Evidence map›Paper›PMID 42249018›Full record

ArticleCancer gene therapy2026

TP53 mutation at codon 179 metabolically reprograms cancer cells to promote invasion.

Debina Sarkar, Gaurav C Gyanwali, Jaishree Patel, Polina Shevchuk, Aaron Jeffs, Adele G Woolley, Selena Wang, Maryam Sardari, Apeksha Bhandarkar, Halima Siddiqui and 10 more

Abstract read
In one paragraph

Article in Cancer gene therapy, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

20 authors.

Debina Sarkar *Department of Pathology and Molecular Medicine, University of Otago, Dunedin, New Zealand.ORCID http://orcid.org/0000-0002-6734-8875
Gaurav C Gyanwali *Department of Pathology and Molecular Medicine, University of Otago, Dunedin, New Zealand.ORCID http://orcid.org/0000-0003-4414-9272
Jaishree PatelDepartment of Pathology and Molecular Medicine, University of Otago, Dunedin, New Zealand.
Polina ShevchukDepartment of Pathology and Molecular Medicine, University of Otago, Dunedin, New Zealand.ORCID http://orcid.org/0009-0009-2747-009X
Aaron JeffsDepartment of Pathology and Molecular Medicine, University of Otago, Dunedin, New Zealand.
Adele G WoolleyDepartment of Pathology and Molecular Medicine, University of Otago, Dunedin, New Zealand.ORCID http://orcid.org/0000-0003-1372-5281
Selena WangDepartment of Pathology and Molecular Medicine, University of Otago, Dunedin, New Zealand.
Maryam SardariDepartment of Pathology and Molecular Medicine, University of Otago, Dunedin, New Zealand.
Apeksha BhandarkarDepartment of Pathology and Molecular Medicine, University of Otago, Dunedin, New Zealand.
Halima SiddiquiMaurice Wilkins Centre for Biodiscovery, Auckland, New Zealand.
Magdalena RatajskaDepartment of Pathology and Molecular Medicine, University of Otago, Dunedin, New Zealand.
Makhdoom SarwarMaurice Wilkins Centre for Biodiscovery, Auckland, New Zealand.
Srinivasaraghavan KannanBioinformatics Institute, Agency for Science, Technology and Research (A*STAR), Singapore, Singapore.ORCID http://orcid.org/0000-0002-9539-5249
Chandra S VermaBioinformatics Institute, Agency for Science, Technology and Research (A*STAR), Singapore, Singapore.
Catherine J DrummondDepartment of Pathology and Molecular Medicine, University of Otago, Dunedin, New Zealand.
Cushla McKinneyDepartment of Pathology and Molecular Medicine, University of Otago, Dunedin, New Zealand.ORCID http://orcid.org/0000-0002-7051-6876
Jisha AntonyDepartment of Pathology and Molecular Medicine, University of Otago, Dunedin, New Zealand.
Sally P McCormickMaurice Wilkins Centre for Biodiscovery, Auckland, New Zealand.
Antony BraithwaiteDepartment of Pathology and Molecular Medicine, University of Otago, Dunedin, New Zealand.ORCID http://orcid.org/0000-0002-8671-5036
Sunali MehtaDepartment of Pathology and Molecular Medicine, University of Otago, Dunedin, New Zealand. sunali.mehta@otago.ac.nz.ORCID http://orcid.org/0000-0002-1777-1245

Funding

Cancer Research Trust New Zealand CRTNZ 2012Manatu Hauora | Health Research Council of New Zealand (HRC) 20/638Manatu Hauora | Health Research Council of New Zealand (HRC) 21/030
6 · The paper itself

Abstract

Mutations in the tumour suppressor, TP53, are prevalent in human cancers yet their functional implications remain unclear. Through comprehensive pan-cancer database analysis, we identified H179 mutations in TP53 as significantly associated with poor disease-free survival across multiple cancer types. Functional studies in lung, ovarian, and prostate cancer cells over-expressing the p53

Indexed as

CodonMutationNeoplasmsTumor Suppressor Protein p53AnimalsCell Line, TumorHumansMetabolic ReprogrammingNeoplasm InvasivenessCodonTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID42249018
PMCPMC13461375

What OpenQuestion holds

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LicenceCC BY
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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.