Evidence map›Paper›PMID 27563822›Full record

ReviewOncotarget2016

The BCR-ABL/NF-κB signal transduction network: a long lasting relationship in Philadelphia positive Leukemias.

Giovanna Carrà, Davide Torti, Sabrina Crivellaro, Cristina Panuzzo, Riccardo Taulli, Daniela Cilloni, Angelo Guerrasio, Giuseppe Saglio, Alessandro Morotti

Open access · diamondAbstract readReview
In one paragraph

Review in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.0field-weighted citation impact, top 12% 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, 32 citations in OpenAlex.

  1. Review
  2. Article
  3. Low Renalase Levels in Newly Diagnosed CML: Dysregulation Sensitive to Modulation by Tyrosine Kinase Inhibitors.Pathophysiology : the official journal of the International Society for Pathophysiology · 2024
    Article
  4. Adaptor protein Abelson interactor 1 in homeostasis and disease.Cell communication and signaling : CCS · 2024
    Review
  5. Review
  6. Article
  7. Article
  8. The Involvement of Canonical NFκB Pathway in Megakaryocyte Differentiation Induction by Nanocurcumin.International journal of hematology-oncology and stem cell research · 2023
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Strategies For Targeting Chronic Myeloid Leukaemia Stem Cells.Blood and lymphatic cancer : targets and therapy · 2019
    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

9 authors at 1 institution in 1 country.

Giovanna CarràDepartment of Clinical and Biological Sciences, University of Turin, Orbassano, Italy.
Davide TortiDepartment of Clinical and Biological Sciences, University of Turin, Orbassano, Italy.
Sabrina CrivellaroDepartment of Clinical and Biological Sciences, University of Turin, Orbassano, Italy.
Cristina PanuzzoDepartment of Clinical and Biological Sciences, University of Turin, Orbassano, Italy.
Riccardo TaulliDepartment of Oncology, University of Turin, Orbassano, Italy.
Daniela CilloniDepartment of Clinical and Biological Sciences, University of Turin, Orbassano, Italy.
Angelo GuerrasioDepartment of Clinical and Biological Sciences, University of Turin, Orbassano, Italy.
Giuseppe SaglioDepartment of Clinical and Biological Sciences, University of Turin, Orbassano, Italy.
Alessandro MorottiDepartment of Clinical and Biological Sciences, University of Turin, Orbassano, Italy.
University of Turin · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The Nuclear Factor-kappa B (NF-κB) family of transcription factors plays a key role in cancer pathogenesis due to the ability to promote cellular proliferation and survival, to induce resistance to chemotherapy and to mediate invasion and metastasis. NF-κB is recruited through different mechanisms involving either canonical (RelA/p50) or non-canonical pathways (RelB/p50 or RelB/p52), which transduce the signals originated from growth-factors, cytokines, oncogenic stress and DNA damage, bacterial and viral products or other stimuli. The pharmacological inhibition of the NF-κB pathway has clearly been associated with significant clinical activity in different cancers. Almost 20 years ago, NF-κB was described as an essential modulator of BCR-ABL signaling in Chronic Myeloid Leukemia and Philadelphia-positive Acute Lymphoblastic Leukemia. This review summarizes the role of NF-κB in BCR-ABL-mediated leukemogenesis and provides new insights on the long lasting BCR-ABL/NF-κB connection.

Indexed as

ApoptosisCell ProliferationFusion Proteins, bcr-ablHumansLeukemia, Myelogenous, Chronic, BCR-ABL PositiveNF-kappa BPrecursor Cell Lymphoblastic Leukemia-LymphomaSignal TransductionFusion Proteins, bcr-ablNF-kappa BBCR-ABLCMLIκB-αNFKBIANF-κB

Identifiers

PMID27563822
PMCPMC5323234
OpenAlexW2514921286

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.