About   Help   FAQ
Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Gt(ROSA)26Sortm1(CAG-MYCN,-luc)Jhsc
targeted mutation 1, Johannes H Schulte
MGI:6196127
Summary 4 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
cn1
Gt(ROSA)26Sortm1(CAG-MYCN,-luc)Jhsc/Gt(ROSA)26Sor+
Ptentm2.1Ppp/Ptentm2.1Ppp
Rb1tm2Brn/Rb1tm2Brn
Tg(Pbsn-cre)4Prb/0
involves: 129 * 129S1/Sv * 129S6/SvEvTac * C57BL/6 * DBA/2 MGI:7277819
cn2
Gt(ROSA)26Sortm1(CAG-MYCN,-luc)Jhsc/Gt(ROSA)26Sor+
Ptentm2.1Ppp/Ptentm2.1Ppp
Rb1tm2Brn/Rb1+
Tg(Pbsn-cre)4Prb/0
involves: 129 * 129S1/Sv * 129S6/SvEvTac * C57BL/6 * DBA/2 MGI:7277820
cn3
Gt(ROSA)26Sortm1(CAG-MYCN,-luc)Jhsc/Gt(ROSA)26Sor+
Ptentm2.1Ppp/Ptentm2.1Ppp
Tg(Pbsn-cre)4Prb/0
involves: 129 * 129S1/Sv * 129S6/SvEvTac * C57BL/6 * DBA/2 MGI:7277821
cn4
Gt(ROSA)26Sortm1(CAG-MYCN,-luc)Jhsc/Gt(ROSA)26Sor+
Tg(Dbh-icre)1Gsc/0
involves: 129S6/SvEvTac * C57BL/6 MGI:6196129


Genotype
MGI:7277819
cn1
Allelic
Composition
Gt(ROSA)26Sortm1(CAG-MYCN,-luc)Jhsc/Gt(ROSA)26Sor+
Ptentm2.1Ppp/Ptentm2.1Ppp
Rb1tm2Brn/Rb1tm2Brn
Tg(Pbsn-cre)4Prb/0
Genetic
Background
involves: 129 * 129S1/Sv * 129S6/SvEvTac * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(CAG-MYCN,-luc)Jhsc mutation (0 available); any Gt(ROSA)26Sor mutation (942 available)
Ptentm2.1Ppp mutation (0 available); any Pten mutation (81 available)
Rb1tm2Brn mutation (3 available); any Rb1 mutation (106 available)
Tg(Pbsn-cre)4Prb mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• median survival time of 12.5 weeks
• castrated mice have a median survival time of 24 weeks

neoplasm
• mice develop large, invasive prostate tumors with androgen receptor (AR)-negative and poorly differentiated foci as early as 8 weeks
• these regions show little resemblance to conventional adenocarcinoma but are negative for neuroendocrine markers, potentially as a transition between conventional adenocarcinoma and neuroendocrine prostate cancer (NEPC) states
• some foci are positive for neuroendocrine markers INSM1, EZH2, and NKX2-1 and some foci display condensed nuclei and scant cytoplasm, characteristic of NEPC morphology
• tumors also include other foci of divergent differentiation like intestinal and squamous, as well as conventional, AR+ adenocarcinoma, but the percentage of conventional adenocarcinoma decreases over time while the percentage of poorly differentiated histology increases over time
• mice do not respond to surgical castration and continue to grow tumors rapidly
• post-castration tumors harbor foci enriched with divergent differentiated histology compared to adenocarcinoma and increased metastatic potential
• onset of metastasis occurs as early as 8 weeks and by 12 weeks, 100% of mice develop distant metastatic lesions; metastases to the lung, liver, lymph nodes, and kidney primarily consist of large and small cell neuroendocrine histologies that are AR-negative

