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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Tg(Cyp1a1-cre/ERT)1Dwi
transgene insertion 1, Douglas J Winton
MGI:3829429
Summary 8 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
cn1
Cdx1tm1Pgr/Cdx1tm1Pgr
Cdx2tm2Fbe/Cdx2tm2Fbe
Tg(Cyp1a1-cre/ERT)1Dwi/0
involves: 129 * C57BL/6 * CBA MGI:5308974
cn2
Apctm1Tno/Apc+
Ptentm2Mak/Ptentm2Mak
Tg(Cyp1a1-cre/ERT)1Dwi/0
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * CBA MGI:3829449
cn3
Stk11tm1Keis/Stk11tm1Keis
Tg(Cyp1a1-cre/ERT)1Dwi/0
involves: 129P2/OlaHsd * C57BL/6 * C57BL/6J * CBA MGI:5789955
cn4
Ptentm2Mak/Ptentm2Mak
Stk11tm1Keis/Stk11tm1Keis
Tg(Cyp1a1-cre/ERT)1Dwi/0
involves: 129P2/OlaHsd * C57BL/6 * C57BL/6J * CBA MGI:5789953
cn5
Ptentm2Mak/Ptentm2Mak
Tg(Cyp1a1-cre/ERT)1Dwi/0
involves: 129P2/OlaHsd * C57BL/6 * C57BL/6J * CBA MGI:5789954
cn6
Cdx2tm2Fbe/Cdx2tm2Fbe
Tg(Cyp1a1-cre/ERT)1Dwi/0
involves: 129P2/OlaHsd * C57BL/6 * CBA MGI:5308973
cn7
Apctm1Tno/Apctm1Tno
Ptentm1Hwu/Ptentm1Hwu
Tg(Cyp1a1-cre/ERT)1Dwi/0
involves: 129S4/SvJae * C57BL/6 * CBA MGI:4943267
cn8
Apctm1Tno/Apctm1Tno
Tg(Cyp1a1-cre/ERT)1Dwi/0
involves: 129S4/SvJae * C57BL/6 * CBA MGI:4943265


Genotype
MGI:5308974
cn1
Allelic
Composition
Cdx1tm1Pgr/Cdx1tm1Pgr
Cdx2tm2Fbe/Cdx2tm2Fbe
Tg(Cyp1a1-cre/ERT)1Dwi/0
Genetic
Background
involves: 129 * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdx1tm1Pgr mutation (1 available); any Cdx1 mutation (13 available)
Cdx2tm2Fbe mutation (0 available); any Cdx2 mutation (22 available)
Tg(Cyp1a1-cre/ERT)1Dwi mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• cystic vesicles appear 1 week after treatment with tamoxifen and BNF, earlier than in mutant mice wild-type for Cdx1

endocrine/exocrine glands
• cystic vesicles appear 1 week after treatment with tamoxifen and BNF, earlier than in mutant mice wild-type for Cdx1




Genotype
MGI:3829449
cn2
Allelic
Composition
Apctm1Tno/Apc+
Ptentm2Mak/Ptentm2Mak
Tg(Cyp1a1-cre/ERT)1Dwi/0
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apctm1Tno mutation (6 available); any Apc mutation (154 available)
Ptentm2Mak mutation (4 available); any Pten mutation (81 available)
Tg(Cyp1a1-cre/ERT)1Dwi mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• tamoxifen- and beta-naphthoflavone-induced mice median survival is 99 days compared to 405 days for wild-type Pten homozygotes or 409 days for wild-type Apc homozygotes

digestive/alimentary system
• 95% of tamoxifen- and beta-naphthoflavone-induced mice exhibit large, flattened, ulcerated lesions in the small intestine unlike control mice homozygous for either a wild-type Pten or Apc allele
• tamoxifen- and beta-naphthoflavone-induced mice develop invasive adenocarcinomas in the small intestines with luminal ulceration, and both acute and chronic inflammation compared to control mice that exhibit begnin neoplasms
• invasion and destruction of the small intestinal wall and peritoneal serosa results in localized peritonitis in tamoxifen- and beta-naphthoflavone-induced mice
• invasion and destruction of the small intestinal wall and peritoneal serosa by adenocarcinomas results in localized peritonitis in tamoxifen- and beta-naphthoflavone-induced mice

