Evidence map›Paper›PMID 29967592›Full record

ReviewFrontiers in endocrinology2018

Androgen Receptor-CaMKK2 Axis in Prostate Cancer and Bone Microenvironment.

Ushashi C Dadwal, Eric S Chang, Uma Sankar

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in endocrinology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

19 citing papers in PubMed, 29 citations in OpenAlex.

  1. Review
  2. Article
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  5. Review
  6. Article
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  9. Article
  10. Roles of calcium signaling in cancer metastasis to bone.Exploration of targeted anti-tumor therapy · 2022
    Review
  11. CaMKK2 Promotes the Progression of Ovarian Carcinoma through the PI3K/PDK1/Akt Axis.Computational and mathematical methods in medicine · 2022
    Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Prostate Cancer Energetics and Biosynthesis.Advances in experimental medicine and biology · 2019
    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

3 authors at 2 institutions in 1 country.

Ushashi C DadwalDepartment of Anatomy and Cell Biology, Indiana University School of Medicine, Indianapolis, IN, United States.
Eric S ChangDepartment of Anatomy and Cell Biology, Indiana University School of Medicine, Indianapolis, IN, United States.
Uma SankarDepartment of Anatomy and Cell Biology, Indiana University School of Medicine, Indianapolis, IN, United States.
Indiana University School of MedicineIndiana University – Purdue University Indianapolis · US

Funding

CaMKK2 Inhibition as a Dual-Action Bone Anabolic and Anti-Catabolic Therapy in OsteoporosisR01AR068332 · NIAMS · INDIANA UNIVERSITY INDIANAPOLIS · PI SANKAR, UMA · 2015 to 2019
$2.1M
NIAMS NIH HHS R01 AR068332
6 · The paper itself

Abstract

The skeletal system is of paramount importance in advanced stage prostate cancer (PCa) as it is the preferred site of metastasis. Complex mechanisms are employed sequentially by PCa cells to home to and colonize the bone. Bone-resident PCa cells then recruit osteoblasts (OBs), osteoclasts (OCs), and macrophages within the niche into entities that promote cancer cell growth and survival. Since PCa is heavily reliant on androgens for growth and survival, androgen-deprivation therapy (ADT) is the standard of care for advanced disease. Although it significantly improves survival rates, ADT detrimentally affects bone health and significantly increases the risk of fractures. Moreover, whereas the majority patients with advanced PCa respond favorably to androgen deprivation, most experience a relapse of the disease to a hormone-refractory form within 1-2 years of ADT. The tumor adapts to surviving under low testosterone conditions by selecting for mutations in the androgen receptor (AR) that constitutively activate it. Thus, AR signaling remains active in PCa cells and aids in its survival under low levels of circulating androgens and additionally allows the cancer cells to manipulate the bone microenvironment to fuel its growth. Hence, AR and its downstream effectors are attractive targets for therapeutic interventions against PCa. Ca

Indexed as

androgen-deprivation therapybone–tumor microenvironmentCAMKK2castrate-resistant prostate cancertreatment induced bone loss

Identifiers

PMID29967592
PMCPMC6015873
OpenAlexW2805358657

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.