endocrine/exocrine glands
• mice develop large, invasive prostate tumors with androgen receptor (AR)-negative and poorly differentiated foci as early as 8 weeks
• these regions show little resemblance to conventional adenocarcinoma but are negative for neuroendocrine markers, potentially as a transition between conventional adenocarcinoma and neuroendocrine prostate cancer (NEPC) states
• some foci are positive for neuroendocrine markers INSM1, EZH2, and NKX2-1 and some foci display condensed nuclei and scant cytoplasm, characteristic of NEPC morphology
• tumors also include other foci of divergent differentiation like intestinal and squamous, as well as conventional, AR+ adenocarcinoma, but the percentage of conventional adenocarcinoma decreases over time while the percentage of poorly differentiated histology increases over time
• mice do not respond to surgical castration and continue to grow tumors rapidly
• post-castration tumors harbor foci enriched with divergent differentiated histology compared to adenocarcinoma and increased metastatic potential

reproductive system
• mice develop large, invasive prostate tumors with androgen receptor (AR)-negative and poorly differentiated foci as early as 8 weeks
• these regions show little resemblance to conventional adenocarcinoma but are negative for neuroendocrine markers, potentially as a transition between conventional adenocarcinoma and neuroendocrine prostate cancer (NEPC) states
• some foci are positive for neuroendocrine markers INSM1, EZH2, and NKX2-1 and some foci display condensed nuclei and scant cytoplasm, characteristic of NEPC morphology
• tumors also include other foci of divergent differentiation like intestinal and squamous, as well as conventional, AR+ adenocarcinoma, but the percentage of conventional adenocarcinoma decreases over time while the percentage of poorly differentiated histology increases over time
• mice do not respond to surgical castration and continue to grow tumors rapidly
• post-castration tumors harbor foci enriched with divergent differentiated histology compared to adenocarcinoma and increased metastatic potential

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
prostate neuroendocrine neoplasm DOID:2992 J:307910




Genotype
MGI:7277820
cn2
Allelic
Composition
Gt(ROSA)26Sortm1(CAG-MYCN,-luc)Jhsc/Gt(ROSA)26Sor+
Ptentm2.1Ppp/Ptentm2.1Ppp
Rb1tm2Brn/Rb1+
Tg(Pbsn-cre)4Prb/0
Genetic
Background
involves: 129 * 129S1/Sv * 129S6/SvEvTac * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(CAG-MYCN,-luc)Jhsc mutation (0 available); any Gt(ROSA)26Sor mutation (942 available)
Ptentm2.1Ppp mutation (0 available); any Pten mutation (81 available)
Rb1tm2Brn mutation (3 available); any Rb1 mutation (106 available)
Tg(Pbsn-cre)4Prb mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• median survival time of 19 weeks

neoplasm
• mice develop large, invasive tumors with androgen receptor (AR)-negative and poorly differentiated foci as early as 12 weeks
• these regions show little resemblance to conventional adenocarcinoma but are negative for neuroendocrine markers, potentially as a transition between conventional adenocarcinoma and neuroendocrine prostate cancer (NEPC) states
• some foci are positive for neuroendocrine markers INSM1, EZH2, and NKX2-1 and some foci display condensed nuclei and scant cytoplasm, characteristic of NEPC morphology
• tumors also include other foci of divergent differentiation like intestinal and squamous, as well as conventional, AR+ adenocarcinoma, but the percentage of conventional adenocarcinoma decreases over time while the percentage of poorly differentiated histology increases over time

endocrine/exocrine glands
• mice develop large, invasive tumors with androgen receptor (AR)-negative and poorly differentiated foci as early as 12 weeks
• these regions show little resemblance to conventional adenocarcinoma but are negative for neuroendocrine markers, potentially as a transition between conventional adenocarcinoma and neuroendocrine prostate cancer (NEPC) states
• some foci are positive for neuroendocrine markers INSM1, EZH2, and NKX2-1 and some foci display condensed nuclei and scant cytoplasm, characteristic of NEPC morphology
• tumors also include other foci of divergent differentiation like intestinal and squamous, as well as conventional, AR+ adenocarcinoma, but the percentage of conventional adenocarcinoma decreases over time while the percentage of poorly differentiated histology increases over time

