Evidence map›Paper›PMID 26579543›Full record

ReviewBioMed research international2015

Mechanisms and Clinical Applications of Genome Instability in Multiple Myeloma.

Antonia Cagnetta, Davide Lovera, Raffaella Grasso, Nicoletta Colombo, Letizia Canepa, Filippo Ballerini, Marino Calvio, Maurizio Miglino, Marco Gobbi, Roberto Lemoli and 1 more

Open access · hybridAbstract readReview
In one paragraph

Review in BioMed research international, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.4field-weighted citation impact, top 35% 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

9 citing papers in PubMed, 14 citations in OpenAlex.

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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

11 authors at 2 institutions in 1 country.

Antonia CagnettaHematology Unit, Department of Internal Medicine (DiMI), University of Genoa, IRCCS AOU San Martino-IST, 1600 Genoa, Italy.
Davide LoveraHematology Unit, Department of Internal Medicine (DiMI), University of Genoa, IRCCS AOU San Martino-IST, 1600 Genoa, Italy.
Raffaella GrassoHematology Unit, Department of Internal Medicine (DiMI), University of Genoa, IRCCS AOU San Martino-IST, 1600 Genoa, Italy.
Nicoletta ColomboHematology Unit, Department of Internal Medicine (DiMI), University of Genoa, IRCCS AOU San Martino-IST, 1600 Genoa, Italy.
Letizia CanepaHematology Unit, Department of Internal Medicine (DiMI), University of Genoa, IRCCS AOU San Martino-IST, 1600 Genoa, Italy.
Filippo BalleriniHematology Unit, Department of Internal Medicine (DiMI), University of Genoa, IRCCS AOU San Martino-IST, 1600 Genoa, Italy.
Marino CalvioHematology Unit, Department of Internal Medicine (DiMI), University of Genoa, IRCCS AOU San Martino-IST, 1600 Genoa, Italy.
Maurizio MiglinoHematology Unit, Department of Internal Medicine (DiMI), University of Genoa, IRCCS AOU San Martino-IST, 1600 Genoa, Italy.
Marco GobbiHematology Unit, Department of Internal Medicine (DiMI), University of Genoa, IRCCS AOU San Martino-IST, 1600 Genoa, Italy.
Roberto LemoliHematology Unit, Department of Internal Medicine (DiMI), University of Genoa, IRCCS AOU San Martino-IST, 1600 Genoa, Italy.
Michele CeaHematology Unit, Department of Internal Medicine (DiMI), University of Genoa, IRCCS AOU San Martino-IST, 1600 Genoa, Italy.
University of Genoa · ITOspedale Policlinico San Martino · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ongoing genomic instability represents a hallmark of multiple myeloma (MM) cells, which manifests largely as whole chromosome- or translocation-based aneuploidy. Importantly, although it supports tumorigenesis, progression and, response to treatment in MM patients, it remains one of the least understood components of malignant transformation in terms of molecular basis. Therefore these aspects make the comprehension of genomic instability a pioneering strategy for novel therapeutic and clinical speculations to use in the management of MM patients. Here we will review mechanisms mediating genomic instability in MM cells with an emphasis placed on pathogenic mutations affecting DNA recombination, replication and repair, telomere function and mitotic regulation of spindle attachment, centrosome function, and chromosomal segregation. We will discuss the mechanisms by which genetic aberrations give rise to multiple pathogenic events required for myelomagenesis and conclude with a discussion of the clinical applications of these findings in MM patients.

Indexed as

AnimalsDNA DamageDNA, NeoplasmGene Expression Regulation, NeoplasticGenes, NeoplasmGenome, HumanGenomic InstabilityHumansModels, GeneticMultiple MyelomaMutationDNA, Neoplasm

Identifiers

PMID26579543
PMCPMC4633548
OpenAlexW1787495625

What OpenQuestion holds

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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.