Evidence map›Paper›PMID 18676840›Full record

ArticleCancer research2008

Reciprocal relationship between O6-methylguanine-DNA methyltransferase P140K expression level and chemoprotection of hematopoietic stem cells.

Michael D Milsom, Moran Jerabek-Willemsen, Chad E Harris, Axel Schambach, Emily Broun, Jeff Bailey, Michael Jansen, David Schleimer, Kalpana Nattamai, Jamie Wilhelm and 7 more

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

15 citing papers in PubMed, 26 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

17 authors at 5 institutions in 3 countries.

Michael D MilsomDivision of Experimental Hematology, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio, USA.
Moran Jerabek-Willemsen
Chad E Harris
Axel Schambach
Emily Broun
Jeff Bailey
Michael Jansen
David Schleimer
Kalpana Nattamai
Jamie Wilhelm
Amanda Watson
Hartmut Geiger
Geoffrey P Margison
Thomas Moritz
Christopher Baum
Jürgen Thomale
David A Williams
Cincinnati Children's Hospital Medical Center · USCancer Research UK Manchester Institute · GBBoston Children's Hospital · USMedizinische Hochschule Hannover · DEUniversity of Duisburg-Essen · DE

Funding

Chemoresistance and Stem Cell SelectionR01DK074310 · NIDDK · CINCINNATI CHILDRENS HOSP MED CTR · PI WILLIAMS, DAVID A · 2006 to 2010
$1.8M
Genetic Reg. of Hematopoietic Stem Cell MobilizationR01HL076604 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI GEIGER, HARTMUT · 2004 to 2007
$1.2M
Cancer Research UKNHLBI NIH HHS R01 HL076604NIDDK NIH HHS R01 DK074310
6 · The paper itself

Abstract

Retroviral-mediated delivery of the P140K mutant O(6)-methylguanine-DNA methyltransferase (MGMT(P140K)) into hematopoietic stem cells (HSC) has been proposed as a means to protect against dose-limiting myelosuppressive toxicity ensuing from chemotherapy combining O(6)-alkylating agents (e.g., temozolomide) with pseudosubstrate inhibitors (such as O(6)-benzylguanine) of endogenous MGMT. Because detoxification of O(6)-alkylguanine adducts by MGMT is stoichiometric, it has been suggested that higher levels of MGMT will afford better protection to gene-modified HSC. However, accomplishing this goal would potentially be in conflict with current efforts in the gene therapy field, which aim to incorporate weaker enhancer elements to avoid insertional mutagenesis. Using a panel of self-inactivating gamma-retroviral vectors that express a range of MGMT(P140K) activity, we show that MGMT(P140K) expression by weaker cellular promoter/enhancers is sufficient for in vivo protection/selection following treatment with O(6)-benzylguanine/temozolomide. Conversely, the highest level of MGMT(P140K) activity did not promote efficient in vivo protection despite mediating detoxification of O(6)-alkylguanine adducts. Moreover, very high expression of MGMT(P140K) was associated with a competitive repopulation defect in HSC. Mechanistically, we show a defect in cellular proliferation associated with elevated expression of MGMT(P140K), but not wild-type MGMT. This proliferation defect correlated with increased localization of MGMT(P140K) to the nucleus/chromatin. These data show that very high expression of MGMT(P140K) has a deleterious effect on cellular proliferation, engraftment, and chemoprotection. These studies have direct translational relevance to ongoing clinical gene therapy studies using MGMT(P140K), whereas the novel mechanistic findings are relevant to the basic understanding of DNA repair by MGMT.

Indexed as

AnimalsComet AssayFluorescent Antibody TechniqueGenetic VectorsHematopoietic Stem CellsMiceMice, Inbred C57BLO(6)-Methylguanine-DNA MethyltransferaseRetroviridaeTransduction, GeneticO(6)-Methylguanine-DNA Methyltransferase

Identifiers

PMID18676840
PMCPMC4337843
OpenAlexW2169125054

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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.