neoplasm
• tamoxifen- and beta-naphthoflavone-induced mice develop invasive adenocarcinomas in the small intestines with luminal ulceration, and both acute and chronic inflammation compared to control mice that exhibit begnin neoplasms
• invasion and destruction of the small intestinal wall and peritoneal serosa results in localized peritonitis in tamoxifen- and beta-naphthoflavone-induced mice

immune system
• invasion and destruction of the small intestinal wall and peritoneal serosa by adenocarcinomas results in localized peritonitis in tamoxifen- and beta-naphthoflavone-induced mice




Genotype
MGI:5789955
cn3
Allelic
Composition
Stk11tm1Keis/Stk11tm1Keis
Tg(Cyp1a1-cre/ERT)1Dwi/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * C57BL/6J * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Stk11tm1Keis mutation (0 available); any Stk11 mutation (34 available)
Tg(Cyp1a1-cre/ERT)1Dwi mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• mice injected with beta-napthoflavone and tamoxifen develop gastric polyps 270 days after induction

renal/urinary system
N
• mice injected with beta-napthoflavone and tamoxifen do not show any abnormal bladder morphology and do not develop bladder tumors




Genotype
MGI:5789953
cn4
Allelic
Composition
Ptentm2Mak/Ptentm2Mak
Stk11tm1Keis/Stk11tm1Keis
Tg(Cyp1a1-cre/ERT)1Dwi/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * C57BL/6J * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptentm2Mak mutation (4 available); any Pten mutation (81 available)
Stk11tm1Keis mutation (0 available); any Stk11 mutation (34 available)
Tg(Cyp1a1-cre/ERT)1Dwi mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Urothelial hyperplasia and increased apoptosis in bladder epithelium of Ptentm2Mak/Ptentm2Mak Stk11tm1Keis/Stk11tm1Keis Tg(Cyp1a1-cre/ERT)1Dwi/0 mice

mortality/aging
• mice injected with beta-napthoflavone and tamoxifen exhibit decreased survival after day 100 of induction, mostly due to bladder blockage

neoplasm
• mice injected with beta-napthoflavone and tamoxifen develop large papillary bladder tumors by day 125 of induction
• tumor tissue shows signs of spindle-shaped cells, squamous metaplasia, focal microvesicular change, and increase in nuclear-cytoplasmic ratio

renal/urinary system
• mice injected with beta-napthoflavone and tamoxifen exhibit enlarged bladders by 125 days of induction
• treatment with rapamycin reduces bladder size
• mice injected with beta-napthoflavone and tamoxifen develop large papillary bladder tumors by day 125 of induction
• tumor tissue shows signs of spindle-shaped cells, squamous metaplasia, focal microvesicular change, and increase in nuclear-cytoplasmic ratio
• by day 100 of induction with beta-napthoflavone and tamoxifen, mucosa of bladders is thickened
• mice injected with beta-napthoflavone and tamoxifen exhibit urothelial hyperplasia by day 50 and 100 of induction
• bladder epithelium of beta-napthoflavone and tamoxifen treated mice shows presence of apoptosis and vacuoles at day 50 of induction
• elevation in proliferation in the urothelium of mice injected with beta-napthoflavone and tamoxifen
• marker analysis indicates that bladder urothelial cells of beta-napthoflavone and tamoxifen injected mice exhibit characteristics of epithelial-mesenchymal transition, with loss of epithelial markers and increases in mesenchymal markers
• treatment with rapamycin reduces urothelial epithelium thickness and suppresses the epithelial-to-mesenchymal transition
• mice injected with beta-napthoflavone and tamoxifen show bladder obstruction due to tumors

growth/size/body
• mice injected with beta-napthoflavone and tamoxifen exhibit enlarged bladders by 125 days of induction
• treatment with rapamycin reduces bladder size

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
urinary bladder cancer DOID:11054 OMIM:109800
J:169565




