Evidence map›Paper›PMID 31827154›Full record

ArticleScientific reports2019

A higher throughput assay for quantification of melphalan-induced DNA damage in peripheral blood mononuclear cells.

Maia van Kan, Kathryn E Burns, Peter Browett, Nuala A Helsby

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.6field-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

3 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. Science advances · 2023
    Article
  3. Article
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

4 authors at 1 institution in 1 country.

Maia van KanDepartment of Molecular Medicine and Pathology, University of Auckland, Auckland, New Zealand.
Kathryn E BurnsDepartment of Molecular Medicine and Pathology, University of Auckland, Auckland, New Zealand.ORCID http://orcid.org/0000-0003-4951-3539
Peter BrowettDepartment of Molecular Medicine and Pathology, University of Auckland, Auckland, New Zealand.
Nuala A HelsbyDepartment of Molecular Medicine and Pathology, University of Auckland, Auckland, New Zealand. n.helsby@auckland.ac.nz.
University of Auckland · NZ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inter-individual differences in DNA adduct formation and repair influence the response to melphalan treatment, however, further clinical investigation of this variability requires a logistically feasible and reproducible bioassay. Our improved fluorescence-based QPCR-block assay is robust, has good precision, and improved throughput. It also incorporates direct PCR amplification from melphalan exposed PBMC using commercially available blood tubes and extraction kits to maximise the utility of this assay for future clinical studies. Using this assay we have demonstrated reproducible inter-individual differences in melphalan-induced QPCR-block across individual PBMC donors. As proof-of-principle we assessed nine healthy donors and found a 7.8 fold range in sensitivity following exposure of PBMC ex vivo. This likely reflects differences in melphalan transport into cells as well as differences in DNA adduct repair proficiency. This improved bioassay may be useful for assessment of these processes in patients about to receive melphalan treatment.

Indexed as

Antineoplastic Agents, AlkylatingDNA DamageHigh-Throughput Screening AssaysHumansLeukocytes, MononuclearMelphalanAntineoplastic Agents, AlkylatingMelphalan

Identifiers

PMID31827154
PMCPMC6906414
OpenAlexW2995033609

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.