Evidence map›Paper›PMID 27983725›Full record

ArticleBlood cancer journal2016

A gene expression inflammatory signature specifically predicts multiple myeloma evolution and patients survival.

C Botta, M T Di Martino, D Ciliberto, M Cucè, P Correale, M Rossi, P Tagliaferri, P Tassone

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Blood cancer journal, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 2 pooled it
3.2field-weighted citation impact, top 8% 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

42 citing papers in PubMed, 2 syntheses or guidelines pooled it, 49 citations in OpenAlex.

  1. Pooled it
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  4. Efficacy of targeted chemokine receptor 4 PET/CT in evaluating active lesions in multiple myeloma, comparison toCancer imaging : the official publication of the International Cancer Imaging Society · 2026
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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

8 authors at 2 institutions in 1 country.

C BottaDepartment of Experimental and Clinical Medicine, Magna Graecia University, Catanzaro, Italy.
M T Di MartinoDepartment of Experimental and Clinical Medicine, Magna Graecia University, Catanzaro, Italy.
D CilibertoDepartment of Experimental and Clinical Medicine, Magna Graecia University, Catanzaro, Italy.
M CucèDepartment of Experimental and Clinical Medicine, Magna Graecia University, Catanzaro, Italy.
P CorrealeDepartment of Oncology, Siena University, Siena, Italy.
M RossiDepartment of Experimental and Clinical Medicine, Magna Graecia University, Catanzaro, Italy.
P TagliaferriDepartment of Experimental and Clinical Medicine, Magna Graecia University, Catanzaro, Italy.
P TassoneDepartment of Experimental and Clinical Medicine, Magna Graecia University, Catanzaro, Italy.
Magna Graecia University · ITUniversity of Siena · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multiple myeloma (MM) is closely dependent on cross-talk between malignant plasma cells and cellular components of the inflammatory/immunosuppressive bone marrow milieu, which promotes disease progression, drug resistance, neo-angiogenesis, bone destruction and immune-impairment. We investigated the relevance of inflammatory genes in predicting disease evolution and patient survival. A bioinformatics study by Ingenuity Pathway Analysis on gene expression profiling dataset of monoclonal gammopathy of undetermined significance, smoldering and symptomatic-MM, identified inflammatory and cytokine/chemokine pathways as the most progressively affected during disease evolution. We then selected 20 candidate genes involved in B-cell inflammation and we investigated their role in predicting clinical outcome, through univariate and multivariate analyses (log-rank test, logistic regression and Cox-regression model). We defined an 8-genes signature (IL8, IL10, IL17A, CCL3, CCL5, VEGFA, EBI3 and NOS2) identifying each condition (MGUS/smoldering/symptomatic-MM) with 84% accuracy. Moreover, six genes (IFNG, IL2, LTA, CCL2, VEGFA, CCL3) were found independently correlated with patients' survival. Patients whose MM cells expressed high levels of Th1 cytokines (IFNG/LTA/IL2/CCL2) and low levels of CCL3 and VEGFA, experienced the longest survival. On these six genes, we built a prognostic risk score that was validated in three additional independent datasets. In this study, we provide proof-of-concept that inflammation has a critical role in MM patient progression and survival. The inflammatory-gene prognostic signature validated in different datasets clearly indicates novel opportunities for personalized anti-MM treatment.

Indexed as

AdultAgedAged, 80 and overComputational BiologyDisease ProgressionFemaleGene Expression Regulation, NeoplasticHumansInflammationMaleMiddle AgedMultiple MyelomaNeoplasm ProteinsSignal TransductionTranscriptomeNeoplasm Proteins

Identifiers

PMID27983725
PMCPMC5223153
OpenAlexW2563021883

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.