Evidence map›Paper›PMID 27533466›Full record

ReviewOncotarget2016

Adenoid cystic carcinoma: emerging role of translocations and gene fusions.

Piotr T Wysocki, Evgeny Izumchenko, Juliet Meir, Patrick K Ha, David Sidransky, Mariana Brait

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 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
6.9field-weighted citation impact, top 3% 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

40 citing papers in PubMed, 72 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Molecular pathology of adenoid cystic carcinoma.Histology and histopathology · 2025
    Review
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  6. Article
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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

6 authors at 3 institutions in 1 country.

Piotr T WysockiDepartment of Otolaryngology and Head & Neck Surgery, Johns Hopkins University, School of Medicine, Baltimore, MD, USA.
Evgeny IzumchenkoDepartment of Otolaryngology and Head & Neck Surgery, Johns Hopkins University, School of Medicine, Baltimore, MD, USA.
Juliet MeirDepartment of Otolaryngology and Head & Neck Surgery, Johns Hopkins University, School of Medicine, Baltimore, MD, USA.
Patrick K HaDepartment of Otolaryngology- Head and Neck Surgery, University of California, San Francisco, CA, USA.
David SidranskyDepartment of Otolaryngology and Head & Neck Surgery, Johns Hopkins University, School of Medicine, Baltimore, MD, USA.
Mariana BraitDepartment of Otolaryngology and Head & Neck Surgery, Johns Hopkins University, School of Medicine, Baltimore, MD, USA.
Johns Hopkins University · USJohns Hopkins Medicine · USUniversity of California, San Francisco · US

Funding

TUMOR SUPPRESOR GENE PROMOTER HYPERMETHYLATION FOR DETECTION OF HEAD AND NECKP50DE019032 · NIDCR · JOHNS HOPKINS UNIVERSITY · PI SIDRANSKY, DAVID · 2007 to 2016
$27.1M
Integrated pathway analysis of altered driver genes in adenoid cystic carcinomaR01DE023227 · NIDCR · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI HA, PATRICK KYONGMIN · 2012 to 2015
$1.6M
NIDCR NIH HHS P50 DE019032NIDCR NIH HHS R01 DE023227
6 · The paper itself

Abstract

Adenoid cystic carcinoma (ACC), the second most common salivary gland malignancy, is notorious for poor prognosis, which reflects the propensity of ACC to progress to clinically advanced metastatic disease. Due to high long-term mortality and lack of effective systemic treatment, the slow-growing but aggressive ACC poses a particular challenge in head and neck oncology. Despite the advancements in cancer genomics, up until recently relatively few genetic alterations critical to the ACC development have been recognized. Although the specific chromosomal translocations resulting in MYB-NFIB fusions provide insight into the ACC pathogenesis and represent attractive diagnostic and therapeutic targets, their clinical significance is unclear, and a substantial subset of ACCs do not harbor the MYB-NFIB translocation. Strategies based on detection of newly described genetic events (such as MYB activating super-enhancer translocations and alterations affecting another member of MYB transcription factor family-MYBL1) offer new hope for improved risk assessment, therapeutic intervention and tumor surveillance. However, the impact of these approaches is still limited by an incomplete understanding of the ACC biology, and the manner by which these alterations initiate and drive ACC remains to be delineated. This manuscript summarizes the current status of gene fusions and other driver genetic alterations in ACC pathogenesis and discusses new therapeutic strategies stemming from the current research.

Indexed as

Gene FusionTranslocation, GeneticCarcinoma, Adenoid CysticHumansOncogene Proteins, FusionSalivary Gland NeoplasmsOncogene Proteins, Fusionadenoid cystic carcinomaMYBMYBL1salivary gland tumortranslocation

Identifiers

PMID27533466
PMCPMC5323230
OpenAlexW2511504476

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.