Overview

JAXTag™

Also Known As:multiple intestinal neoplasia, Min

Heterozygotes of this strain develop anemia and are highly susceptible to spontaneous intestinal adenoma formation. Homozygous C57BL/6J-Apc^Min/J mice are not viable. The increased incidence of colorectal adenomas renders these mice a useful model of colon cancer. A small number of C57BL/6J-Apc^Min heterozygous female mice develop mammary tumors.

Donating Investigator

Dr. Alexandra Shedlovsky, University of Wisconsin , Madison

Dr. William F. Dove, University of Wisconsin- Madison

Genetic overview

Genetic Background	Generation
	Contact Technical Support (2019-05-22 00:00:00)

Apc^Min

Allele Type	Gene Symbol	Gene Name
Chemically induced (ENU)	Apc	adenomatosis polyposis coli

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Research Applications

Cancer Research
Mouse/Human Gene Homologs

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Base Price

Starting at:

$371.78 Domestic price for female 4-week

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Details

Detailed Description

The C57BL/6J-Apc^Min/J strain is highly susceptible to spontaneous intestinal adenoma formation. Homozygous mice are not viable. It was initially reported that one hundred percent of the C57BL/6J-Apc^Min heterozygous mice raised on a high fat diet develop in excess of 30 adenomas throughout the intestinal tract and most die by 120 days of age. Heterozygotes also develop anemia. (Moser et al., 1990, Su et al., 1992). A small number of C57BL/6J-Apc^Min heterozygous female mice develop mammary tumors. A subsequent publication indicates that this strain may carry a dominant modifier (Mom2) gene that reduces the number and incidence of polyp formation in C57BL/6J-Apc^Min heterozygous mice (Silverman et al., 2002).

This strain ships with a JAXTag^TM affixed. Learn more about JAXTag^TM.

Development

Following N-ethyl-N-nitrosourea (ENU) treatments to induce mutations in founder C57BL/6J mice, a forward genetic screen identified a AKR/JxB6 F1 female displaying circling behavior. This female was mated to C57BL/6J males. Some progeny from this backcross developed adult onset anemia and multiple intestinal neoplasia (Min). A tumor suppressor gene, Apc (adenomatosis polyposis coli), mutations of which have been identified in colorectal cancers and familial adenomatous polyposis (FAP), was found to cosegregate with the Min phenotype. Sequencing of Apc identified a T to A transversion of nucleotide 2549 resulting in a Leucine to a Stop codon nonsense mutation. The circling behavior was determined to be a separate heritable trait and was eliminated through subsequent crosses to C57BL/6J. These Apc^Min mice maintained on a C57BL/6J background when they were sent to The Jackson Laboratory in 1992.

Control Suggestions

Wild-type from the colony
000664 C57BL/6J

Additional Information

Considerations for Choosing Controls

Selected References

Moser AR; Pitot HC; Dove WF. 1990. A dominant mutation that predisposes to multiple intestinal neoplasia in the mouse. Science 247(4940):322-4PubMed: 2296722 MGI: J:10209
Su LK; Kinzler KW; Vogelstein B; Preisinger AC; Moser AR; Luongo C; Gould KA; Dove WF. 1992. Multiple intestinal neoplasia caused by a mutation in the murine homolog of the APC gene [published erratum appears in Science 1992 May 22;256(5060):1114] Science 256(5057):668-70PubMed: 1350108 MGI: J:830

View All References

Genetics

Apc^Min

Allele Symbol: Apc^Min

Allele Name	multiple intestinal neoplasia
Allele Type	Chemically induced (ENU)
Allele Synonym(s)	Apc^Δ850; Apc^-; Apc^delta850; Min; Min-
Gene Symbol and Name	Apc, adenomatosis polyposis coli
Gene Synonym(s)
Strain of Origin	C57BL/6J
Chromosome	18
Molecular Note	A transversion point mutation that alters nucleotide 2549 from a T to an A (mRNA: NM_001360980.1; protein: NM_007462.3). This converts codon 850 from one encoding a leucine to a stop codon (p.Leu850*), truncating the expected polypeptide.
Mutations Made By	Dr. William Dove, University of Wisconsin- Madison

Disease/Phenotype

Disease Terms

Model with phenotypic similarity to human disease where etiologies involve orthologs. Human genes are associated with this disease. Orthologs of those genes appear in the mouse genotype(s).

Research Areas By Phenotype

This mouse can be used to support research in many areas including:

Genotype: Apc^Min related

Cancer Research
- Increased Tumor Incidence
  - Mammary Gland Tumors
  - Adenomas: intestinal adenomas
  - Other Tissues/Organs: GI tract (stomach, intestine, colon)
  - Adenomas
  - Other Tissues/Organs
Mouse/Human Gene Homologs
- adenomatosis polyposis coli

Mammalian Phenotype Terms by Genotype

The following phenotype information is associated with a similar, but not exact match to this JAX^® Mice strain

Genotype: Apc^Min/Apc⁺
(MA/MyJ x C57BL/6J-Apc)F1

digestive/alimentary phenotype

decreased intestinal adenoma incidence
- Background Sensitivity - decrease in the average number of tumors per mouse (6 vs 29) relative to heterozygous mice on an inbred C57BL/6J background
- however, all heterozygous mice developed tumors

mortality/aging

extended life span
- Background Sensitivity - relative to heterozygous mice on an inbred C57BL/6J background

neoplasm

decreased intestinal adenoma incidence
- however, all heterozygous mice developed tumors
- Background Sensitivity - decrease in the average number of tumors per mouse (6 vs 29) relative to heterozygous mice on an inbred C57BL/6J background

