Evidence map›Paper›PMID 19056696›Full record

ArticleGenome research2009

A sequence-level map of chromosomal breakpoints in the MCF-7 breast cancer cell line yields insights into the evolution of a cancer genome.

Oliver A Hampton, Petra Den Hollander, Christopher A Miller, David A Delgado, Jian Li, Cristian Coarfa, Ronald A Harris, Stephen Richards, Steven E Scherer, Donna M Muzny and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Genome research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.

0numbers the graph read from it
0cells of the map it votes in
77citing 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

77 citing papers in PubMed, 130 citations in OpenAlex.

  1. Review
  2. Sample and Library Preparation for PacBio Long-Read Sequencing in Grapevine.Methods in molecular biology (Clifton, N.J.) · 2024
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  15. Identifying fusion transcripts using next generation sequencing.Wiley interdisciplinary reviews. RNA · 2016
    Review
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  19. Article
  20. PacBio Sequencing and Its Applications.Genomics, proteomics & bioinformatics · 2015
    Review

17 more citing papers are in PubMed but not listed here.

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

13 authors at 1 institution in 1 country.

Oliver A HamptonBioinformatics Research Laboratory, Baylor College of Medicine, Houston, Texas 77030, USA.
Petra Den Hollander
Christopher A Miller
David A Delgado
Jian Li
Cristian Coarfa
Ronald A Harris
Stephen Richards
Steven E Scherer
Donna M Muzny
Richard A Gibbs
Adrian V Lee
Aleksandar Milosavljevic
Baylor College of Medicine · US

Funding

Clone-Array Pooled Shotgun IndexingR01HG002583 · NHGRI · BAYLOR COLLEGE OF MEDICINE · PI MILOSAVLJEVIC, ALEKSANDAR · 2002 to 2004
$1.5M
Multiplexed Methods for the Study of Chromosomal Aberrations in CancerR33CA114151 · NCI · BAYLOR COLLEGE OF MEDICINE · PI MILOSAVLJEVIC, ALEKSANDAR · 2007 to 2009
$690k
NCI NIH HHS R21 CA128496NCI NIH HHS R33 CA114151NHGRI NIH HHS 1 R01 HG02583NHGRI NIH HHS R01 HG002583
6 · The paper itself

Abstract

By applying a method that combines end-sequence profiling and massively parallel sequencing, we obtained a sequence-level map of chromosomal aberrations in the genome of the MCF-7 breast cancer cell line. A total of 157 distinct somatic breakpoints of two distinct types, dispersed and clustered, were identified. A total of 89 breakpoints are evenly dispersed across the genome. A majority of dispersed breakpoints are in regions of low copy repeats (LCRs), indicating a possible role for LCRs in chromosome breakage. The remaining 68 breakpoints form four distinct clusters of closely spaced breakpoints that coincide with the four highly amplified regions in MCF-7 detected by array CGH located in the 1p13.1-p21.1, 3p14.1-p14.2, 17q22-q24.3, and 20q12-q13.33 chromosomal cytobands. The clustered breakpoints are not significantly associated with LCRs. Sequences flanking most (95%) breakpoint junctions are consistent with double-stranded DNA break repair by nonhomologous end-joining or template switching. A total of 79 known or predicted genes are involved in rearrangement events, including 10 fusions of coding exons from different genes and 77 other rearrangements. Four fusions result in novel expressed chimeric mRNA transcripts. One of the four expressed fusion products (RAD51C-ATXN7) and one gene truncation (BRIP1 or BACH1) involve genes coding for members of protein complexes responsible for homology-driven repair of double-stranded DNA breaks. Another one of the four expressed fusion products (ARFGEF2-SULF2) involves SULF2, a regulator of cell growth and angiogenesis. We show that knock-down of SULF2 in cell lines causes tumorigenic phenotypes, including increased proliferation, enhanced survival, and increased anchorage-independent growth.

Indexed as

Cell Line, TumorChromosome BreakageGenes, NeoplasmGenome, HumanBreast NeoplasmsChromosome MappingChromosomes, Artificial, BacterialDNA RepairEvolution, MolecularGene Expression ProfilingHumansLocus Control RegionModels, BiologicalMutant Chimeric ProteinsSequence Analysis, DNAMutant Chimeric Proteins

Identifiers

PMID19056696
PMCPMC2652200
OpenAlexW2129843621

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.