Evidence map›Paper›PMID 27285986›Full record

ArticleOncotarget2016

Clonal evolution in relapsed and refractory diffuse large B-cell lymphoma is characterized by high dynamics of subclones.

Thomas Melchardt, Clemens Hufnagl, David M Weinstock, Nadja Kopp, Daniel Neureiter, Wolfgang Tränkenschuh, Hubert Hackl, Lukas Weiss, Gabriel Rinnerthaler, Tanja N Hartmann and 3 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
3.9field-weighted citation impact, top 7% 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

32 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. Article
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

13 authors at 4 institutions in 3 countries.

Thomas MelchardtThird Medical Department at The Paracelsus Medical University Salzburg, Salzburg, Austria.
Clemens HufnaglThird Medical Department at The Paracelsus Medical University Salzburg, Salzburg, Austria.
David M WeinstockDepartment of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA.
Nadja KoppDepartment of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA.
Daniel NeureiterInstitute of Pathology, Paracelsus Medical University Salzburg, Salzburg, Austria.
Wolfgang TränkenschuhInstitute of Pathology, Paracelsus Medical University Salzburg, Salzburg, Austria.
Hubert HacklDivision of Bioinformatics, Biocenter, Medical University of Innsbruck, Innsbruck, Austria.
Lukas WeissThird Medical Department at The Paracelsus Medical University Salzburg, Salzburg, Austria.
Gabriel RinnerthalerThird Medical Department at The Paracelsus Medical University Salzburg, Salzburg, Austria.
Tanja N HartmannThird Medical Department at The Paracelsus Medical University Salzburg, Salzburg, Austria.
Richard GreilThird Medical Department at The Paracelsus Medical University Salzburg, Salzburg, Austria.
Oliver WeigertUniversity Hospital of The Ludwig-Maximilians-University Munich, Medical Department III, Laboratory for Experimental Leukemia and Lymphoma Research (ELLF), Munich, Germany.
Alexander EgleThird Medical Department at The Paracelsus Medical University Salzburg, Salzburg, Austria.
Paracelsus Medical University · ATDana-Farber Cancer Institute · USLudwig-Maximilians-Universität München · DEUniversität Innsbruck · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Little information is available about the role of certain mutations for clonal evolution and the clinical outcome during relapse in diffuse large B-cell lymphoma (DLBCL). Therefore, we analyzed formalin-fixed-paraffin-embedded tumor samples from first diagnosis, relapsed or refractory disease from 28 patients using next-generation sequencing of the exons of 104 coding genes. Non-synonymous mutations were present in 74 of the 104 genes tested. Primary tumor samples showed a median of 8 non-synonymous mutations (range: 0-24) with the used gene set. Lower numbers of non-synonymous mutations in the primary tumor were associated with a better median OS compared with higher numbers (28 versus 15 months, p=0.031). We observed three patterns of clonal evolution during relapse of disease: large global change, subclonal selection and no or minimal change possibly suggesting preprogrammed resistance. We conclude that targeted re-sequencing is a feasible and informative approach to characterize the molecular pattern of relapse and it creates novel insights into the role of dynamics of individual genes.

Indexed as

Mutation RateAdultAgedAged, 80 and overClonal EvolutionFemaleHigh-Throughput Nucleotide SequencingHumansLymphoma, Large B-Cell, DiffuseMaleMiddle AgedMutationNeoplasm Recurrence, LocalTreatment FailureYoung Adultclonal evolutionDLBCLsubclonal selectionTP53tumor heterogeneity

Identifiers

PMID27285986
PMCPMC5239491
OpenAlexW2414958612

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.