 14642.
Ian R KlecknerDepartment of Surgery, Cancer Control, University of Rochester Medical Center, Rochester, New York, 14642.
Aminah JatoiDepartment of Oncology, Mayo Medical School, Rochester, Minnesota, 55905.
Edward M SchwarzDepartment of Orthopaedics, Center for Musculoskeletal Research, University of Rochester Medical Center, Rochester, New York, 14642.
Richard F DunneDepartment of Surgery, Cancer Control, University of Rochester Medical Center, Rochester, New York, 14642.
University of Rochester Medical Center · USMayo Clinic in Arizona · US

Funding

UNIVERSITY OF ROCHESTER--CCOP RESEARCH BASEU10CA037420 · NCI · UNIVERSITY OF ROCHESTER · PI MORROW, GARY R · 1985 to 2014
$21.1M
Rochester Resource-Based Center for Bone, Muscle and Orthopaedic Research (ROCSTARR) (Overall Application)P30AR069655 · NIAMS · UNIVERSITY OF ROCHESTER · PI Edward M. Schwarz · 2016 to 2026
$7.8M
Cancer Control Research Training Curriculum (R25T)R25CA102618 · NCI · UNIVERSITY OF ROCHESTER · PI JANELSINS, MICHELLE C, MORROW, GARY R · 2004 to 2018
$6.7M
The Effects of Exercise on Chemotherapy-Induced Peripheral Neuropathy, Inflammation, and Interoceptive Brain CircuitryK07CA221931 · NCI · UNIVERSITY OF ROCHESTER · PI KLECKNER, IAN ROBERT · 2018 to 2022
$795k
NCI NIH HHS K07 CA221931NCI NIH HHS R25 CA102618NCI NIH HHS U10 CA037420NIAMS NIH HHS P30 AR069655
6 · The paper itself

Abstract

Progressive skeletal muscle wasting in cancer cachexia involves a process of dysregulated protein synthesis and breakdown. This catabolism may be the result of mal-nutrition, and an upregulation of both pro-inflammatory cytokines and the ubiquitin proteasome pathway (UPP), which can subsequently increase myostatin and activin A release. The skeletal muscle wasting associated with cancer cachexia is clinically significant, it can contribute to treatment toxicity or the premature discontinuation of treatments resulting in increases in morbidity and mortality. Thus, there is a need for further investigation into the pathophysiology of muscle wasting in cancer cachexia to develop effective prophylactic and therapeutic interventions. Several studies have identified a central role for chronic-systemic inflammation in initiating and perpetuating muscle wasting in patients with cancer. Interestingly, while exercise has shown efficacy in improving muscle quality, only recently have investigators begun to assess the impact that exercise has on chronic-systemic inflammation. To put this new information into context with established paradigms, here we review several biological pathways (e.g. dysfunctional inflammatory response, hypothalamus pituitary adrenal axis, and increased myostatin/activin A activity) that may be responsible for the muscle wasting in patients with cancer. Additionally, we discuss the potential impact that exercise has on these pathways in the treatment of cancer-related muscle wasting. Exercise is an attractive intervention for muscle wasting in this population, partially because it disrupts chronic-systemic inflammation mediated catabolism. Most importantly, exercise is a potent stimulator of muscle synthesis, and therefore this therapy may reverse muscle damage caused by cancer cachexia.

Indexed as

Cancer CachexiaChronic-Systemic InflammationExerciseMuscle Wasting

Identifiers

PMID31134216
PMCPMC6534125
OpenAlexW2891012290

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.