Evidence map›Paper›PMID 35589715›Full record

ArticleNature communications2022

Different hotspot p53 mutants exert distinct phenotypes and predict outcome of colorectal cancer patients.

Ori Hassin, Nishanth Belugali Nataraj, Michal Shreberk-Shaked, Yael Aylon, Rona Yaeger, Giulia Fontemaggi, Saptaparna Mukherjee, Martino Maddalena, Adi Avioz, Ortal Iancu and 11 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed, 2 pooled it
9.9field-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

68 citing papers in PubMed, 2 syntheses or guidelines pooled it, 97 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Revisiting tumor immunogenicity through the lens of mutant p53: Implications for cancer immunotherapy.Apoptosis : an international journal on programmed cell death · 2026
    Review
  5. Programmable ZBTB7A RNA NMolecular cancer · 2026
    Article
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  20. Rapid Exploratory Data Visualization for Cancer Genomics.Methods in molecular biology (Clifton, N.J.) · 2026
    Article

8 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

21 authors at 3 institutions in 2 countries.

Ori HassinDepartment of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel.ORCID http://orcid.org/0000-0002-4959-9662
Nishanth Belugali NatarajDepartment of Biological Regulation, Weizmann Institute of Science, Rehovot, Israel.ORCID http://orcid.org/0000-0003-2970-6739
Michal Shreberk-ShakedDepartment of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel.
Yael AylonDepartment of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel.ORCID http://orcid.org/0000-0001-5821-9548
Rona YaegerDepartment of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Giulia FontemaggiOncogenomic and Epigenetic Unit, IRCCS Regina Elena National Cancer Institute, Rome, Italy.ORCID http://orcid.org/0000-0001-8332-8842
Saptaparna MukherjeeDepartment of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel.
Martino MaddalenaDepartment of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel.
Adi AviozDepartment of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel.
Ortal IancuThe Institute for Advanced Materials and Nanotechnology, The Mina and Everard Goodman Faculty of Life Sciences, Bar-Ilan University, Ramat-Gan, Israel.
Giuseppe MallelPathology Department, Curesponse Ltd, Rehovot, Israel.ORCID http://orcid.org/0000-0002-8673-7526
Anat GershoniDepartment of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel.
Inna GroshevaDepartment of Immunology, Weizmann Institute of Science, Rehovot, Israel.
Ester FeldmesserDepartment of Life Sciences Core Facilities, Weizmann Institute of Science, Rehovot, Israel.ORCID http://orcid.org/0000-0002-7017-4861
Shifra Ben-DorDepartment of Life Sciences Core Facilities, Weizmann Institute of Science, Rehovot, Israel.ORCID http://orcid.org/0000-0001-9604-1939
Ofra GolaniDepartment of Life Sciences Core Facilities, Weizmann Institute of Science, Rehovot, Israel.ORCID http://orcid.org/0000-0002-9793-236X
Ayal HendelThe Institute for Advanced Materials and Nanotechnology, The Mina and Everard Goodman Faculty of Life Sciences, Bar-Ilan University, Ramat-Gan, Israel.ORCID http://orcid.org/0000-0002-3388-6202
Giovanni BlandinoOncogenomic and Epigenetic Unit, IRCCS Regina Elena National Cancer Institute, Rome, Italy.
David KelsenDepartment of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY, USA.ORCID http://orcid.org/0000-0001-6139-438X
Yosef YardenDepartment of Biological Regulation, Weizmann Institute of Science, Rehovot, Israel.ORCID http://orcid.org/0000-0003-4168-7884
Moshe OrenDepartment of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel. moshe.oren@weizmann.ac.il.ORCID http://orcid.org/0000-0003-4311-7172
Weizmann Institute of Science · ILBar-Ilan University · ILMemorial 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
NCI NIH HHS P30 CA008748
6 · The paper itself

Abstract

The TP53 gene is mutated in approximately 60% of all colorectal cancer (CRC) cases. Over 20% of all TP53-mutated CRC tumors carry missense mutations at position R175 or R273. Here we report that CRC tumors harboring R273 mutations are more prone to progress to metastatic disease, with decreased survival, than those with R175 mutations. We identify a distinct transcriptional signature orchestrated by p53R273H, implicating activation of oncogenic signaling pathways and predicting worse outcome. These features are shared also with the hotspot mutants p53R248Q and p53R248W. p53R273H selectively promotes rapid CRC cell spreading, migration, invasion and metastasis. The transcriptional output of p53R273H is associated with preferential binding to regulatory elements of R273 signature genes. Thus, different TP53 missense mutations contribute differently to cancer progression. Elucidation of the differential impact of distinct TP53 mutations on disease features may make TP53 mutational information more actionable, holding potential for better precision-based medicine.

Indexed as

Colorectal NeoplasmsTumor Suppressor Protein p53Genes, p53HumansMutationPhenotypeTumor Suppressor Protein p53

Identifiers

PMID35589715
PMCPMC9120190
OpenAlexW4280559744

What OpenQuestion holds

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Registered trials

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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.