Evidence map›Paper›PMID 34192538›Full record

ArticleCell reports2021

p53-intact cancers escape tumor suppression through loss of long noncoding RNA Dino.

Christina B Marney, Erik S Anderson, Mutayyaba Adnan, Kai-Lin Peng, Ya Hu, Nils Weinhold, Adam M Schmitt

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 18% 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

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.

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  16. A mechanistic view of long noncoding RNAs in cancer.Wiley interdisciplinary reviews. RNA · 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

7 authors at 1 institution in 1 country.

Christina B MarneyDivision of Translational Oncology, Department of Radiation Oncology, Memorial Sloan Kettering Cancer Center, New York, NY 10128, USA.
Erik S AndersonDivision of Translational Oncology, Department of Radiation Oncology, Memorial Sloan Kettering Cancer Center, New York, NY 10128, USA.
Mutayyaba AdnanDivision of Translational Oncology, Department of Radiation Oncology, Memorial Sloan Kettering Cancer Center, New York, NY 10128, USA.
Kai-Lin PengDivision of Translational Oncology, Department of Radiation Oncology, Memorial Sloan Kettering Cancer Center, New York, NY 10128, USA.
Ya HuDivision of Translational Oncology, Department of Radiation Oncology, Memorial Sloan Kettering Cancer Center, New York, NY 10128, USA.
Nils WeinholdDivision of Translational Oncology, Department of Radiation Oncology, Memorial Sloan Kettering Cancer Center, New York, NY 10128, USA.
Adam M SchmittDivision of Translational Oncology, Department of Radiation Oncology, Memorial Sloan Kettering Cancer Center, New York, NY 10128, USA. Electronic address: schmitta@mskcc.org.
Memorial Sloan Kettering Cancer Center · US

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Nicholas D Socci · 1985 to 2026
$347.4M
Investigating long noncoding RNAs as regulators of the p53 pathway functions.R35GM124909 · NIGMS · SLOAN-KETTERING INST CAN RESEARCH · PI SCHMITT, ADAM · 2017 to 2021
$2.2M
NCI NIH HHS P30 CA008748NIGMS NIH HHS R35 GM124909
6 · The paper itself

Abstract

Many long noncoding RNA (lncRNA) genes exist near cancer-associated loci, yet evidence connecting lncRNA functions to recurrent genetic alterations in cancer are lacking. Here, we report that DINO, the lncRNA transcribed from the cancer-associated DINO/CDKN1A locus, suppresses tumor formation independent of p21, the protein encoded at the locus. Loss of one or two alleles of Dino impairs p53 signaling and apoptosis, resulting in a haplo-insufficient tumor suppressor phenotype in genetically defined mouse models of tumorigenesis. A discrete region of the DINO/CDKN1A locus is recurrently hypermethylated in human cancers, silencing DINO but not CDKN1A, the gene encoding p21. Hypermethylation silences DINO, impairs p53 signaling pathway in trans, and is mutually exclusive with TP53 alterations, indicating that DINO and TP53 comprise a common tumor suppressor module. Therefore, DINO encodes a lncRNA essential for tumor suppression that is recurrently silenced in human cancers as a mechanism to escape p53-dependent tumor suppression.

Indexed as

Genes, Tumor SuppressorAllelesAnimalsApoptosisCell Line, TumorCyclin-Dependent Kinase Inhibitor p21DNA MethylationEpistasis, GeneticGenetic LociGenetic Predisposition to DiseaseHaploinsufficiencyHumansMaleMiceMice, Inbred C57BLMutationCDKN1A protein, humanCyclin-Dependent Kinase Inhibitor p21DINOL lncRNA, humanRNA, Long NoncodingTumor Suppressor Protein p53cancerDINODNA methylationlong noncoding RNAp53tumor suppression

Identifiers

PMID34192538
PMCPMC8287872
OpenAlexW3175222119

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.