Detection of a novel, primate-specific 'kill switch' tumor suppression mechanism that may fundamentally control cancer risk in humans: an unexpected twist in the basic biology of TP53.

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.

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.

Who cites it

7 citing papers in PubMed, 11 citations in OpenAlex.

1. Medicinal plants: nutritional, immunological and therapeutic role in treating cancer-related malnutrition: a comprehensive review.Cancer cell international · 2025
   Review
2. A mathematically rigorous algorithm to define, compute and assess relevance of the probable dissociation constants in characterizing a biochemical network.Scientific reports · 2024
   Article
3. A lex naturalis delineates components of a human-specific, adrenal androgen-dependent, p53-mediated 'kill switch' tumor suppression mechanism.Endocrine-related cancer · 2020
   Review
4. Can postfertile life stages evolve as an anticancer mechanism?PLoS biology · 2019
   Article
5. Bioinformatics and functional analyses of key genes in smoking-associated lung adenocarcinoma.Oncology letters · 2019
   Article
6. Species-specific mechanisms of tumor suppression are fundamental drivers of vertebrate speciation: critical implications for the 'war on cancer'.Endocrine-related cancer · 2019
   Article
7. Components of the human-specific, p53-mediated "kill switch" tumor suppression mechanism are usurped by human tumors, creating the possibility of therapeutic exploitation.Cancer drug resistance (Alhambra, Calif.) · 2019
   Article

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

Authors and funding

1 author.

Funding

No grant is acknowledged in the PubMed record.

Abstract

Indexed as