Evidence map›Paper›PMID 28240214›Full record

ReviewTrends in molecular medicine2016

Genomic Alterations of Non-Coding Regions Underlie Human Cancer: Lessons from T-ALL.

Adrian Rivera-Reyes, Katharina E Hayer, Craig H Bassing

Abstract readReview
In one paragraph

Review in Trends in molecular medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
–field-weighted citation impact
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

8 citing papers in PubMed.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Non-Coding RNA Networks in ALK-Positive Anaplastic-Large Cell Lymphoma.International journal of molecular sciences · 2019
    Review
  8. Review
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.

Adrian Rivera-ReyesDivision of Cancer Pathobiology, Department of Pathology and Laboratory Medicine, Center for Childhood Cancer Research, Children's Hospital of Philadelphia, Philadelphia, PA 19104, USA; Cell and Molecular Biology Graduate Group, Department of Pathology and Laboratory Medicine, Abramson Family Cancer Research Institute, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA 19104, USA.
Katharina E HayerDivision of Cancer Pathobiology, Department of Pathology and Laboratory Medicine, Center for Childhood Cancer Research, Children's Hospital of Philadelphia, Philadelphia, PA 19104, USA.
Craig H BassingDivision of Cancer Pathobiology, Department of Pathology and Laboratory Medicine, Center for Childhood Cancer Research, Children's Hospital of Philadelphia, Philadelphia, PA 19104, USA; Cell and Molecular Biology Graduate Group, Department of Pathology and Laboratory Medicine, Abramson Family Cancer Research Institute, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA 19104, USA. Electronic address: bassing@email.chop.edu.

Funding

TRAINING PROGRAM IN CELL AND MOLECULAR BIOLOGYT32GM007229 · NIGMS · UNIVERSITY OF PENNSYLVANIA · PI BARTOLOMEI, MARISA S. · 1985 to 2023
$14.0M
DNA Double Strand Break Mediated Feedback Inhibition of V(D)J RecombinationR01AI112621 · NIAID · CHILDREN'S HOSP OF PHILADELPHIA · PI BASSING, CRAIG H · 2015 to 2019
$1.9M
DNA Double Strand Break Mediated Feedback Inhibition of V(D)J RecombinationR56AI112621 · NIAID · CHILDREN'S HOSP OF PHILADELPHIA · PI BASSING, CRAIG H · 2014 to 2014
$420k
NIAID NIH HHS R01 AI112621NIAID NIH HHS R56 AI112621NIGMS NIH HHS T32 GM007229
6 · The paper itself

Abstract

It has been appreciated for decades that somatic genomic alterations that change coding sequences of proto-oncogenes, translocate enhancers/promoters near proto-oncogenes, or create fusion oncogenes can drive cancer by inducing oncogenic activities. An explosion of genome-wide technologies over the past decade has fueled discoveries of the roles of three-dimensional chromosome structure and powerful cis-acting elements (super-enhancers) in regulating gene transcription. In recent years, studies of human T cell acute lymphoblastic leukemia (T-ALL) using genome-wide technologies have provided paradigms for how non-coding genomic region alterations can disrupt 3D chromosome architecture or establish super-enhancers to activate oncogenic transcription of proto-oncogenes. These studies raise important issues to consider with the objective of leveraging basic knowledge into new diagnostic and therapeutic opportunities for cancer patients.

Indexed as

Gene Expression Regulation, LeukemicBasic Helix-Loop-Helix ProteinsEctopic Gene ExpressionGenome, HumanHumansPrecursor T-Cell Lymphoblastic Leukemia-LymphomaProto-Oncogene ProteinsT-Cell Acute Lymphocytic Leukemia Protein 1Transcriptional ActivationBasic Helix-Loop-Helix ProteinsProto-Oncogene ProteinsTAL1 protein, humanT-Cell Acute Lymphocytic Leukemia Protein 1

Identifiers

PMID28240214
PMCPMC5330204

What OpenQuestion holds

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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.