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Our mouse models of pulmonary adenocarcinoma are based upon the KP model, in which Cre controls expression of oncogenic Kras G12D and deletion of Trp53 , to which we have added alterations in Dicer1 expression. Cre expression, and thus tumorigenesis, is controlled by infecting mice with viral vectors that express Cre, in either a cell type independent (left panel) or cell type specific (middle and right panels) manner. In all models except KP, expression of Cre also deletes one allele of Dicer1 in those cells. In KPDT-1 mice, we express Cre in Club cells, using an adenoviral vector, and mutate Dicer1 in ATII cells, using a <t>lentiviral</t> vector. In KPDT-2 mice, we reverse these cell types, expressing Cre in ATII cells and mutating Dicer1 in Club cells. Mutation of Dicer1 in a non-tumor bearing cell population accelerates tumor progression and shortens expected survival dramatically in KPDT-1 mice and modestly in KPDT-2 mice.
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Our mouse models of pulmonary adenocarcinoma are based upon the KP model, in which Cre controls expression of oncogenic Kras G12D and deletion of Trp53 , to which we have added alterations in Dicer1 expression. Cre expression, and thus tumorigenesis, is controlled by infecting mice with viral vectors that express Cre, in either a cell type independent (left panel) or cell type specific (middle and right panels) manner. In all models except KP, expression of Cre also deletes one allele of Dicer1 in those cells. In KPDT-1 mice, we express Cre in Club cells, using an adenoviral vector, and mutate Dicer1 in ATII cells, using a <t>lentiviral</t> vector. In KPDT-2 mice, we reverse these cell types, expressing Cre in ATII cells and mutating Dicer1 in Club cells. Mutation of Dicer1 in a non-tumor bearing cell population accelerates tumor progression and shortens expected survival dramatically in KPDT-1 mice and modestly in KPDT-2 mice.
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Our mouse models of pulmonary adenocarcinoma are based upon the KP model, in which Cre controls expression of oncogenic Kras G12D and deletion of Trp53 , to which we have added alterations in Dicer1 expression. Cre expression, and thus tumorigenesis, is controlled by infecting mice with viral vectors that express Cre, in either a cell type independent (left panel) or cell type specific (middle and right panels) manner. In all models except KP, expression of Cre also deletes one allele of Dicer1 in those cells. In KPDT-1 mice, we express Cre in Club cells, using an adenoviral vector, and mutate Dicer1 in ATII cells, using a <t>lentiviral</t> vector. In KPDT-2 mice, we reverse these cell types, expressing Cre in ATII cells and mutating Dicer1 in Club cells. Mutation of Dicer1 in a non-tumor bearing cell population accelerates tumor progression and shortens expected survival dramatically in KPDT-1 mice and modestly in KPDT-2 mice.
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Our mouse models of pulmonary adenocarcinoma are based upon the KP model, in which Cre controls expression of oncogenic Kras G12D and deletion of Trp53 , to which we have added alterations in Dicer1 expression. Cre expression, and thus tumorigenesis, is controlled by infecting mice with viral vectors that express Cre, in either a cell type independent (left panel) or cell type specific (middle and right panels) manner. In all models except KP, expression of Cre also deletes one allele of Dicer1 in those cells. In KPDT-1 mice, we express Cre in Club cells, using an adenoviral vector, and mutate Dicer1 in ATII cells, using a <t>lentiviral</t> vector. In KPDT-2 mice, we reverse these cell types, expressing Cre in ATII cells and mutating Dicer1 in Club cells. Mutation of Dicer1 in a non-tumor bearing cell population accelerates tumor progression and shortens expected survival dramatically in KPDT-1 mice and modestly in KPDT-2 mice.
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Our mouse models of pulmonary adenocarcinoma are based upon the KP model, in which Cre controls expression of oncogenic Kras G12D and deletion of Trp53 , to which we have added alterations in Dicer1 expression. Cre expression, and thus tumorigenesis, is controlled by infecting mice with viral vectors that express Cre, in either a cell type independent (left panel) or cell type specific (middle and right panels) manner. In all models except KP, expression of Cre also deletes one allele of Dicer1 in those cells. In KPDT-1 mice, we express Cre in Club cells, using an adenoviral vector, and mutate Dicer1 in ATII cells, using a <t>lentiviral</t> vector. In KPDT-2 mice, we reverse these cell types, expressing Cre in ATII cells and mutating Dicer1 in Club cells. Mutation of Dicer1 in a non-tumor bearing cell population accelerates tumor progression and shortens expected survival dramatically in KPDT-1 mice and modestly in KPDT-2 mice.
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Our mouse models of pulmonary adenocarcinoma are based upon the KP model, in which Cre controls expression of oncogenic Kras G12D and deletion of Trp53 , to which we have added alterations in Dicer1 expression. Cre expression, and thus tumorigenesis, is controlled by infecting mice with viral vectors that express Cre, in either a cell type independent (left panel) or cell type specific (middle and right panels) manner. In all models except KP, expression of Cre also deletes one allele of Dicer1 in those cells. In KPDT-1 mice, we express Cre in Club cells, using an adenoviral vector, and mutate Dicer1 in ATII cells, using a <t>lentiviral</t> vector. In KPDT-2 mice, we reverse these cell types, expressing Cre in ATII cells and mutating Dicer1 in Club cells. Mutation of Dicer1 in a non-tumor bearing cell population accelerates tumor progression and shortens expected survival dramatically in KPDT-1 mice and modestly in KPDT-2 mice.
