Evidence map›Paper›PMID 26046463›Full record

Trial reportOncotarget2015

Whole-exome sequencing of primary plasma cell leukemia discloses heterogeneous mutational patterns.

Ingrid Cifola, Marta Lionetti, Eva Pinatel, Katia Todoerti, Eleonora Mangano, Alessandro Pietrelli, Sonia Fabris, Laura Mosca, Vittorio Simeon, Maria Teresa Petrucci and 10 more

Open access · diamondAbstract readClinical Trial, Phase IIMulticenter Study
In one paragraph

Trial report in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
5.3field-weighted citation impact, top 4% 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

41 citing papers in PubMed, 63 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Identification of High-Risk Multiple Myeloma With a Plasma Cell Leukemia-Like Transcriptomic Profile.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2022
    Article
  8. [Update on biology of primary plasma cell leukemia].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2022
    Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. Review
  16. Article
  17. Review
  18. Article
  19. Molecular basis of clonal evolution in multiple myeloma.International journal of hematology · 2020
    Review
  20. 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

20 authors at 12 institutions in 1 country.

Ingrid CifolaInstitute for Biomedical Technologies, National Research Council, Milan, Italy.
Marta LionettiDepartment of Clinical Sciences and Community Health, University of Milan, Milan, Italy.
Eva PinatelInstitute for Biomedical Technologies, National Research Council, Milan, Italy.
Katia TodoertiLaboratory of Pre-Clinical and Translational Research, IRCCS-CROB, Referral Cancer Center of Basilicata, Rionero in Vulture (PZ), Italy.
Eleonora ManganoInstitute for Biomedical Technologies, National Research Council, Milan, Italy.
Alessandro PietrelliInstitute for Biomedical Technologies, National Research Council, Milan, Italy.
Sonia FabrisDepartment of Clinical Sciences and Community Health, University of Milan, Milan, Italy.
Laura MoscaDepartment of Clinical Sciences and Community Health, University of Milan, Milan, Italy.
Vittorio SimeonLaboratory of Pre-Clinical and Translational Research, IRCCS-CROB, Referral Cancer Center of Basilicata, Rionero in Vulture (PZ), Italy.
Maria Teresa PetrucciHematology, Department of Cellular Biotechnologies and Hematology, La Sapienza University, Rome, Italy.
Fortunato MorabitoHematology Unit, Azienda Ospedaliera di Cosenza, Cosenza, Italy.
Massimo OffidaniHematologic Clinic, Azienda Ospedaliero-Universitaria Ospedali Riuniti di Ancona, Ancona, Italy.
Francesco Di RaimondoDepartment of Biomedical Sciences, Division of Hematology, Ospedale Ferrarotto, University of Catania, Catania, Italy.
Antonietta FalconeHematology Unit, IRCCS "Casa Sollievo della Sofferenza" Hospital, San Giovanni Rotondo, Italy.
Tommaso CaravitaDepartment of Hematology, Ospedale S. Eugenio, Tor Vergata University, Rome, Italy.
Cristina BattagliaInstitute for Biomedical Technologies, National Research Council, Milan, Italy.
Gianluca De BellisInstitute for Biomedical Technologies, National Research Council, Milan, Italy.
Antonio PalumboDivision of Hematology, University of Torino, A.O.U. San Giovanni Battista, Torino, Italy.
Pellegrino MustoScientific Direction, IRCCS-CROB, Referral Cancer Center of Basilicata, Rionero in Vulture (PZ), Italy.
Antonino NeriDepartment of Clinical Sciences and Community Health, University of Milan, Milan, Italy.
National Research Council · ITUniversity of Milan · ITFondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico · ITIstituti di Ricovero e Cura a Carattere Scientifico · ITAzienda Ospedaliera di Cosenza · ITAzienda Ospedaliero Universitaria San Giovanni Battista · ITCasa Sollievo della Sofferenza · ITCentro di Riferimento Oncologico della Basilicata · ITOspedali Riuniti di Ancona · ITSapienza University of Rome · ITSt. Eugenio Hospital · ITUniversity of Catania · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Primary plasma cell leukemia (pPCL) is a rare and aggressive form of plasma cell dyscrasia and may represent a valid model for high-risk multiple myeloma (MM). To provide novel information concerning the mutational profile of this disease, we performed the whole-exome sequencing of a prospective series of 12 pPCL cases included in a Phase II multicenter clinical trial and previously characterized at clinical and molecular levels. We identified 1, 928 coding somatic non-silent variants on 1, 643 genes, with a mean of 166 variants per sample, and only few variants and genes recurrent in two or more samples. An excess of C > T transitions and the presence of two main mutational signatures (related to APOBEC over-activity and aging) occurring in different translocation groups were observed. We identified 14 candidate cancer driver genes, mainly involved in cell-matrix adhesion, cell cycle, genome stability, RNA metabolism and protein folding. Furthermore, integration of mutation data with copy number alteration profiles evidenced biallelically disrupted genes with potential tumor suppressor functions. Globally, cadherin/Wnt signaling, extracellular matrix and cell cycle checkpoint resulted the most affected functional pathways. Sequencing results were finally combined with gene expression data to better elucidate the biological relevance of mutated genes. This study represents the first whole-exome sequencing screen of pPCL and evidenced a remarkable genetic heterogeneity of mutational patterns. This may provide a contribution to the comprehension of the pathogenetic mechanisms associated with this aggressive form of PC dyscrasia and potentially with high-risk MM.

Indexed as

ExomeCluster AnalysisDNA Mutational AnalysisHumansLeukemia, Plasma Cellmultiple myelomamutationsplasma cell leukemiawhole-exome sequencing

Identifiers

PMID26046463
PMCPMC4627327
OpenAlexW1549044564

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Registered trials

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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.