Evidence map›Paper›PMID 26343726›Full record

ReviewCancers2015

The Role of Hedgehog Signaling in Tumor Induced Bone Disease.

Shellese A Cannonier, Julie A Sterling

Open access · goldAbstract readReview
In one paragraph

Review in Cancers, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

14 citing papers in PubMed, 25 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. The Biological Function of MicroRNAs in Bone Tumors.International journal of molecular sciences · 2022
    Review
  7. Cholesterol and Hedgehog Signaling: Mutual Regulation and Beyond.Frontiers in cell and developmental biology · 2022
    Review
  8. Review
  9. Article
  10. Systemic delivery of a Gli inhibitor via polymeric nanocarriers inhibits tumor-induced bone disease.Journal of controlled release : official journal of the Controlled Release Society · 2019
    Article
  11. Review
  12. Article
  13. Article
  14. Osteoblasts Are the Centerpiece of the Metastatic Bone Microenvironment.Endocrinology and metabolism (Seoul, Korea) · 2016
    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.

Shellese A CannonierDepartment of Veterans Affairs, Tennessee Valley Healthcare System, Nashville, TN 37235, USA. shellese.a.cannonier@vanderbilt.edu.
Julie A SterlingDepartment of Veterans Affairs, Tennessee Valley Healthcare System, Nashville, TN 37235, USA. Julie.sterling@vanderbilt.edu.
VA Tennessee Valley Healthcare System · US

Funding

Vanderbilt/Meharry Initiative for Minority Student DvptR25GM062459 · NIGMS · VANDERBILT UNIVERSITY · PI VELEZ EDWARDS, DIGNA R · 2002 to 2020
$10.4M
The Role of Mechanotransduction in Progression of Tumor-induced Bone DiseaseR01CA163499 · NCI · VANDERBILT UNIVERSITY · PI GUELCHER, SCOTT A, RHOADES (STERLING), JULIE A · 2012 to 2016
$1.5M
Targeting the Bone Microenvironment to Reduce Tumor-induced Bone DiseaseI01BX001957 · VA · VETERANS HEALTH ADMINISTRATION · PI RHOADES (STERLING), JULIE A · 2013 to 2025
–
BLRD VA I01 BX001957NCI NIH HHS R01 CA163499NIGMS NIH HHS R25 GM062459
6 · The paper itself

Abstract

Despite significant progress in cancer treatments, tumor induced bone disease continues to cause significant morbidities. While tumors show distinct mutations and clinical characteristics, they behave similarly once they establish in bone. Tumors can metastasize to bone from distant sites (breast, prostate, lung), directly invade into bone (head and neck) or originate from the bone (melanoma, chondrosarcoma) where they cause pain, fractures, hypercalcemia, and ultimately, poor prognoses and outcomes. Tumors in bone secrete factors (interleukins and parathyroid hormone-related protein) that induce RANKL expression from osteoblasts, causing an increase in osteoclast mediated bone resorption. While the mechanisms involved varies slightly between tumor types, many tumors display an increase in Hedgehog signaling components that lead to increased tumor growth, therapy failure, and metastasis. The work of multiple laboratories has detailed Hh signaling in several tumor types and revealed that tumor establishment in bone can be controlled by both canonical and non-canonical Hh signaling in a cell type specific manner. This review will explore the role of Hh signaling in the modulation of tumor induced bone disease, and will shed insight into possible therapeutic interventions for blocking Hh signaling in these tumors.

Indexed as

bonecancerGliHedgehog signalingmetastasis

Identifiers

PMID26343726
PMCPMC4586789
OpenAlexW1628412869

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.