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Our mouse models of pulmonary adenocarcinoma are based upon the KP model, in which Cre controls expression of oncogenic Kras G12D and deletion of Trp53 , to which we have added alterations in Dicer1 expression. Cre expression, and thus tumorigenesis, is controlled by infecting mice with viral vectors that express Cre, in either a cell type independent (left panel) or cell type specific (middle and right panels) manner. In all models except KP, expression of Cre also deletes one allele of Dicer1 in those cells. In KPDT-1 mice, we express Cre in Club cells, using an adenoviral vector, and mutate Dicer1 in ATII cells, using a <t>lentiviral</t> vector. In KPDT-2 mice, we reverse these cell types, expressing Cre in ATII cells and mutating Dicer1 in Club cells. Mutation of Dicer1 in a non-tumor bearing cell population accelerates tumor progression and shortens expected survival dramatically in KPDT-1 mice and modestly in KPDT-2 mice.
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Our mouse models of pulmonary adenocarcinoma are based upon the KP model, in which Cre controls expression of oncogenic Kras G12D and deletion of Trp53 , to which we have added alterations in Dicer1 expression. Cre expression, and thus tumorigenesis, is controlled by infecting mice with viral vectors that express Cre, in either a cell type independent (left panel) or cell type specific (middle and right panels) manner. In all models except KP, expression of Cre also deletes one allele of Dicer1 in those cells. In KPDT-1 mice, we express Cre in Club cells, using an adenoviral vector, and mutate Dicer1 in ATII cells, using a <t>lentiviral</t> vector. In KPDT-2 mice, we reverse these cell types, expressing Cre in ATII cells and mutating Dicer1 in Club cells. Mutation of Dicer1 in a non-tumor bearing cell population accelerates tumor progression and shortens expected survival dramatically in KPDT-1 mice and modestly in KPDT-2 mice.
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Our mouse models of pulmonary adenocarcinoma are based upon the KP model, in which Cre controls expression of oncogenic Kras G12D and deletion of Trp53 , to which we have added alterations in Dicer1 expression. Cre expression, and thus tumorigenesis, is controlled by infecting mice with viral vectors that express Cre, in either a cell type independent (left panel) or cell type specific (middle and right panels) manner. In all models except KP, expression of Cre also deletes one allele of Dicer1 in those cells. In KPDT-1 mice, we express Cre in Club cells, using an adenoviral vector, and mutate Dicer1 in ATII cells, using a <t>lentiviral</t> vector. In KPDT-2 mice, we reverse these cell types, expressing Cre in ATII cells and mutating Dicer1 in Club cells. Mutation of Dicer1 in a non-tumor bearing cell population accelerates tumor progression and shortens expected survival dramatically in KPDT-1 mice and modestly in KPDT-2 mice.
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lentiviral packaging plasmid pspax2  (Addgene inc)
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Our mouse models of pulmonary adenocarcinoma are based upon the KP model, in which Cre controls expression of oncogenic Kras G12D and deletion of Trp53 , to which we have added alterations in Dicer1 expression. Cre expression, and thus tumorigenesis, is controlled by infecting mice with viral vectors that express Cre, in either a cell type independent (left panel) or cell type specific (middle and right panels) manner. In all models except KP, expression of Cre also deletes one allele of Dicer1 in those cells. In KPDT-1 mice, we express Cre in Club cells, using an adenoviral vector, and mutate Dicer1 in ATII cells, using a <t>lentiviral</t> vector. In KPDT-2 mice, we reverse these cell types, expressing Cre in ATII cells and mutating Dicer1 in Club cells. Mutation of Dicer1 in a non-tumor bearing cell population accelerates tumor progression and shortens expected survival dramatically in KPDT-1 mice and modestly in KPDT-2 mice.
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Our mouse models of pulmonary adenocarcinoma are based upon the KP model, in which Cre controls expression of oncogenic Kras G12D and deletion of Trp53 , to which we have added alterations in Dicer1 expression. Cre expression, and thus tumorigenesis, is controlled by infecting mice with viral vectors that express Cre, in either a cell type independent (left panel) or cell type specific (middle and right panels) manner. In all models except KP, expression of Cre also deletes one allele of Dicer1 in those cells. In KPDT-1 mice, we express Cre in Club cells, using an adenoviral vector, and mutate Dicer1 in ATII cells, using a lentiviral vector. In KPDT-2 mice, we reverse these cell types, expressing Cre in ATII cells and mutating Dicer1 in Club cells. Mutation of Dicer1 in a non-tumor bearing cell population accelerates tumor progression and shortens expected survival dramatically in KPDT-1 mice and modestly in KPDT-2 mice.

