Evidence map›Paper›PMID 24677373›Full record

ReviewClinical cancer research : an official journal of the American Association for Cancer Research2014

Molecular mechanisms of bone metastasis and associated muscle weakness.

David L Waning, Theresa A Guise

Abstract readReview
In one paragraph

Review in Clinical cancer research : an official journal of the American Association for Cancer Research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
4.3field-weighted citation impact, top 4% 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

60 citing papers in PubMed, 99 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Article
  6. 2D and 3D In Vitro Co-culture for Cancer and Bone Cell Interaction Studies.Methods in molecular biology (Clifton, N.J.) · 2025
    Article
  7. Molecular communication from bone to skeletal muscle: an overview.Frontiers in cell and developmental biology · 2025
    Review
  8. Review
  9. Review
  10. Review
  11. RAS‑stimulated release of exosomalInternational journal of molecular medicine · 2023
    Article
  12. Muscle and Bone Defects in Metastatic Disease.Current osteoporosis reports · 2022
    Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Extracellular Vesicles in Tumors: A Potential Mediator of Bone Metastasis.Frontiers in cell and developmental biology · 2021
    Review
  19. Cachexia, a Systemic Disease beyond Muscle Atrophy.International journal of molecular sciences · 2020
    Review
  20. The Etiology and Impact of Muscle Wasting in Metastatic Cancer.Cold Spring Harbor perspectives in medicine · 2020
    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 at 1 institution in 1 country.

David L WaningAuthors' Affiliation: Division of Endocrinology, Department of Medicine, Indiana University, Indianapolis, Indiana.
Theresa A GuiseAuthors' Affiliation: Division of Endocrinology, Department of Medicine, Indiana University, Indianapolis, Indiana tguise@iu.edu.
Indiana University – Purdue University Indianapolis · US

Funding

TGFbeta IN THE BONE MICROENVIRONMENT: ROLE IN TUMOR METASTASISR01CA069158 · NCI · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI GUISE, THERESA A · 2001 to 2012
$2.8M
Differential TGF-Beta Signaling in Bone Microenviroment: Impact on Tumor GrowthU01CA143057 · NCI · INDIANA UNIVERSITY INDIANAPOLIS · PI BHOWMICK, NEIL A., GUISE, THERESA A · 2011 to 2015
$2.7M
(PQ9) Novel therapeutic approaches to chemotherapy-induced muscle.R21CA205437 · NCI · PENNSYLVANIA STATE UNIV HERSHEY MED CTR · PI WANING, DAVID L · 2016 to 2017
$372k
NCI NIH HHS R01 CA069158NCI NIH HHS R01CA69158NCI NIH HHS U01 CA143057NCI NIH HHS U01CA143057
6 · The paper itself

Abstract

Bone is a preferred site for breast cancer metastasis and leads to pathologic bone loss due to increased osteoclast-induced bone resorption. The homing of tumor cells to the bone depends on the support of the bone microenvironment in which the tumor cells prime the premetastatic niche. The colonization and growth of tumor cells then depend on adaptations in the invading tumor cells to take advantage of normal physiologic responses by mimicking bone marrow cells. This concerted effort by tumor cells leads to uncoupled bone remodeling in which the balance of osteoclast-driven bone resorption and osteoblast-driven bone deposition is lost. Breast cancer bone metastases often lead to osteolytic lesions due to hyperactive bone resorption. Release of growth factors from bone matrix during resorption then feeds a "vicious cycle" of bone destruction leading to many skeletal-related events. In addition to activity in bone, some of the factors released during bone resorption are also known to be involved in skeletal muscle regeneration and contraction. In this review, we discuss the mechanisms that lead to osteolytic breast cancer bone metastases and the potential for cancer-induced bone-muscle cross-talk leading to skeletal muscle weakness.

Indexed as

AnimalsBone NeoplasmsBreast NeoplasmsFemaleHumansMuscle WeaknessPrognosis

Identifiers

PMID24677373
PMCPMC4058425
OpenAlexW1981111508

What OpenQuestion holds

Textmetadata
LicenceTDM
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.