Evidence map›Paper›PMID 19225112›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2009

A panel of isogenic human cancer cells suggests a therapeutic approach for cancers with inactivated p53.

Surojit Sur, Raymond Pagliarini, Fred Bunz, Carlo Rago, Luis A Diaz, Kenneth W Kinzler, Bert Vogelstein, Nickolas Papadopoulos

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 200 papers.

0numbers the graph read from it
0cells of the map it votes in
200citing papers in PubMed
12.1field-weighted citation impact, top 1% 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

200 citing papers in PubMed, 298 citations in OpenAlex.

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140 more citing papers are in PubMed but not listed here.

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 1 country.

Surojit SurThe Howard Hughes Medical Institute and The Ludwig Center for Cancer Genetics and Therapeutics, Baltimore, MD 21231, USA.
Raymond Pagliarini
Fred Bunz
Carlo Rago
Luis A Diaz
Kenneth W Kinzler
Bert Vogelstein
Nickolas Papadopoulos
Cancer Genetics (United States) · USHoward Hughes Medical Institute · USSidney Kimmel Cancer Center · USSidney Kimmel Comprehensive Cancer Center · US

Funding

Tumor Antigens for Individual Signatures and TherapyP50CA062924 · NCI · JOHNS HOPKINS UNIVERSITY · PI LENNON, ANNE MARIE · 1993 to 2022
$54.6M
MOLECULAR GENETIC ANALYSIS OF COLORECTAL CANCERR37CA043460 · NCI · JOHNS HOPKINS UNIVERSITY · PI VOGELSTEIN, BERT · 1997 to 2016
$7.4M
Genes from the FAP LocusR37CA057345 · NCI · JOHNS HOPKINS UNIVERSITY · PI KINZLER, KENNETH W. · 2002 to 2016
$7.4M
TRAINING IN ANTICANCER DRUG DEVELOPMENTT32CA009243 · NCI · JOHNS HOPKINS UNIVERSITY · PI STIVERS, JAMES T. · 1985 to 2012
$6.2M
THE P53 GENE IN HUMAN NEOPLASIAR01CA043460 · NCI · JOHNS HOPKINS UNIVERSITY · PI VOGELSTEIN, BERT · 1986 to 1995
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Howard Hughes Medical InstituteNCI NIH HHS CA 09243NCI NIH HHS CA 43460NCI NIH HHS CA 62924NCI NIH HHS P50 CA062924NCI NIH HHS R37 CA043460NCI NIH HHS R37 CA057345NCI NIH HHS T32 CA009243
6 · The paper itself

Abstract

Through targeted homologous recombination, we developed a panel of matched colorectal cancer cell lines that differ only with respect to their endogenous TP53 status. We then used these lines to define the genes whose expression was altered after DNA damage induced by ionizing radiation. Transcriptome analyses revealed a consistent up-regulation of polo-like kinase 1 (PLK1) as well as other genes controlling the G(2)/M transition in the cells whose TP53 genes were inactivated compared with those with WT TP53 genes. This led to the hypothesis that the viability of stressed cells without WT TP53 depended on PLK1. This hypothesis was validated by demonstrating that stressed cancer cells without WT TP53 alleles were highly sensitive to PLK1 inhibitors, both in vivo and in vitro.

Indexed as

AllelesAnimalsAntineoplastic AgentsCell Line, TumorCyclin-Dependent Kinase Inhibitor p21G1 PhaseGene Expression ProfilingGene TargetingGenotypeHumansImidazolesMiceNeoplasmsPiperazinesPteridinesTranscription, GeneticAntineoplastic AgentsBI 2536Cyclin-Dependent Kinase Inhibitor p21Imidazolesnutlin 3PiperazinesPteridinesTumor Suppressor Protein p53

Identifiers

PMID19225112
PMCPMC2656188
OpenAlexW2165582413

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.