Evidence map›Paper›PMID 21553146›Full record

ArticleCancer immunology, immunotherapy : CII2011

Increased PRAME antigen-specific killing of malignant cell lines by low avidity CTL clones, following treatment with 5-Aza-2'-Deoxycytidine.

Mengyong Yan, Nourredine Himoudi, B Piku Basu, Rebecca Wallace, Edmund Poon, Stuart Adams, Fyeza Hasan, Shao-An Xue, Natalie Wilson, Angus Dalgleish and 2 more

Open access · greenAbstract read
In one paragraph

Article in Cancer immunology, immunotherapy : CII, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

19 citing papers in PubMed, 31 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

12 authors at 4 institutions in 1 country.

Mengyong YanUnit of Molecular Haematology and Cancer Biology, University College London Institute of Child Health, 30 Guilford Street, London WC1N 1EH, UK.
Nourredine Himoudi
B Piku Basu
Rebecca Wallace
Edmund Poon
Stuart Adams
Fyeza Hasan
Shao-An Xue
Natalie Wilson
Angus Dalgleish
Owen Williams
John Anderson
University College London · GBSt George's Hospital · GBSt George's, University of London · GBThe Royal Free Hospital · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The cancer testis antigen Preferentially Expressed Antigen of Melanoma (PRAME) is overexpressed in many solid tumours and haematological malignancies whilst showing minimal expression in normal tissues and is therefore a promising target for immunotherapy. HLA-A0201-restricted peptide epitopes from PRAME have previously been identified as potential immunogens to drive antigen-specific autologous CTL responses, capable of lysing PRAME expressing tumour cells. CTL lines, from 13 normal donors and 10 melanoma patients, all of whom were HLA-A0201 positive, were generated against the PRAME peptide epitope PRA(100-108). Specific killing activity against PRA(100-108) peptide-pulsed targets was weak compared with CTL lines directed against known immunodominant peptides. Moreover, limiting dilution cloning from selected PRAME-specific CTL lines resulted in the generation of a clone of only low to intermediate avidity. Addition of the demethylating agent 5-aza-2'-Deoxycytidine (DAC) increased PRAME expression in 7 out of 11 malignant cell lines including several B lineage leukaemia lines and also increased class I expression. Pre-treatment of target cells was associated with increased sensitivity to antigen-specific killing by the low avidity CTL. When CTL, as well as of the target cells, were treated, the antigen-specific killing was further augmented. Interestingly, one HLA-A0201-negative DAC-treated line (RAJI) showed increased sensitivity to killing by clones despite a failure of expression of PRAME or HLA-A0201. Together these data point to a general increased augmentation of cancer immunogenocity by DAC involving both antigen-specific and non-specific mechanisms.

Indexed as

Antibody AffinityAntigens, NeoplasmAntimetabolites, AntineoplasticAzacitidineCell Line, TumorCytotoxicity, ImmunologicDecitabineHL-60 CellsHLA-A2 AntigenHumansImmunotherapy, AdoptiveK562 CellsNeoplasmsT-Lymphocytes, CytotoxicTransfectionAntigens, NeoplasmAntimetabolites, AntineoplasticAzacitidineDecitabineHLA-A*02:01 antigenHLA-A2 AntigenPRAME protein, human

Identifiers

PMID21553146
PMCPMC11029732
OpenAlexW2045522616

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Registered trials

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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.