Evidence map›Paper›PMID 25768405›Full record

ArticleBlood cancer journal2015

The relationship of TP53 R72P polymorphism to disease outcome and TP53 mutation in myelodysplastic syndromes.

K L McGraw, L M Zhang, D E Rollison, A A Basiorka, W Fulp, B Rawal, A Jerez, D L Billingsley, H-Y Lin, S E Kurtin and 20 more

Open access · goldAbstract read
In one paragraph

Article in Blood cancer journal, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.7field-weighted citation impact, top 14% 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

6 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
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  3. International journal of molecular sciences · 2020
    Review
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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

30 authors at 10 institutions in 5 countries.

K L McGrawHematology Department, H Lee Moffitt Cancer Center, Tampa, FL, USA.
L M ZhangMolecular Genomics Core Lab, H Lee Moffitt Cancer Center, Tampa, FL, USA.
D E RollisonCancer Epidemiology, H Lee Moffitt Cancer Center, Tampa, FL, USA.
A A Basiorka1] Hematology Department, H Lee Moffitt Cancer Center, Tampa, FL, USA [2] Cancer Biology PhD Program, University of South Florida, Tampa, FL, USA.
W FulpBiostatistics and Bioinformatics Department, H Lee Moffitt Cancer Center, Tampa, FL, USA.
B RawalMayo Clinic, Biostatistics-Division of Health Sciences Research, Jacksonville, FL, USA.
A JerezCleveland Clinic, Taussig Cancer Institute, Cleveland, OH, USA.
D L BillingsleyCelgene Corporation, Tampa, FL, USA.
H-Y LinBiostatistics and Bioinformatics Department, H Lee Moffitt Cancer Center, Tampa, FL, USA.
S E KurtinArizona Cancer Center, Tucson, AZ, USA.
S YoderMolecular Genomics Core Lab, H Lee Moffitt Cancer Center, Tampa, FL, USA.
Y ZhangBiostatistics and Bioinformatics Department, H Lee Moffitt Cancer Center, Tampa, FL, USA.
K GuintaCleveland Clinic, Taussig Cancer Institute, Cleveland, OH, USA.
M MalloInstitut de Recerca Contra la Leucèmia Josep Carreras (IJC) Badalona, Barcelona, Spain.
F SoléInstitut de Recerca Contra la Leucèmia Josep Carreras (IJC) Badalona, Barcelona, Spain.
M J CalasanzHematology Department, Hospital Universitario La Fe, Valencia, Spain.
J CerveraHematology Department, Hospital Universitario La Fe, Valencia, Spain.
E SuchHematology Department, Hospital Universitario La Fe, Valencia, Spain.
T GonzálezGenomics Medicine Public Foundation, Hospital Clinico Universitario, Santiago de Compostela, Spain.
T J NevillBritish Columbia Cancer Agency, Vancouver, BC, Canada.
T HaferlachMunich Leukemia Laboratory, Munich, Germany.
A E SmithKing's College London, King's College Hospital, London, UK.
A KulasekararajKing's College London, King's College Hospital, London, UK.
G MuftiKing's College London, King's College Hospital, London, UK.
A KarsanBritish Columbia Cancer Agency, Vancouver, BC, Canada.
J P MaciejewskiCleveland Clinic, Taussig Cancer Institute, Cleveland, OH, USA.
L SokolHematology Department, H Lee Moffitt Cancer Center, Tampa, FL, USA.
P K Epling-BurnetteImmunology Department, H Lee Moffitt Cancer Center, Tampa, FL, USA.
S WeiImmunology Department, H Lee Moffitt Cancer Center, Tampa, FL, USA.
A F ListHematology Department, H Lee Moffitt Cancer Center, Tampa, FL, USA.
Moffitt Cancer Center · USCleveland Clinic · USHospital Universitari i Politècnic La Fe · ESBC Cancer Agency · CAFundación Josep Carreras Contra la Leucemia · ESKing's College Hospital · GBArizona Oncology · USKing's College London · GBMayo Clinic in Florida · USMunich Leukemia Laboratory (Germany) · DE

Funding

TRANSLATIONAL RESEARCHP30CA076292 · NCI · UNIVERSITY OF SOUTH FLORIDA · PI John L. Cleveland · 1998 to 2026
$93.5M
Integrative Molecular Epidemiology WorkshopR25CA174664 · NCI · AMERICAN ASSOCIATION FOR CANCER RESEARCH · PI Shelley S Tworoger · 2013 to 2026
$2.8M
Tumor Immunology Training Program -1 T32 CA115308-A1T32CA115308 · NCI · H. LEE MOFFITT CANCER CTR & RES INST · PI WRIGHT, KENNETH LYNN · 2007 to 2017
$2.8M
Phosphatase Targets of Lenalidomide in Myelodysplastic SyndromeR01CA131076 · NCI · H. LEE MOFFITT CANCER CTR & RES INST · PI LIST, ALAN F · 2008 to 2012
$2.2M
NCI NIH HHS 5 R01 CA131076-04NCI NIH HHS P30 CA076292NCI NIH HHS R01 CA131076NCI NIH HHS R25 CA174664NCI NIH HHS T32 CA115308
6 · The paper itself

Abstract

Nonsynonymous TP53 exon 4 single-nucleotide polymorphism (SNP), R72P, is linked to cancer and mutagen susceptibility. R72P associations with specific cancer risk, particularly hematological malignancies, have been conflicting. Myelodysplastic syndrome (MDS) with chromosome 5q deletion is characterized by erythroid hypoplasia arising from lineage-specific p53 accumulation resulting from ribosomal insufficiency. We hypothesized that apoptotically diminished R72P C-allele may influence predisposition to del(5q) MDS. Bone marrow and blood DNA was sequenced from 705 MDS cases (333 del(5q), 372 non-del(5q)) and 157 controls. Genotype distribution did not significantly differ between del(5q) cases (12.6% CC, 38.1% CG, 49.2% GG), non-del(5q) cases (9.7% CC, 44.6% CG, 45.7% GG) and controls (7.6% CC, 37.6% CG, 54.8% GG) (P=0.13). Allele frequency did not differ between non-del(5q) and del(5q) cases (P=0.91) but trended towards increased C-allele frequency comparing non-del(5q) (P=0.08) and del(5q) (P=0.10) cases with controls. Median lenalidomide response duration increased proportionate to C-allele dosage in del(5q) patients (2.2 (CC), 1.3 (CG) and 0.89 years (GG)). Furthermore, C-allele homozygosity in del(5q) was associated with prolonged overall and progression-free survival and non-terminal interstitial deletions that excluded 5q34, whereas G-allele homozygozity was associated with inferior outcome and terminal deletions involving 5q34 (P=0.05). These findings comprise the largest MDS R72P SNP analysis.

Indexed as

Chromosome DeletionAdolescentAdultAgedAged, 80 and overGene FrequencyHumansKaplan-Meier EstimateMaleMiddle AgedMutationMyelodysplastic SyndromesPolymorphism, Single NucleotideTreatment OutcomeTumor Suppressor Protein p53TP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID25768405
PMCPMC4382654
OpenAlexW2018993327

What OpenQuestion holds

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LicenceCC BY-NC-SA
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.