Evidence map›Paper›PMID 27343063›Full record

ReviewCalcified tissue international2017

Adipose, Bone, and Myeloma: Contributions from the Microenvironment.

Michelle M McDonald, Heather Fairfield, Carolyne Falank, Michaela R Reagan

Abstract readReview
In one paragraph

Review in Calcified tissue international, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
8.2field-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

29 citing papers in PubMed, 52 citations in OpenAlex.

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  19. New agents in the Treatment of Myeloma Bone Disease.Calcified tissue international · 2018
    Review
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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

4 authors at 3 institutions in 2 countries.

Michelle M McDonaldGarvan Institute of Medical Research, 384 Victoria Street, Sydney, NSW, 2010, Australia. m.mcdonald@garvan.org.au.
Heather FairfieldMaine Medical Center Research Institute, 81 Research Drive, Scarborough, ME, 04074, USA.
Carolyne FalankMaine Medical Center Research Institute, 81 Research Drive, Scarborough, ME, 04074, USA.
Michaela R ReaganMaine Medical Center Research Institute, 81 Research Drive, Scarborough, ME, 04074, USA. Mreagan@mmc.org.ORCID 0000-0003-2884-6481
Maine Medical Center · USGarvan Institute of Medical Research · AUTufts University · US

Funding

Interdisciplinary Study of Marrow Adiposity, Mineral Metabolism & Energy BalanceR24DK092759 · NIDDK · MAINEHEALTH · PI HOROWITZ, MARK C, MACDOUGALD, ORMOND A · 2011 to 2019
$13.0M
Progenitor Cell Analysis CoreP30GM106391 · NIGMS · MAINEHEALTH · PI FRIESEL, ROBERT E · 2013 to 2017
$5.7M
NIDDK NIH HHS R24 DK092759NIGMS NIH HHS P30 GM106391
6 · The paper itself

Abstract

Researchers globally are working towards finding a cure for multiple myeloma (MM), a destructive blood cancer diagnosed yearly in ~750,000 people worldwide (Podar et al. in Expert Opin Emerg Drugs 14:99-127, 2009). Although MM targets multiple organ systems, it is the devastating skeletal destruction experienced by over 90 % of patients that often most severely impacts patient morbidity, pain, and quality of life. Preventing bone disease is therefore a priority in MM treatment, and understanding how and why myeloma cells target the bone marrow (BM) is fundamental to this process. This review focuses on a key area of MM research: the contributions of the bone microenvironment to disease origins, progression, and drug resistance. We describe some of the key cell types in the BM niche: osteoclasts, osteoblasts, osteocytes, adipocytes, and mesenchymal stem cells. We then focus on how these key cellular players are, or could be, regulating a range of disease-related processes spanning MM growth, drug resistance, and bone disease (including osteolysis, fracture, and hypercalcemia). We summarize the literature regarding MM-bone cell and MM-adipocyte relationships and subsequent phenotypic changes or adaptations in MM cells, with the aim of providing a deeper understanding of how myeloma cells grow in the skeleton to cause bone destruction. We identify avenues and therapies that intervene in these networks to stop tumor growth and/or induce bone regeneration. Overall, we aim to illustrate how novel therapeutic target molecules, proteins, and cellular mediators may offer new avenues to attack this disease while reviewing currently utilized therapies.

Indexed as

Tumor MicroenvironmentAdipocytesBone and BonesBone MarrowHumansMultiple MyelomaAdipocyteBMATBone marrowBone marrow adiposeBone microenvironmentMGUSMultiple myeloma (MM)

Identifiers

PMID27343063
PMCPMC5396178
OpenAlexW2475153636

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.