Evidence map›Paper›PMID 19625708›Full record

ArticleBlood2009

The preferentially expressed antigen in melanoma (PRAME) inhibits myeloid differentiation in normal hematopoietic and leukemic progenitor cells.

Vivian G Oehler, Katherine A Guthrie, Carrie L Cummings, Kathleen Sabo, Brent L Wood, Ted Gooley, Taimei Yang, Mirjam T Epping, Yaping Shou, Era Pogosova-Agadjanyan and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 2 pooled it
3.3field-weighted citation impact, top 7% 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

42 citing papers in PubMed, 2 syntheses or guidelines pooled it, 83 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
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  9. Identification ofGenes · 2022
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  20. Identification of Preferentially Expressed Antigen of Melanoma as a Potential Tumor Suppressor in Lung Adenocarcinoma.Medical science monitor : international medical journal of experimental and clinical research · 2016
    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

14 authors at 4 institutions in 2 countries.

Vivian G OehlerClinical Research Division, Fred Hutchinson Cancer Research Center, Seattle, WA, USA. voehler@u.washington.edu
Katherine A Guthrie
Carrie L Cummings
Kathleen Sabo
Brent L Wood
Ted Gooley
Taimei Yang
Mirjam T Epping
Yaping Shou
Era Pogosova-Agadjanyan
Paula Ladne
Derek L Stirewalt
Janis L Abkowitz
Jerald P Radich
Fred Hutch Cancer Center · USUniversity of Washington · USNovartis (United States) · USThe Netherlands Cancer Institute · NL

Funding

VIRUS-MEDIATED MYELOSUPPRESSIONP01CA018029 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI STEPHANIE J LEE · 1985 to 2026
$128.4M
CORE--VECTOR PRODUCTIONP30DK056465 · NIDDK · FRED HUTCHINSON CANCER RESEARCH CENTER · PI HEIMFELD, SHELLY · 1999 to 2014
$14.9M
Integrating Diagnostics with Therapeutic Strategies in Chronic Myeloid LeukemiaR01CA140371 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI OEHLER, VIVIAN G · 2009 to 2013
$1.8M
Examination of imatinib mesylate resistance in CMLK23CA106796 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI OEHLER, VIVIAN G · 2004 to 2008
$668k
NCI NIH HHS CA106796NCI NIH HHS CA18029NCI NIH HHS K23 CA106796NCI NIH HHS P01 CA018029NCI NIH HHS R01 CA140371NIDDK NIH HHS P30 DK056465
6 · The paper itself

Abstract

The preferentially expressed antigen in melanoma (PRAME) is expressed in several hematologic malignancies, but either is not expressed or is expressed at only low levels in normal hematopoietic cells, making it a target for cancer therapy. PRAME is a tumor-associated antigen and has been described as a corepressor of retinoic acid signaling in solid tumor cells, but its function in hematopoietic cells is unknown. PRAME mRNA expression increased with chronic myeloid leukemia (CML) disease progression and its detection in late chronic-phase CML patients before tyrosine kinase inhibitor therapy was associated with poorer therapeutic responses and ABL tyrosine kinase domain point mutations. In leukemia cell lines, PRAME protein expression inhibited granulocytic differentiation only in cell lines that differentiate along this lineage after all-trans retinoic acid (ATRA) exposure. Forced PRAME expression in normal hematopoietic progenitors, however, inhibited myeloid differentiation both in the presence and absence of ATRA, and this phenotype was reversed when PRAME was silenced in primary CML progenitors. These observations suggest that PRAME inhibits myeloid differentiation in certain myeloid leukemias, and that its function in these cells is lineage and phenotype dependent. Lastly, these observations suggest that PRAME is a target for both prognostic and therapeutic applications.

Indexed as

Cell DifferentiationGene Expression Regulation, LeukemicAntigens, NeoplasmAntineoplastic AgentsCell Line, TumorDisease ProgressionFemaleGene SilencingGranulocytesHematopoietic Stem CellsHumansLeukemia, Myelogenous, Chronic, BCR-ABL PositiveMaleNeoplastic Stem CellsPrognosisProtein Kinase InhibitorsAntigens, NeoplasmAntineoplastic AgentsPRAME protein, humanProtein Kinase InhibitorsProto-Oncogene Proteins c-ablTretinoin

Identifiers

PMID19625708
PMCPMC2759652
OpenAlexW2151883962

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.