Journal: bioRxiv

Article Title: Cell-type Specific Alteration of Dicer1 Accelerates Tumor Progression in Mouse Models of KRAS-driven Lung Adenocarcinoma

doi: 10.64898/2026.05.29.728740

Figure Lengend Snippet: Our mouse models of pulmonary adenocarcinoma are based upon the KP model, in which Cre controls expression of oncogenic Kras G12D and deletion of Trp53 , to which we have added alterations in Dicer1 expression. Cre expression, and thus tumorigenesis, is controlled by infecting mice with viral vectors that express Cre, in either a cell type independent (left panel) or cell type specific (middle and right panels) manner. In all models except KP, expression of Cre also deletes one allele of Dicer1 in those cells. In KPDT-1 mice, we express Cre in Club cells, using an adenoviral vector, and mutate Dicer1 in ATII cells, using a lentiviral vector. In KPDT-2 mice, we reverse these cell types, expressing Cre in ATII cells and mutating Dicer1 in Club cells. Mutation of Dicer1 in a non-tumor bearing cell population accelerates tumor progression and shortens expected survival dramatically in KPDT-1 mice and modestly in KPDT-2 mice.

Article Snippet: For PCR reactions, DNA from mouse strain 006225 (JAX, Bar Harbor, ME) was used to generate an hSPC promoter fragment and from strain 000664 (JAX, Bar Harbor, ME) to generate a mCC10 promoter fragment. pLEX307-iCre was created by inserting the iCre ORF downstream of the EF1 promoter in plasmid pLEX_307 (Addgene #41392, Watertown, MA) Lentiviral packaging was performed in human 293T/17 cells (ATCC CRL-11268, Manassas, VA) cells using packaging plasmids obtained from Addgene (pMD2.g, Addgene #12259; pMDLg/pRRE, Addgene #12251; pRSV-Rev, Addgene #12253).

Techniques: Expressing, Plasmid Preparation, Mutagenesis