Evidence map›Paper›PMID 27135981›Full record

ReviewCurrent opinion in hematology2016

Oncogenic Notch signaling in T-cell and B-cell lymphoproliferative disorders.

Mark Y Chiang, Vedran Radojcic, Ivan Maillard

Open access · greenAbstract readReview
In one paragraph

Review in Current opinion in hematology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
2.3field-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

35 citing papers in PubMed, 45 citations in OpenAlex.

  1. Review
  2. Review
  3. Notch Inhibitors and BH3 Mimetics in T-Cell Acute Lymphoblastic Leukemia.International journal of molecular sciences · 2024
    Review
  4. Article
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  11. The influence ofHGG advances · 2023
    Article
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  15. miRNAs in Lymphocytic Leukaemias-The miRror of Drug Resistance.International journal of molecular sciences · 2022
    Review
  16. Review
  17. Review
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  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

3 authors at 1 institution in 1 country.

Mark Y ChiangaDepartment of Internal Medicine, Division of Hematology-Oncology bLife Sciences Institute cDepartment of Cell and Developmental Biology, University of Michigan, Ann Arbor, Michigan, USA.
Vedran Radojcic
Ivan Maillard
University of Michigan–Ann Arbor · US

Funding

Notch Signaling in AlloimmunityR01AI091627 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI PEAR, WARREN S · 2011 to 2025
$6.0M
Direct coregulation of Notch1 by Zmiz1 in T-cell leukemiaR01CA196604 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CHIANG, MARK Y · 2015 to 2019
$1.8M
NCI NIH HHS R01 CA196604NIAID NIH HHS R01 AI091627
6 · The paper itself

Abstract

purpose of reviewThis article highlights recent discoveries about Notch activation and its oncogenic functions in lymphoid malignancies, and discusses the therapeutic potential of Notch inhibition. RECENT

findingsNOTCH mutations arise in a broad spectrum of lymphoid malignancies and are increasingly scrutinized as putative therapeutic targets. In T-cell acute lymphoblastic leukemia (T-ALL), NOTCH1 mutations affect the extracellular negative regulatory region and lead to constitutive Notch activation, although mutated receptors remain sensitive to Notch ligands. Other NOTCH1 mutations in T-ALL and NOTCH1/2 mutations in multiple B-cell malignancies truncate the C-terminal proline (P), glutamic acid (E), serine (S), threonine (T)-rich (PEST) domain, leading to decreased Notch degradation after ligand-mediated activation. Thus, targeting Notch ligand-receptor interactions could provide therapeutic benefits. In addition, we discuss recent reports on clinical testing of Notch inhibitors in T-ALL that influenced contemporary thinking on the challenges of targeting Notch in cancer. We review advances in the laboratory to address these challenges in regards to drug targets, the Notch-driven metabolome, and the sophisticated protein-protein interactions at Notch-dependent superenhancers that underlie oncogenic Notch functions. SUMMARY: Notch signaling is a recurrent oncogenic pathway in multiple T- and B-cell lymphoproliferative disorders. Understanding the complexity and consequences of Notch activation is critical to define optimal therapeutic strategies targeting the Notch pathway.

Indexed as

Signal TransductionAnimalsBiomarkersB-LymphocytesCell Transformation, NeoplasticDrug Resistance, NeoplasmGene Expression Regulation, NeoplasticHumansLymphoproliferative DisordersMolecular Targeted TherapyProtein BindingReceptors, NotchT-LymphocytesBiomarkersReceptors, Notch

Identifiers

PMID27135981
PMCPMC4962559
OpenAlexW2342789489

What OpenQuestion holds

Textmetadata
LicenceTDM
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.