Genotype
MGI:5789954
cn5
Allelic
Composition
Ptentm2Mak/Ptentm2Mak
Tg(Cyp1a1-cre/ERT)1Dwi/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * C57BL/6J * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptentm2Mak mutation (4 available); any Pten mutation (81 available)
Tg(Cyp1a1-cre/ERT)1Dwi mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
renal/urinary system
N
• mice injected with beta-napthoflavone and tamoxifen do not show any abnormal bladder morphology and do not develop bladder tumors




Genotype
MGI:5308973
cn6
Allelic
Composition
Cdx2tm2Fbe/Cdx2tm2Fbe
Tg(Cyp1a1-cre/ERT)1Dwi/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdx2tm2Fbe mutation (0 available); any Cdx2 mutation (22 available)
Tg(Cyp1a1-cre/ERT)1Dwi mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• 4 weeks after treatment with tamoxifen and BNF a bias towards the production of secretory cells is detected with an excess of mucous-secreting cells in the upper part of the crypts and towards the bases of the villi
• 4 weeks after treatment with tamoxifen and BNF crypts become sealed off into cystic vesicles and display a severe degree of hypoproliferation
• by 6 weeks after treatment cystic vesicles persist and are often filled with mucous and detritus
• cystic vesicles continue to persist 19-62 weeks after treatment although the surface epithelium consists of unrecombined cells
• abnormal and frequently moribund 4 weeks after treatment with tamoxifen and BNF
• an excess of Paneth cells are found by 19-62 weeks after treatment and these cells contain an abnormally abundant number of normal looking secretory granules
• in some mice polyps containing large irregular vesicles develop after treatment with tamoxifen and BNF
• by 6 weeks after treatment in isolated areas of the distal ileum recombined crypts have replaced the villi
• beyond 19 weeks these recombined regions develop into antral-like branched tubular glands secreting PASpositive, Alcian Blue-negative mucous
• 4 weeks after treatment with tamoxifen and BNF villi are misshapen
• 4 weeks after treatment with tamoxifen and beta-naphthoflavone (BNF) the gut becomes abnormally viscid
• by 6 weeks after treatment dying Paneth cells are commonly seen
• by 6 weeks after treatment dying Paneth cells are commonly seen

cellular
• recombined cells fail to migrate out of the crypts and up the villi in the intestine

endocrine/exocrine glands
• 4 weeks after treatment with tamoxifen and BNF crypts become sealed off into cystic vesicles and display a severe degree of hypoproliferation
• by 6 weeks after treatment cystic vesicles persist and are often filled with mucous and detritus
• cystic vesicles continue to persist 19-62 weeks after treatment although the surface epithelium consists of unrecombined cells
• abnormal and frequently moribund 4 weeks after treatment with tamoxifen and BNF
• an excess of Paneth cells are found by 19-62 weeks after treatment and these cells contain an abnormally abundant number of normal looking secretory granules




Genotype
MGI:4943267
cn7
Allelic
Composition
Apctm1Tno/Apctm1Tno
Ptentm1Hwu/Ptentm1Hwu
Tg(Cyp1a1-cre/ERT)1Dwi/0
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apctm1Tno mutation (6 available); any Apc mutation (154 available)
Ptentm1Hwu mutation (16 available); any Pten mutation (81 available)
Tg(Cyp1a1-cre/ERT)1Dwi mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
renal/urinary system
• mice develop hyperplastic lesions in the bladder unlike wild-type mice that are larger than in Apctm1Tno/Apctm1Tno Tg(Cyp1a1-cre/ERT)1Dwi mice




Genotype
MGI:4943265
cn8
Allelic
Composition
Apctm1Tno/Apctm1Tno
Tg(Cyp1a1-cre/ERT)1Dwi/0
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apctm1Tno mutation (6 available); any Apc mutation (154 available)
Tg(Cyp1a1-cre/ERT)1Dwi mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
renal/urinary system
• mice develop hyperplastic lesions in the bladder unlike wild-type mice





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last database update
04/16/2024
MGI 6.23
The Jackson Laboratory