scholarly journals Establishment and characterization of MRT cell lines from genetically engineered mouse models and the influence of genetic background on their development

2012 ◽  
Vol 132 (12) ◽  
pp. 2767-2777 ◽  
Author(s):  
Yasumichi Kuwahara ◽  
E. Lorena Mora-Blanco ◽  
Fatima Banine ◽  
Arlin B. Rogers ◽  
Christopher Fletcher ◽  
...  
Keyword(s):  
Mouse Models ◽  
Cell Lines ◽  
Genetic Background ◽  
Genetically Engineered ◽  
Genetically Engineered Mouse Models

scholarly journals 804 Characterization of amelanotic melanomas from genetically-engineered mouse models

2019 ◽  
Vol 139 (5) ◽  
pp. S139
Author(s):  
S.R. Florell ◽  
F. Clayton ◽  
H. Rahman ◽  
S. Holmen ◽  
C. Burd ◽  
...  
Keyword(s):  
Mouse Models ◽  
Genetically Engineered ◽  
Genetically Engineered Mouse Models

scholarly journals Possible pitfalls investigating cell death responses in genetically engineered mouse models and derived cell lines

Methods ◽  
2013 ◽  
Vol 61 (2) ◽  
pp. 130-137 ◽  
Author(s):  
Claudia Manzl ◽  
Florian Baumgartner ◽  
Lukas Peintner ◽  
Fabian Schuler ◽  
Andreas Villunger
Keyword(s):  
Cell Death ◽  
Mouse Models ◽  
Cell Lines ◽  
Genetically Engineered ◽  
Genetically Engineered Mouse Models

scholarly journals Characterization of genetically engineered mouse models carrying Col2a1-cre-induced deletions of Lrp5 and/or Lrp6

Bone Research ◽  
2016 ◽  
Vol 4 (1) ◽  
Author(s):  
Cassie A Schumacher ◽  
Danese M Joiner ◽  
Kennen D Less ◽  
Melissa Oosterhouse Drewry ◽  
Bart O Williams
Keyword(s):  
Mouse Models ◽  
Genetically Engineered ◽  
Genetically Engineered Mouse Models

scholarly journals DIPG-41. DISSECTING THE MECHANISTIC BASIS FOR ACVR1 AND PIK3CA MUTATION CO-OCCURRENCE IN DIFFUSE MIDLINE GLIOMAS USING GENETICALLY ENGINEERED MOUSE MODELS

2020 ◽  
Vol 22 (Supplement_3) ◽  
pp. iii295-iii295
Author(s):  
Annette Wu ◽  
Tak Mak ◽  
Jerome Fortin
Keyword(s):  
Mouse Models ◽  
Pik3ca Mutation ◽  
Cell Lineage ◽  
Gene Expression Signature ◽  
Genetically Engineered ◽  
Genetically Engineered Mouse Models ◽  
Dismal Prognosis ◽  
Human Pathology ◽  
Genes Encoding ◽  
Mechanistic Basis

Abstract Diffuse midline gliomas (DMGs) are aggressive childhood brain tumors with a dismal prognosis. Most of these tumors carry K27M mutations in histone H3-encoding genes, particularly H3F3A and HIST1H3B. In addition, activating mutations in ACVR1 and PIK3CA co-occur in a subset of DMGs. To understand how these lesions drive the development of DMGs, we generated genetically engineered mouse models in which Acvr1G328V, Hist1h3bK27M, and Pik3caH1047R are targeted to the OLIG2-expressing cell lineage. Animals carrying Acvr1G328V and Pik3caH1047R, with (“AHPO”) or without (“APO”) Hist1h3bK27M, developed high-grade diffuse gliomas involving midline and forebrain regions. Neither Acvr1G328V nor Pik3caH1047R drove tumorigenesis by themselves, but Acvr1G328V was sufficient to cause oligodendroglial differentiation arrest, pointing to a role in the earliest stages of gliomas formation. Transcriptomic analyses of AHPO and APO tumors indicated a predominantly proneural and oligodendrocyte precursor-like gene expression signature, consistent with the corresponding human pathology. Genes encoding transcription factors (TFs) with dual roles in controlling glial and neuronal differentiation were upregulated in tumors. Some of these genes were mildly induced by Acvr1G328V alone. Functional experiments using CRISPR/Cas9-mediated gene editing in patient-derived cell lines confirmed a role for some of these TFs in controlling DMG cell fitness. Overall, our results suggest that Pik3caH1047R consolidates Acvr1G328V-induced glial differentiation arrest to drive DMG development and progression.

scholarly journals Mutational landscape of EGFR-, MYC-, and Kras-driven genetically engineered mouse models of lung adenocarcinoma

2016 ◽  
Vol 113 (42) ◽  
pp. E6409-E6417 ◽  
Author(s):  
David G. McFadden ◽  
Katerina Politi ◽  
Arjun Bhutkar ◽  
Frances K. Chen ◽  
Xiaoling Song ◽  
...  
Keyword(s):  
Lung Adenocarcinoma ◽  
Mouse Models ◽  
Cancer Progression ◽  
Large Scale ◽  
Human Cancer ◽  
Genetically Engineered ◽  
Model Systems ◽  
Driver Mutations ◽  
Genetic Profile ◽  
Genetically Engineered Mouse Models

Genetically engineered mouse models (GEMMs) of cancer are increasingly being used to assess putative driver mutations identified by large-scale sequencing of human cancer genomes. To accurately interpret experiments that introduce additional mutations, an understanding of the somatic genetic profile and evolution of GEMM tumors is necessary. Here, we performed whole-exome sequencing of tumors from three GEMMs of lung adenocarcinoma driven by mutant epidermal growth factor receptor (EGFR), mutant Kirsten rat sarcoma viral oncogene homolog (Kras), or overexpression of MYC proto-oncogene. Tumors from EGFR- and Kras-driven models exhibited, respectively, 0.02 and 0.07 nonsynonymous mutations per megabase, a dramatically lower average mutational frequency than observed in human lung adenocarcinomas. Tumors from models driven by strong cancer drivers (mutant EGFR and Kras) harbored few mutations in known cancer genes, whereas tumors driven by MYC, a weaker initiating oncogene in the murine lung, acquired recurrent clonal oncogenic Kras mutations. In addition, although EGFR- and Kras-driven models both exhibited recurrent whole-chromosome DNA copy number alterations, the specific chromosomes altered by gain or loss were different in each model. These data demonstrate that GEMM tumors exhibit relatively simple somatic genotypes compared with human cancers of a similar type, making these autochthonous model systems useful for additive engineering approaches to assess the potential of novel mutations on tumorigenesis, cancer progression, and drug sensitivity.

Genetically Engineered Mouse Models of Esophageal Cancer

2021 ◽  
pp. 112757
Author(s):  
Reihaneh Alsadat Mahmoudian ◽  
Moein Farshchian ◽  
Mohammad Reza Abbaszadegan
Keyword(s):  
Esophageal Cancer ◽  
Mouse Models ◽  
Genetically Engineered ◽  
Genetically Engineered Mouse Models
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