Evidence map›Paper›PMID 19948237›Full record

ReviewSeminars in cell & developmental biology2010

Tumor-stroma co-evolution in prostate cancer progression and metastasis.

Sajni Josson, Yasuhiro Matsuoka, Leland W K Chung, Haiyen E Zhau, Ruoxiang Wang

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Seminars in cell & developmental biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed
8.6field-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

72 citing papers in PubMed, 135 citations in OpenAlex.

  1. Article
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  7. Review
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  15. Prostate zones and cancer: lost in transition?Nature reviews. Urology · 2022
    Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Review

12 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

5 authors at 2 institutions in 1 country.

Sajni JossonUro-Oncology Research, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA, USA.
Yasuhiro Matsuoka
Leland W K Chung
Haiyen E Zhau
Ruoxiang Wang
Cedars-Sinai Medical Center · USEmory University · US

Funding

Prostate Cancer Bone Metastasis: Biology and TargetingP01CA098912 · NCI · EMORY UNIVERSITY · PI TIGHIOUART, MOURAD · 2003 to 2019
$24.0M
Beta 2-Microglobulin signaling and targeting in bone metastasisR01CA122602 · NCI · CEDARS-SINAI MEDICAL CENTER · PI CHUNG, LELAND W.K. · 2009 to 2013
$1.5M
NCI NIH HHS P01 CA098912NCI NIH HHS R01 CA122602
6 · The paper itself

Abstract

Cancer development is complex and involves several layers of interactions and pleotropic signaling mechanisms leading to progression. Cancer cells associate with resident stromal fibroblasts, smooth muscle cells, macrophages, endothelium, neurons and migrating cells at metastatic sites and phenotypically and genotypically activate them. These become an integral part of the cancer cell community through activated cell signaling mechanisms. During this process, the cancer cells and cells in the cancer microenvironment "co-evolve" in part due to oxidative stress, and acquire the ability to mimic other cell types (which can be termed osteomimicry, vasculomimicry, neuromimicry and stem cell mimicry), and undergo transition from epithelium to mesenchyme with definitive morphologic and behavioral modifications. In our laboratory, we demonstrated that prostate cancer cells co-evolve in their genotypic and phenotypic characters with stroma and acquire osteomimetic properties allowing them to proliferate and survive in the skeleton as bone metastasis. Several signaling interactions in the bone microenvironment, mediated by reactive oxygen species, soluble and membrane bound factors, such as superoxide, beta2-microglobulin and RANKL have been described. Targeting the signaling pathways in the cancer-associated stromal microenvironment in combination with known conventional therapeutic modalities could have a synergistic effect on cancer treatment. Since cancer cells are constantly interacting and acquiring adaptive and survival changes primarily directed by their microenvironment, it is imperative to delineate these interactions and co-target both cancer and stroma to improve the treatment and overall survival of cancer patients.

Indexed as

Stromal CellsBone NeoplasmsDisease ProgressionHumansMaleNeoplasm MetastasisOsteoblastsOsteoprotegerinOxidative StressProstatic NeoplasmsRANK LigandOsteoprotegerinRANK Ligand

Identifiers

PMID19948237
PMCPMC3388105
OpenAlexW2046701189

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.