ReviewMedical oncology (Northwood, London, England)2006
Bone disease in multiple myeloma.
Review in Medical oncology (Northwood, London, England), 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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.
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.
Who cites it
2 citing papers in PubMed, 18 citations in OpenAlex.
- Preventing osteolytic lesions and osteomyelitis in multiple myeloma.Journal of bone oncology · 2022Review
- BCL-B (BCL2L10) is overexpressed in patients suffering from multiple myeloma (MM) and drives an MM-like disease in transgenic mice.The Journal of experimental medicine · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A new understanding of the regulation of bone resorption developed with the discovery of receptor activator of nuclear factor-kappaB, receptor activator of nuclear factor-kappaB ligand, and osteoprotegerin in 1997-1998. The RANK signaling system is abnormally regulated in multiple myeloma, and this favors increased osteoclast function, which early in the disease is compensated by increased osteoblast function. Later in the disease osteoblast activity decreases, resulting in osteolytic lesions. We review the factors implicated in osteoclast and osteoblast function. Among these are receptor activator of nuclear factor-kappaB, receptor activator of nuclear factor-kappaB ligand, osteoprotegerin, hepatocyte growth factor, macrophage inflammatory protein-1alpha, bone morphogenetic proteins, and the Wnt system. Bisphosphonates are the only drugs used in routine clinical management; however, the complex regulation system of bone homeostasis offers a number of of possible targets for therapy, which are discussed.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.