ArticleNature communications2016
Clonal dynamics following p53 loss of heterozygosity in Kras-driven cancers.
Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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
48 citing papers in PubMed, 74 citations in OpenAlex.
- Diet-Induced Phospholipid Remodeling Dictates Ferroptosis Sensitivity and Tumorigenesis in the Pancreas.Cancer discovery · 2026Article
- The sleeping threat: targeting cancer dormancy to transform metastasis therapy.Nature reviews. Cancer · 2026Review
- Article
- Beta cell-derived cholecystokinin drives obesity-associated pancreatic adenocarcinoma development.Nature communications · 2026Article
- Tracing the evolution of single-cell 3D genomes in Kras-driven cancers.Nature genetics · 2025Article
- Mapping lung cancer ventilation dynamics using functional imaging and lung mechanics.Disease models & mechanisms · 2025Article
- Coexistence of P53 and KRAS mutations enhances ERK1/2 signaling by inducing EGR1 expression through mutp53 and c-JUN interaction.Oncogene · 2025Article
- FGFR2 Abrogation Intercepts Pancreatic Ductal Adenocarcinoma Development.Cancer research · 2025Article
- A comprehensive single-cell breast tumor atlas defines epithelial and immune heterogeneity and interactions predicting anti-PD-1 therapy response.Cell reports. Medicine · 2024Article
- Article
- A genetic mosaic mouse model illuminates the pre-malignant progression of basal-like breast cancer.Disease models & mechanisms · 2023Article
- Decoding the obesity-cancer connection: lessons from preclinical models of pancreatic adenocarcinoma.Life science alliance · 2023Review
- Article
- Reprogramming of tissue metabolism during cancer metastasis.Trends in cancer · 2023Review
- Skip to the end: metastasis before tumorigenesis.Nature genetics · 2022Article
- NF1 loss of function as an alternative initiating event in pancreatic ductal adenocarcinoma.Cell reports · 2022Article
- ZFP281 drives a mesenchymal-like dormancy program in early disseminated breast cancer cells that prevents metastatic outgrowth in the lung.Nature cancer · 2022Article
- Review
- Interplays of glucose metabolism and KRAS mutation in pancreatic ductal adenocarcinoma.Cell death & disease · 2022Review
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Although it has become increasingly clear that cancers display extensive cellular heterogeneity, the spatial growth dynamics of genetically distinct clones within developing solid tumours remain poorly understood. Here we leverage mosaic analysis with double markers (MADM) to trace subclonal populations retaining or lacking p53 within oncogenic Kras-initiated lung and pancreatic tumours. In both models, p53 constrains progression to advanced adenocarcinomas. Comparison of lineage-related p53 knockout and wild-type clones reveals a minor role of p53 in suppressing cell expansion in lung adenomas. In contrast, p53 loss promotes both the initiation and expansion of low-grade pancreatic intraepithelial neoplasia (PanINs), likely through differential expression of the p53 regulator p19ARF. Strikingly, lineage-related cells are often dispersed in lung adenomas and PanINs, contrasting with more contiguous growth of advanced subclones. Together, these results support cancer type-specific suppressive roles of p53 in early tumour progression and offer insights into clonal growth patterns during tumour development.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.