Evidence map›Paper›PMID 28838991›Full record

ArticleHaematologica2017

SYK inhibition thwarts the BAFF - B-cell receptor crosstalk and thereby antagonizes Mcl-1 in chronic lymphocytic leukemia.

Cody Paiva, Taylor A Rowland, Bhargava Sreekantham, Claire Godbersen, Scott R Best, Prabhjot Kaur, Marc M Loriaux, Stephen E F Spurgeon, Olga V Danilova, Alexey V Danilov

Open access · goldAbstract read
In one paragraph

Article in Haematologica, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.2field-weighted citation impact, top 20% 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

24 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Aberrant B-Cell Activation in Systemic Lupus Erythematosus.Kidney diseases (Basel, Switzerland) · 2022
    Review
  12. Article
  13. Article
  14. Pharmacologic Targeting of Mcl-1 Induces Mitochondrial Dysfunction and Apoptosis in B-Cell Lymphoma Cells in aClinical cancer research : an official journal of the American Association for Cancer Research · 2021
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  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

10 authors at 3 institutions in 1 country.

Cody PaivaKnight Cancer Institute, Oregon Health and Science University, Portland, OR, USA.
Taylor A RowlandKnight Cancer Institute, Oregon Health and Science University, Portland, OR, USA.
Bhargava SreekanthamKnight Cancer Institute, Oregon Health and Science University, Portland, OR, USA.
Claire GodbersenGeisel School of Medicine at Dartmouth, Hanover, NH, USA.
Scott R BestKnight Cancer Institute, Oregon Health and Science University, Portland, OR, USA.
Prabhjot KaurGeisel School of Medicine at Dartmouth, Hanover, NH, USA.
Marc M LoriauxKnight Cancer Institute, Oregon Health and Science University, Portland, OR, USA.
Stephen E F SpurgeonKnight Cancer Institute, Oregon Health and Science University, Portland, OR, USA.
Olga V DanilovaPathology, Portland VA Medical Center, Portland, OR, USA.
Alexey V DanilovKnight Cancer Institute, Oregon Health and Science University, Portland, OR, USA danilov@ohsu.edu.
Oregon Health & Science University · USDartmouth College · USPortland VA Medical Center · US

Funding

Molecular and Cellular Biology at DartmouthT32GM008704 · NIGMS · DARTMOUTH COLLEGE · PI COMPTON, DUANE A. · 1998 to 2018
$6.8M
NIGMS NIH HHS T32 GM008704
6 · The paper itself

Abstract

Although small molecule inhibitors of B-cell receptor-associated kinases have revolutionized therapy in chronic lymphocytic leukemia (CLL), responses are incomplete. Pro-survival signaling emanating from the microenvironment may foster therapeutic resistance of the malignant B cells resident in the protective lymphoid niches. B-cell activating factor (BAFF) is critical to the survival of both healthy and neoplastic B cells. However, the pro-survival pathways triggered by BAFF have not been fully characterized. Here we show that BAFF elicited resistance to spontaneous and drug-induced apoptosis in stromal co-cultures, induced activation of both canonical and non-canonical NFκB signaling pathways, and triggered B-cell receptor signaling in CLL cells, independently of

Indexed as

Signal TransductionAnimalsB-Cell Activating FactorCell Line, TumorCell SurvivalCHO CellsCluster AnalysisCricetulusGene Expression ProfilingHumansImmunoglobulin Heavy ChainsImmunohistochemistryLeukemia, Lymphocytic, Chronic, B-CellModels, BiologicalMyeloid Cell Leukemia Sequence 1 ProteinNF-kappa BB-Cell Activating FactorImmunoglobulin Heavy ChainsMCL1 protein, humanMyeloid Cell Leukemia Sequence 1 ProteinNF-kappa BProto-Oncogene Proteins c-bcl-2Receptors, Antigen, B-CellSyk KinaseTNF Receptor-Associated Factor 2TNF Receptor-Associated Factor 3TNFSF13B protein, human

Identifiers

PMID28838991
PMCPMC5664393
OpenAlexW2746851788

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.