ArticleCancer research2015
TP53 Silencing Bypasses Growth Arrest of BRAFV600E-Induced Lung Tumor Cells in a Two-Switch Model of Lung Tumorigenesis.
Article in Cancer research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 22 citations in OpenAlex.
- Preclinical Modeling of Pathway-Targeted Therapy of Human Lung Cancer in the Mouse.Cold Spring Harbor perspectives in medicine · 2024Review
- Oncogenic context shapes the fitness landscape of tumor suppression.Nature communications · 2023Article
- Tissue specificity of oncogenic BRAF targeted to lung and thyroid through a shared lineage factor.iScience · 2023Article
- FoxA1 and FoxA2 control growth and cellular identity in NKX2-1-positive lung adenocarcinoma.Developmental cell · 2022Article
- Early differential responses elicited by BRAFCell death & disease · 2022Article
- Article
- Mutationally-activated PI3'-kinase-α promotes de-differentiation of lung tumors initiated by the BRAFeLife · 2019Article
- A Transgenic MMTV-Flippase Mouse Line for Molecular Engineering in Mammary Gland and Breast Cancer Mouse Models.Journal of mammary gland biology and neoplasia · 2019Article
- p53 loss does not permit escape from BrafOncogene · 2017Article
- TFAP2C promotes lung tumorigenesis and aggressiveness through miR-183- and miR-33a-mediated cell cycle regulation.Oncogene · 2017Article
- Context-Dependent Effects of Amplified MAPK Signaling during Lung Adenocarcinoma Initiation and Progression.Cell reports · 2017Article
- The Regulation of Cellular Functions by the p53 Protein: Cellular Senescence.Cold Spring Harbor perspectives in medicine · 2017Review
- Nucleolus-derived mediators in oncogenic stress response and activation of p53-dependent pathways.Histochemistry and cell biology · 2016Review
- The generation and characterization of novel Col1a1FRT-Cre-ER-T2-FRT and Col1a1FRT-STOP-FRT-Cre-ER-T2 mice for sequential mutagenesis.Disease models & mechanisms · 2015Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Lung carcinogenesis is a multistep process in which normal lung epithelial cells are converted to cancer cells through the sequential acquisition of multiple genetic or epigenetic events. Despite the utility of current genetically engineered mouse (GEM) models of lung cancer, most do not allow temporal dissociation of the cardinal events involved in lung tumor initiation and cancer progression. Here we describe a novel two-switch GEM model for BRAF(V600E)-induced lung carcinogenesis allowing temporal dissociation of these processes. In mice carrying a Flp recombinase-activated allele of Braf (Braf(FA)) in conjunction with Cre-regulated alleles of Trp53, Cdkn2a, or c-MYC, we demonstrate that secondary genetic events can promote bypass of the senescence-like proliferative arrest displayed by BRAF(V600E)-induced lung adenomas, leading to malignant progression. Moreover, restoring or activating TP53 in cultured BRAF(V600E)/TP53(Null) or BRAF(V600E)/INK4A-ARF(Null) lung cancer cells triggered a G1 cell-cycle arrest regardless of p19(ARF) status. Perhaps surprisingly, neither senescence nor apoptosis was observed upon TP53 restoration. Our results establish a central function for the TP53 pathway in restricting lung cancer development, highlighting the mechanisms that limit malignant progression of BRAF(V600E)-initiated tumors.
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