Evidence map›Paper›PMID 24140083›Full record

ReviewPharmacology & therapeutics2014

Targeting tumor-stromal interactions in bone metastasis.

Mark Esposito, Yibin Kang

Open access · greenAbstract readReview
In one paragraph

Review in Pharmacology & therapeutics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
83citing papers in PubMed, 1 pooled it
7.1field-weighted citation impact, top 2% 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

83 citing papers in PubMed, 1 synthesis or guideline pooled it, 128 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Review
  5. Review
  6. Review
  7. Sema3A Affect Osteolytic Bone Metastasis of Non-small Cell Lung Cancer.Recent patents on anti-cancer drug discovery · 2025
    Article
  8. Review
  9. Review
  10. Review
  11. Heterogeneity and prognosis of single organ metastases in gastric cancer.Translational gastroenterology and hepatology · 2024
    Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Article
  20. Article

23 more citing papers are in PubMed but not listed here.

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.

Mark EspositoDepartment of Molecular Biology, Princeton University, Princeton, NJ 08544, United States.
Yibin KangDepartment of Molecular Biology, Princeton University, Princeton, NJ 08544, United States. Electronic address: ykang@princeton.edu.
Princeton University · US

Funding

PREDOCTORAL TRAINING PROGRAM IN GENETICST32GM007388 · NIGMS · PRINCETON UNIVERSITY · PI CRISTEA, ILEANA M. · 1985 to 2022
$27.4M
Metadherin in Metastasis and Chemoresistance of Breast CancerR01CA134519 · NCI · PRINCETON UNIVERSITY · PI KANG, YIBIN · 2008 to 2012
$1.6M
The Role of miRNAs in Epithelial-Mesenchymal Transition and MetastasisR01CA141062 · NCI · PRINCETON UNIVERSITY · PI KANG, YIBIN · 2010 to 2014
$1.6M
NCI NIH HHS R01 CA134519NCI NIH HHS R01 CA141062NIGMS NIH HHS T32 GM007388
6 · The paper itself

Abstract

Bone metastasis is a frequent occurrence in late stage solid tumors, including breast cancers, prostate or lung. However, the causes for this proclivity have only recently been elucidated. Significant progress has been made in the past decade toward understanding the molecular underpinnings of bone metastasis, and much of this research reveals a crucial role of the host stroma in each step of the metastatic cascade. Tumor-stromal interactions are crucial in engineering a pre-metastatic niche, accommodating metastatic seeding, and establishing the vicious cycle of bone metastasis. Current treatments in bone metastasis focus on latter steps of the metastatic cascade, with most treatments targeting the process of bone remodeling; however, emerging research identifies many other candidates as promising targets. Host stromal cells including platelets and endothelial cells are important in the early steps of metastatic homing, attachment and extravasation while a variety of immune cells, parenchymal cells and mesenchymal cells of the bone marrow are important in the establishment of overt, immune-suppressed metastatic lesions. Many participants during these steps have been identified and functionally validated. Significant contributors include integrins, (αvβ3, α2β1, α4β1), TGFβ family members, bone resident proteins (BSP, OPG, SPARC, OPN), RANKL, and PTHrP. In this review, we will discuss the contribution of host stromal cells to pre-metastatic niche conditioning, seeding, dormancy, bone-remodeling, immune regulation, and chemotherapeutic shielding in bone metastasis. Research exploring these interactions between bone metastases and stromal cells has yielded many therapeutic targets, and we will discuss both the current and future therapeutic avenues in treating bone metastasis.

Indexed as

AnimalsBone NeoplasmsBone RemodelingHumansNeoplasmsStromal CellsBone metastasiscirculating tumor cellCTCDCdendritic celldisseminated tumor cellDTChematopoietic stem cellHSCImmune surveillancemesenchymal stem cellMetastatic nicheMSCnatural killerNKOsteoclast inhibitorsregulatory T cellT(reg)Tumor dormancyTumor–stromal interactions

Identifiers

PMID24140083
PMCPMC3947254
OpenAlexW2088518437

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.