reproductive system
• mice develop large, invasive tumors with androgen receptor (AR)-negative and poorly differentiated foci as early as 12 weeks
• these regions show little resemblance to conventional adenocarcinoma but are negative for neuroendocrine markers, potentially as a transition between conventional adenocarcinoma and neuroendocrine prostate cancer (NEPC) states
• some foci are positive for neuroendocrine markers INSM1, EZH2, and NKX2-1 and some foci display condensed nuclei and scant cytoplasm, characteristic of NEPC morphology
• tumors also include other foci of divergent differentiation like intestinal and squamous, as well as conventional, AR+ adenocarcinoma, but the percentage of conventional adenocarcinoma decreases over time while the percentage of poorly differentiated histology increases over time

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
prostate neuroendocrine neoplasm DOID:2992 J:307910




Genotype
MGI:7277821
cn3
Allelic
Composition
Gt(ROSA)26Sortm1(CAG-MYCN,-luc)Jhsc/Gt(ROSA)26Sor+
Ptentm2.1Ppp/Ptentm2.1Ppp
Tg(Pbsn-cre)4Prb/0
Genetic
Background
involves: 129 * 129S1/Sv * 129S6/SvEvTac * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(CAG-MYCN,-luc)Jhsc mutation (0 available); any Gt(ROSA)26Sor mutation (942 available)
Ptentm2.1Ppp mutation (0 available); any Pten mutation (81 available)
Tg(Pbsn-cre)4Prb mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• median survival time of 26 weeks
• castrated mice have a median survival time of 44 weeks

neoplasm
• mice develop prostate tumors that have primarily high-grade prostatic intraepithelial neoplasia at earlier time points
• tumors regress post-castration but resume growth 24 weeks post-castration

endocrine/exocrine glands
• mice develop prostate tumors that have primarily high-grade prostatic intraepithelial neoplasia at earlier time points
• tumors regress post-castration but resume growth 24 weeks post-castration

reproductive system
• mice develop prostate tumors that have primarily high-grade prostatic intraepithelial neoplasia at earlier time points
• tumors regress post-castration but resume growth 24 weeks post-castration




Genotype
MGI:6196129
cn4
Allelic
Composition
Gt(ROSA)26Sortm1(CAG-MYCN,-luc)Jhsc/Gt(ROSA)26Sor+
Tg(Dbh-icre)1Gsc/0
Genetic
Background
involves: 129S6/SvEvTac * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(CAG-MYCN,-luc)Jhsc mutation (0 available); any Gt(ROSA)26Sor mutation (942 available)
Tg(Dbh-icre)1Gsc mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• mice develop abdominal tumors with an incidence of 76%
• tumor onset occurs between 26-337 days of age, with a mean age of 79.6 days
• tumors arise from the superior cervical ganglion, the adrenals, or the celiac ganglion
• histology indicates small round cell tumor with cells harboring neurosecretory vesicles and express markers indicative of neuroblastoma
• neuroblastomas are characterized by genomic aberrations syntenic to human neuroblastomas

endocrine/exocrine glands
• hyperplastic cells are present in the adrenal medulla of some adrenal glands in 0-day old pups and most 14 and 28 day old mice
• at 28 days of age, the adrenal medulla has an atypical, nodal tissue architecture

nervous system
• mice develop abdominal tumors with an incidence of 76%
• tumor onset occurs between 26-337 days of age, with a mean age of 79.6 days
• tumors arise from the superior cervical ganglion, the adrenals, or the celiac ganglion
• histology indicates small round cell tumor with cells harboring neurosecretory vesicles and express markers indicative of neuroblastoma
• neuroblastomas are characterized by genomic aberrations syntenic to human neuroblastomas

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
neuroblastoma DOID:769 J:222527





Contributing Projects:
Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB)), Gene Ontology (GO)
Citing These Resources
Funding Information
Warranty Disclaimer, Privacy Notice, Licensing, & Copyright
Send questions and comments to User Support.
last database update
04/23/2024
MGI 6.23
The Jackson Laboratory