Evidence map›Paper›PMID 26178348›Full record

ArticleCell cycle (Georgetown, Tex.)2015

Pathways to chromothripsis.

Robert Ivkov, Fred Bunz

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

6 citing papers in PubMed, 13 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

2 authors at 2 institutions in 1 country.

Robert Ivkova Department of Radiation Oncology and Molecular Radiation Sciences ; The Kimmel Cancer Center at Johns Hopkins ; Baltimore MD USA.
Fred Bunza Department of Radiation Oncology and Molecular Radiation Sciences ; The Kimmel Cancer Center at Johns Hopkins ; Baltimore MD USA.
Sidney Kimmel Cancer Center · USUniversity of Baltimore · US

Funding

Targeting the ATR pathway in p53-deficient cancersR01CA157535 · NCI · JOHNS HOPKINS UNIVERSITY · PI BUNZ, FRED · 2011 to 2015
$1.7M
NCI NIH HHS R01 CA157535
6 · The paper itself

Abstract

Chromothripsis is a recently recognized mode of genetic instability that generates chromosomes with strikingly large numbers of segmental re-arrangements. While the characterization of these derivative chromosomes has provided new insights into the processes by which cancer genomes can evolve, the underlying signaling events and molecular mechanisms remain unknown. In medulloblastomas, chromothripsis has been observed to occur in the context of mutational inactivation of p53 and activation of the canonical Hedgehog (Hh) pathway. Recent studies have illuminated mechanistic links between these 2 signaling pathways, including a novel PTCH1 homolog that is regulated by p53. Here, we integrate this new pathway into a hypothetical model for the catastrophic DNA breakage that appears to trigger profound chromosomal rearrangements.

Indexed as

Chromosomal InstabilityModels, GeneticDNA BreaksGene Expression Regulation, NeoplasticGene RearrangementHedgehog ProteinsNeoplasmsRepressor ProteinsSignal TransductionTumor Suppressor Protein p53Hedgehog ProteinsPTCHD4 protein, humanRepressor ProteinsTumor Suppressor Protein p53chromothripsishedgehogmedulloblastomap53PTCH53

Identifiers

PMID26178348
PMCPMC4825555
OpenAlexW2148833567

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.