Evidence map›Paper›PMID 24625551›Full record

ArticleLeukemia2014

p53 haploinsufficiency and functional abnormalities in multiple myeloma.

P J Teoh, T H Chung, S Sebastian, S N Choo, J Yan, S B Ng, R Fonseca, W J Chng

Abstract read
PubMed Publisher
In one paragraph

Article in Leukemia, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
4.0field-weighted citation impact, top 5% 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

55 citing papers in PubMed, 77 citations in OpenAlex.

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  6. The genomic and epigenomic landscapes of hemizygous genes across crops with contrasting reproductive systems.Proceedings of the National Academy of Sciences of the United States of America · 2025
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  14. Assessment of Bone Marrow Biopsy and Cytogenetic Findings in Patients with Multiple MyelomaTurkish journal of haematology : official journal of Turkish Society of Haematology · 2022
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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

8 authors at 4 institutions in 2 countries.

P J Teoh1] Department of Medicine, Yong Loo Lin School of Medicine, National University of Singapore, Singapore [2] Cancer Science Institute of Singapore, National University of Singapore, Singapore.
T H ChungCancer Science Institute of Singapore, National University of Singapore, Singapore.
S SebastianDepartment of Hematology-Oncology, Mayo Clinic, Scottsdale, AZ, USA.
S N ChooDepartment of Pathology, National University Cancer Institute of Singapore, National University Health System, Singapore.
J YanCancer Science Institute of Singapore, National University of Singapore, Singapore.
S B Ng1] Department of Pathology, National University Cancer Institute of Singapore, National University Health System, Singapore [2] Department of Pathology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore.
R FonsecaDepartment of Hematology-Oncology, Mayo Clinic, Scottsdale, AZ, USA.
W J Chng1] Department of Medicine, Yong Loo Lin School of Medicine, National University of Singapore, Singapore [2] Cancer Science Institute of Singapore, National University of Singapore, Singapore [3] Department of Haematology-Oncology, National University Cancer Institute of Singapore, National University Health System, Singapore.
National University Cancer Institute, Singapore · SGNational University of Singapore · SGMayo Clinic · USMayo Clinic in Arizona · US

Funding

TISSUE BANK AND CLINICAL/LABORATORY DATABASEP01CA062242 · NCI · MAYO CLINIC ROCHESTER · PI FONSECAR, RAFAEL · 1994 to 2009
$12.9M
CHROMOSOMAL ABNORMALITIES IN MYELOMA AS DETECTED BY FISHR01CA083724 · NCI · MAYO CLINIC COLL OF MEDICINE, ROCHESTER · PI FONSECA, RAFAEL · 2000 to 2013
$4.0M
NCI NIH HHS CA90297052NCI NIH HHS P01 CA62242NCI NIH HHS R01 CA83724
6 · The paper itself

Abstract

Hemizygous deletion of 17p13, which harbors the TP53 gene, has been identified in >10% of newly diagnosed multiple myeloma (MM) patients and is associated with poor prognosis. To date, there is no conclusive evidence that TP53 is the critical gene. Furthermore, the functional effect of TP53 haploinsufficiency is not well characterized. By utilizing human myeloma cell lines, we showed that TP53 hemizygous loss was associated with decreased basal expression level with a partially or severely inactivated p53 response upon genotoxic and non-genotoxic stress. The pathway deficiency was manifested as defective p53 transcriptional activities, together with significant resistance to apoptosis. In some cases with p53 WT/- and no p53 protein expression, the remaining allele was silenced by promoter hypermethylation. We also developed a p53 target gene signature to summarize the complexity of the p53 pathway abnormalities in MM and showed that it is strongly associated with genomic complexity and patient survival. In conclusion, this study identified TP53 as the critical gene located in 17p13, and revealed its haploinsufficiency properties in MM. Furthermore, we have elucidated that multiple mechanisms can deregulate the p53 functions and that this has important prognostic impact in MM.

Indexed as

Genes, p53HaploinsufficiencyAllelesApoptosisCell Line, TumorCell ProliferationCell SurvivalChromosomes, Human, Pair 17Comparative Genomic HybridizationDNA MethylationGene DeletionGene SilencingHumansMultiple MyelomaPrognosisPromoter Regions, GeneticTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID24625551
OpenAlexW2114366538

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.