Evidence map›Paper›PMID 26351841›Full record

ArticlePloS one2015

Use of Genome Engineering to Create Patient Specific MLL Translocations in Primary Human Hematopoietic Stem and Progenitor Cells.

Erin H Breese, Corina Buechele, Catherine Dawson, Michael L Cleary, Matthew H Porteus

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
4.3field-weighted citation impact, top 6% 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

17 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
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  7. Murine Models of Acute Myeloid Leukaemia.International journal of molecular sciences · 2019
    Review
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  10. Blood advances · 2018
    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

5 authors at 1 institution in 1 country.

Erin H BreeseDivision of Pediatric Hematology/Oncology, Department of Pediatrics, Stanford University, Stanford, California, United States of America.
Corina BuecheleDepartment of Pathology, Stanford University, Stanford, California, United States of America.
Catherine DawsonDivision of Pediatric Hematology/Oncology, Department of Pediatrics, Stanford University, Stanford, California, United States of America.
Michael L ClearyDepartment of Pathology, Stanford University, Stanford, California, United States of America.
Matthew H PorteusDivision of Pediatric Stem Cell Transplantation and Regenerative Medicine, Department of Pediatrics, Stanford University, Stanford, California, United States of America.
Stanford University · US

Funding

Molecular Targeting of MLL and Associated FactorsR01CA116606 · NCI · STANFORD UNIVERSITY · PI CLEARY, MICHAEL L · 2005 to 2020
$4.7M
NCI NIH HHS R01 CA116606
6 · The paper itself

Abstract

One of the challenging questions in cancer biology is how a normal cell transforms into a cancer cell. There is strong evidence that specific chromosomal translocations are a key element in this transformation process. Our studies focus on understanding the developmental mechanism by which a normal stem or progenitor cell transforms into leukemia. Here we used engineered nucleases to induce simultaneous specific double strand breaks in the MLL gene and two different known translocation partners (AF4 and AF9), which resulted in specific chromosomal translocations in K562 cells as well as primary hematopoietic stem and progenitor cells (HSPCs). The initiation of a specific MLL translocation in a small number of HSPCs likely mimics the leukemia-initiating event that occurs in patients. In our studies, the creation of specific MLL translocations in CD34+ cells was not sufficient to transform cells in vitro. Rather, a variety of fates was observed for translocation positive cells including cell loss over time, a transient proliferative advantage followed by loss of the clone, or a persistent proliferative advantage. These studies highlight the application of genome engineering tools in primary human HSPCs to induce and prospectively study the consequences of initiating translocation events in leukemia pathogenesis.

Indexed as

DNA Breaks, Double-StrandedTranslocation, GeneticCell LineCell Transformation, NeoplasticHematopoietic Stem CellsHistone-Lysine N-MethyltransferaseHumansMyeloid-Lymphoid Leukemia ProteinHistone-Lysine N-MethyltransferaseKMT2A protein, humanMyeloid-Lymphoid Leukemia Protein

Identifiers

PMID26351841
PMCPMC4564237
OpenAlexW2161148585

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.