Evidence map›Paper›PMID 27858941›Full record

ReviewCell death and differentiation2017

Block one, unleash a hundred. Mechanisms of DAB2IP inactivation in cancer.

Arianna Bellazzo, Giulio Di Minin, Licio Collavin

Open access · bronzeAbstract readReview
In one paragraph

Review in Cell death and differentiation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

46 citing papers in PubMed, 66 citations in OpenAlex.

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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

3 authors at 2 institutions in 2 countries.

Arianna BellazzoLaboratorio Nazionale CIB, AREA Science Park, Trieste 34149, Italy.
Giulio Di MininInstitute of Molecular Health Sciences, Swiss Federal Institute of Technology, ETH Hönggerberg, Zurich 8093, Switzerland.
Licio CollavinLaboratorio Nazionale CIB, AREA Science Park, Trieste 34149, Italy.ORCID 0000-0001-6815-5381
University of Trieste · ITETH Zurich · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

One of the most defining features of cancer is aberrant cell communication; therefore, a molecular understanding of the intricate network established among tumor cells and their microenvironment could significantly improve comprehension and clinical management of cancer. The tumor suppressor DAB2IP (Disabled homolog 2 interacting protein), also known as AIP1 (ASK1 interacting protein), has an important role in this context, as it modulates signal transduction by multiple inflammatory cytokines and growth factors. DAB2IP is a Ras-GAP, and negatively controls Ras-dependent mitogenic signals. In addition, acting as a signaling adaptor, DAB2IP modulates other key oncogenic pathways, including TNFα/NF-κB, WNT/β-catenin, PI3K/AKT, and androgen receptors. Therefore, DAB2IP inactivation can provide a selective advantage to tumors initiated by a variety of driver mutations. In line with this role, DAB2IP expression is frequently impaired by methylation in cancer. Interestingly, recent studies reveal that tumor cells can employ other sophisticated mechanisms to disable DAB2IP at the post-transcriptional level. We review the mechanisms and consequences of DAB2IP inactivation in cancer, with the purpose to support and improve research aimed to counteract such mechanisms. We suggest that DAB2IP reactivation in cancer cells could be a strategy to coordinately dampen multiple oncogenic pathways, potentially limiting progression of a wide spectrum of tumors.

Indexed as

AnimalsDrug Resistance, NeoplasmHumansJNK Mitogen-Activated Protein KinasesMAP Kinase Kinase Kinase 5NeoplasmsNeoplastic Stem Cellsras GTPase-Activating ProteinsSignal TransductionUbiquitinDAB2IP protein, humanJNK Mitogen-Activated Protein KinasesMAP Kinase Kinase Kinase 5ras GTPase-Activating ProteinsUbiquitin

Identifiers

PMID27858941
PMCPMC5260500
OpenAlexW2556270292

What OpenQuestion holds

Textmetadata
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.