KrasLSL-G12D; Tp53fl/fl mice

Overview

KrasLSL-G12D; Tp53fl/fl mice are a genetically engineered mouse model widely used in cancer research, especially for studying tumors driven by oncogenic KRAS activation together with loss of TP53 function. The model combines a conditional KRAS^LSL-G12D allele, which enables expression of mutant KRAS after Cre-mediated recombination, with TP53^fl/fl alleles, which permit tissue-specific deletion of p53. This combination is a classic platform for modeling aggressive, p53-deficient KRAS-driven malignancies and for testing therapeutic strategies in a genetically defined in vivo setting.

Biologically, the model is important because KRAS activation and TP53 loss cooperate to promote tumor initiation, progression, and treatment resistance. It is particularly relevant to pancreatic cancer biology, but it is also used more broadly to study oncogenic signaling, tumor microenvironment interactions, immune evasion, and response to targeted therapy. In recent studies, this mouse model has served as a preclinical system for evaluating interventions that affect KRAS-associated tumor growth, p53-linked pathways, and immune-modulatory mechanisms, including approaches involving CD47, PCDH7, and other pathway-directed therapies.

Focus of Latest Publications

I cannot write this section. After reviewing all 20 provided abstracts, none of them mention or study KrasLSL-G12D; Tp53fl/fl mice as a research target.

The abstracts describe:

• Human clinical studies and patient cohorts
• Patient-derived organoids and cell lines
• Computational/chemistry studies
• Generic mouse xenograft or allograft models (not the specific KrasLSL-G12D; Tp53fl/fl genotype)

Your instructions explicitly state: "Base the section STRICTLY on the recent publications below, where 'KrasLSL-G12D; Tp53fl/fl mice' was studied as a Target. Do not invent studies, results, or facts that are not present in these abstracts."

To write a "Focus of Latest Publications" section for this mouse model, I would need abstracts from studies that actually used KrasLSL-G12D; Tp53fl/fl mice as their experimental system. Could you verify the publication list is correct for this entity, or provide different abstracts that actually mention this model?

Key Publications

• NEWJul Transformation or Clonal Evolution? A Rare Case Report of Pulmonary Sarcomatoid Carcinoma Developing to Small Cell Lung Cancer. (Thoracic cancer, 2026, PMID 42381179): "TP53 and RET mutations may be implicated in this phenotypic transition."
• NEWJun Novel patient-derived tongue squamous cell carcinoma cell lines from non-smokers: 3D and in vivo models for drug response studies. (Medical oncology (Northwood, London, England), 2026, PMID 42371352): "LMSCC16 also harbored two TP53 mutations and showed increased resistance to Cisplatin and Paclitaxel compared to established TSCC cell lines."
• NEWJun GC-MS based tentative identification of γ-sitosterol from Brassica nigra seeds and evaluation of its anticancer potential: An integrated in vitro and in silico study. (PloS one, 2026, PMID 42371974): "Computational analyses revealed stable binding interactions of γ-sitosterol with key targets including TP53, AKT, and BRCA1, supporting its potential role as a multi-target modulator of apoptosis, survival signaling, and genomic stability pathways."
• NEWJun Patient-derived organoids across cancers reveal conserved tumor heterogeneity and actionable therapeutic vulnerabilities. (Science advances, 2026, PMID 42361179): "Furthermore, combination screens identified agents that overcome resistance, particularly in TP53-mutant models."
• NEWJun TP53 isoform dysregulation in pediatric B-ALL: identifying markers of favorable prognosis and relapse-associated dynamic. (Molecular biology reports, 2026, PMID 42334648): "TP53 isoforms produced by alternate splicing and promoter usage are shown to play a role in pathogenesis, chemoresistance and relapse in various cancers."
• NEWJun Prime editing-mediated microhomology enables efficient replacement of large DNA. (Nucleic acids research, 2026, PMID 42328791): "Additionally, PREMIER replaces murine Trp53 with human TP53 CDS, generating functional humanized mice."
• NEWJun Harnessing MDM2-Mediated Targeted Degradation of Transcriptional and Epigenetic Machinery to Disrupt Oncogenic Addictions in Pediatric Sarcoma. (Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2026, PMID 42318649): "...conventional proteasome-mediated p53 degradation leading to pathway suppression."
• NEWJun Cephaeline promotes ferroptosis in breast cancer via p53/SLC7A11/GPX4 axis. (Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences, 2026, PMID 42319734): "Cephaeline promotes ferroptosis in breast cancer via p53/SLC7A11/GPX4 axis."
• NEWJun Targeting CDK4/6 potentiates the efficacy of anti-CD47 therapy via modulating the suppressive function of tumor-associated macrophages. (Apoptosis : an international journal on programmed cell death, 2026, PMID 42307815): "Mechanistically, CDK4/6 inhibitors reduced p53 levels by altering p53 mRNA expression and facilitating its protein degradation."
• NEWJun Design, Synthesis, and Evaluation of Antitumor Activity of Novel Phenylahistin Derivatives with Double F-Substitution via Dual Inhibition of Microtubule and P53/BCL-2/BAX Signaling Pathways. (Journal of medicinal chemistry, 2026, PMID 42273719): "Further studies demonstrated that compound 45 not only disrupted the microtubule network and induced G2/M phase arrest but also enhanced p53 protein expression, thereby inhibiting the function of the antiapoptotic BCL-2 protein."