Evidence map›Paper›PMID 34885058›Full record

ReviewCancers2021

Genome Instability in Multiple Myeloma: Facts and Factors.

Anna Y Aksenova, Anna S Zhuk, Artem G Lada, Irina V Zotova, Elena I Stepchenkova, Ivan I Kostroma, Sergey V Gritsaev, Youri I Pavlov

Open access · goldAbstract readReview
In one paragraph

Review in Cancers, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
4.1field-weighted citation impact, top 5% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.

  1. Pooled it
  2. Review
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  6. Article
  7. Review
  8. The FGF/FGFR/c-Myc axis as a promising therapeutic target in multiple myeloma.Journal of experimental & clinical cancer research : CR · 2024
    Review
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  12. Article
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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 5 institutions in 2 countries.

Anna Y AksenovaLaboratory of Amyloid Biology, St. Petersburg State University, 199034 St. Petersburg, Russia.ORCID 0000-0002-1601-1615
Anna S ZhukInternational Laboratory "Computer Technologies", ITMO University, 197101 St. Petersburg, Russia.ORCID 0000-0001-8683-9533
Artem G LadaDepartment of Microbiology and Molecular Genetics, University of California, Davis, CA 95616, USA.
Irina V ZotovaDepartment of Genetics and Biotechnology, St. Petersburg State University, 199034 St. Petersburg, Russia.ORCID 0000-0001-6393-5645
Elena I StepchenkovaDepartment of Genetics and Biotechnology, St. Petersburg State University, 199034 St. Petersburg, Russia.ORCID 0000-0002-5854-8701
Ivan I KostromaRussian Research Institute of Hematology and Transfusiology, 191024 St. Petersburg, Russia.ORCID 0000-0003-3768-0831
Sergey V GritsaevRussian Research Institute of Hematology and Transfusiology, 191024 St. Petersburg, Russia.ORCID 0000-0001-7586-4709
Youri I PavlovEppley Institute for Research in Cancer, Fred and Pamela Buffett Cancer Center, University of Nebraska Medical Center, Omaha, NE 68198, USA.ORCID 0000-0003-1179-5796
St Petersburg University · RURussian Research Institute of Hematology and Transfusiology · RUITMO University · RUUniversity of California, Davis · USUniversity of Nebraska Medical Center · US

Funding

Russian Science Foundation 20-15-00081
6 · The paper itself

Abstract

Multiple myeloma (MM) is a malignant neoplasm of terminally differentiated immunoglobulin-producing B lymphocytes called plasma cells. MM is the second most common hematologic malignancy, and it poses a heavy economic and social burden because it remains incurable and confers a profound disability to patients. Despite current progress in MM treatment, the disease invariably recurs, even after the transplantation of autologous hematopoietic stem cells (ASCT). Biological processes leading to a pathological myeloma clone and the mechanisms of further evolution of the disease are far from complete understanding. Genetically, MM is a complex disease that demonstrates a high level of heterogeneity. Myeloma genomes carry numerous genetic changes, including structural genome variations and chromosomal gains and losses, and these changes occur in combinations with point mutations affecting various cellular pathways, including genome maintenance. MM genome instability in its extreme is manifested in mutation

Indexed as

chromothripsisDNA repairediting deaminasesgenome instabilitykataegismultiple myelomatranslocations

Identifiers

PMID34885058
PMCPMC8656811
OpenAlexW3217035673

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.