Tg(tetO/CMV-KRAS*G12C)9.1Msmi Transgene Detail MGI Mouse (MGI:3693226)

Tg(tetO/CMV-KRAS*G12C)9.1Msmi
Transgene Detail

Nomenclature

Symbol:	Tg(tetO/CMV-KRAS*G12C)9.1Msmi
Name:	transgene insertion 9.1, Mark Miller
MGI ID:	MGI:3693226
Synonyms:	Ki-ras^G12C
Transgene:	Tg(tetO/CMV-KRAS*G12C)9.1Msmi Location: unknown

Transgene
origin

Strain of Origin:

FVB/NTac

Transgene
description

Transgene Type:	Transgenic (random, expressed)
Mutation:	Insertion
	A genomic segment including the KRAS^G12C mutation was cloned from the H358 human lung bronchioalveolar cell line and placed under the regulation of a tetracycline-inducible (tetO)/cytomegalovirus (CMV) promoter. Copy number is estimated at 22. (J:102839)

Find Mice (IMSR)

Mouse strains and cell lines available from the International Mouse Strain Resource (IMSR)

Carrying this Mutation:

Mouse Strains: 1 strain available Cell Lines: 0 lines available

Phenotype
summary

Phenotype Summary by Mammalian Phenotype terms

(show or hide all annotated terms)

Genotypes are listed in the next section.

Key:

hm	homozygous	ht	heterozygous
cn	conditional genotype	cx	complex: > 1 genome feature
tg	involves transgenes	ot	other: hemizygous, indeterminate,...
N	normal phenotype		expected model not found

Affected Systems	Genotypes:	tg1	tg2
respiratory system		√	√
abnormal lung morphology		√	√
abnormal respiratory alveolar epithelial cell morphology		√	√
abnormal respiratory system physiology		√
abnormal surfactant physiology		√
		tg1	tg2
tumorigenesis		√	√
increased tumor incidence		√	√
lung adenoma		√	√
lung adenocarcinoma			√

Phenotypic
data by
genotype

Phenotypic Data by Genotype

(show or hide all phenotypic details)

Genotype	Allelic Composition	Genetic Background
tg1	Tg(SFTPC-rtTA)5Jaw/0 Tg(tetO/CMV-KRAS*G12C)9.1Msmi/0	involves: FVB/N
respiratory system abnormal lung morphology (J:102839) after 12 days of doxycycline (DOX) treatement, small, hyperplastic lung foci are detected; untreated mice have normal lungs abnormal respiratory alveolar epithelial cell morphology (J:102839) after 5 weeks of DOX treatment, extensive epithelial hyperplasia of alveolar region of lung is observed; untreated mice have normal lungs abnormal respiratory system physiology (J:102839) abnormal surfactant physiology (J:102839) alveolar lipoproteinosis is regularly found, indicating abnormal surfactant metabolism tumorigenesis increased tumor incidence (J:102839) after 3 months treatment, visible macroscopic lesions are found; tumor incidence at 3 months is 55%, with multiplicity of 1.7 tumors/mouse lesions are <1mm in size early hyperplastic lesions are of alveologenic origin at 6 and 9 months DOX treatment, visible lesions increase in number; multiplicity is 10.2 and 12.5 tumors/mouse after 9 and 12 months, lower than Scgb1a1/KRAS bitransgenic mice; treated monotransgenic mice show no incidence when DOX treatment was stopped after 9 months, within 2 weeks only 4 tumors are visible on lung surface and by 1 month, no tumors are visible, and with minimal hyperplastic foci microscopically detectable, showing no proliferation (or apoptosis) lung adenoma (J:102839)
Genotype	Allelic Composition	Genetic Background
tg2	Tg(Scgb1a1-rtTA)1Jaw/0 Tg(tetO/CMV-KRAS*G12C)9.1Msmi/0	involves: FVB/N
respiratory system abnormal lung morphology (J:102839) after 12 days of doxycycline (DOX) treatement, small, hyperplastic lung foci are detected; untreated mice have normal lungs abnormal respiratory alveolar epithelial cell morphology (J:102839) after 5 weeks of DOX treatment, extensive epithelial hyperplasia of alveolar region of lung is observed; untreated mice have normal lungs tumorigenesis increased tumor incidence (J:102839) after 3 months treatment, visible macroscopic lesions are found; tumor incidence at 3 months is 55%, with multiplicity of 3.5 tumors/mouse lesions are <1mm in size early hyperplastic lesions are of bronchiolar origin at 6 and 9 months DOX treatment, visible lesions increase in number; multiplicity is 28.8 and 34 tumors/mouse after 9 and 12 months, higher than SFTPC/KRAS bitransgenic mice; treated monotransgenic mice show no tumor incidence when DOX treatment was stopped after 9 months, within 2 weeks only 4 tumors are visible on lung surface; these remain after 1 months; minimal hyperplastic foci microscopically are detectable, showing no proliferation (or apoptosis) lung adenoma (J:102839) single adenoma was detected at 3 months; at 6, 9, and 12 months of treatment, incidence increases; mice develop higher incidence of proliferative changes with lower latency than SFTPC/KRAS mice lung adenocarcinoma (J:102839) at 12 months of treatment, 2 adenomas have progressed to low grade carcinomas

References

Original:	J:102839 Floyd HS et al., "Conditional expression of the mutant Ki-rasG12C allele results in formation of benign lung adenomas: development of a novel mouse lung tumor model." Carcinogenesis 2005 Dec;26(12):2196-206
All:	4 reference(s)

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