Genotype: Apc^Min/Apc^Min
involves: C57BL/6J * CAST/EiJ

mortality/aging

embryonic lethality, complete penetrance
- inferred from no recovery of mice homozygous for embryos typed as homozygous for the identifying, linked B6 D18Mitl4 marker among a significant number of E10.5 and E13.5 progeny
- at E13.5 decidual swellings were necrotic with remnants of trophoblast giant cells
- at E10.5 histological analysis shows trophoblast giant cells and a small cluster of embryonic cells, source unknown

Genotype: Apc^Min/Apc⁺
(AKR/J x C57BL/6J-Apc)F1

cellular phenotype

aneuploidy
- quantitative polymerase chain reaction analysis of all intestinal adenomas sampled showed loss of Chr 18 carrying the wild-type Apc⁺ allele

digestive/alimentary phenotype

increased intestinal adenocarcinoma incidence
- a range of 1 to 12 with an average of 3 adenomas were found per mouse

decreased intestinal adenoma incidence
- however, all heterozygous mice developed tumors
- Background Sensitivity - decrease in the average number of tumors per mouse (6 vs 29) relative to heterozygous mice on an inbred C57BL/6J background

homeostasis/metabolism phenotype

increased incidence of tumors by chemical induction

mortality/aging

extended life span
- Background Sensitivity - relative to heterozygous mice on an inbred C57BL/6J background

neoplasm

decreased intestinal adenoma incidence
- Background Sensitivity - decrease in the average number of tumors per mouse (6 vs 29) relative to heterozygous mice on an inbred C57BL/6J background
- however, all heterozygous mice developed tumors

increased intestinal adenocarcinoma incidence
- a range of 1 to 12 with an average of 3 adenomas were found per mouse

increased incidence of tumors by chemical induction

Genotype: Apc^Min/Apc⁺
B6.Cg-Brca2 Apc

endocrine/exocrine gland phenotype

increased mammary gland tumor incidence
- tumors with predominantly squamous differentiation, moderate to marked inflammation in and around tumors is observed, with areas of fibrosis; in some cases, squamous component becomes cystic and is filled with keratinous debris
- invasion or metastases into the mammary lymph nodes was not observed during time course of study
- tumors in male and female mice are adenoacanthomas, characterized by undifferentiated acini and tubules with centrally confined squamous cells and keratin; most tumors contain proportions of adenomatous and squamous cell types
- by 65 days after ENU treatment, 100% of females develop mammary tumors with a multiplicity of 6.7 +/- 2.8
- males develop tumors at a very low incidence and with a tumor multiplicity of 0.4 +/- 0.5, whereas no wild-type or Brca2-heterozygous males developed mammary tumors

abnormal mammary gland development
- in ENU treated mice, male mammary ducts are elongated and in most males have extended to the lymph node of the fourth mammary gland, whereas wild-type and Brca2-heterozygous males are born with a small mammary gland rudiment, which grows no further, and no nipple
- Normal - no differences are observed in branching of female mammary glands among genotypes or wild-type females
- no nipple

abnormal ovarian folliculogenesis
- arrested follicular development is 6-fold more prevalent compared to ENU-treated Brca2-deficient mice

absent corpus luteum
- absent in 26% of ENU-treated females

absent mature ovarian follicles

absent nipple

adrenal gland hyperplasia
- females exhibit some adrenal hyperplasia, while none is observed in males

ovary atrophy
- complete loss of follicles (ovarian atrophy) is observed in about 25% of ENU-treated mutants, whereas almost no incidence is observed in ENU-treated wild-type or Brca2-mutant females

abnormal ovarian follicle morphology
- remaining follicles are degenerating in ENU-treated females

growth/size/body region phenotype

decreased body weight
- body weight of mice at time of sacrifice differs significantly from Brca2-heterozygous and wild-type animals; mice show lower weight gain from start to end of experiment compared to other experimental genotypes

integument phenotype

abnormal mammary gland development
- in ENU treated mice, male mammary ducts are elongated and in most males have extended to the lymph node of the fourth mammary gland, whereas wild-type and Brca2-heterozygous males are born with a small mammary gland rudiment, which grows no further, and no nipple
- Normal - no differences are observed in branching of female mammary glands among genotypes or wild-type females
- no nipple

increased mammary gland tumor incidence
- by 65 days after ENU treatment, 100% of females develop mammary tumors with a multiplicity of 6.7 +/- 2.8
- males develop tumors at a very low incidence and with a tumor multiplicity of 0.4 +/- 0.5, whereas no wild-type or Brca2-heterozygous males developed mammary tumors
- tumors in male and female mice are adenoacanthomas, characterized by undifferentiated acini and tubules with centrally confined squamous cells and keratin; most tumors contain proportions of adenomatous and squamous cell types
- invasion or metastases into the mammary lymph nodes was not observed during time course of study
- tumors with predominantly squamous differentiation, moderate to marked inflammation in and around tumors is observed, with areas of fibrosis; in some cases, squamous component becomes cystic and is filled with keratinous debris

absent nipple

mammalian phenotype

reproductive system phenotype
- Normal - only observed in 1/9 ENU-treated males, similar to wild-type males (1/9)

neoplasm

increased mammary gland tumor incidence
- males develop tumors at a very low incidence and with a tumor multiplicity of 0.4 +/- 0.5, whereas no wild-type or Brca2-heterozygous males developed mammary tumors
- tumors in male and female mice are adenoacanthomas, characterized by undifferentiated acini and tubules with centrally confined squamous cells and keratin; most tumors contain proportions of adenomatous and squamous cell types
- tumors with predominantly squamous differentiation, moderate to marked inflammation in and around tumors is observed, with areas of fibrosis; in some cases, squamous component becomes cystic and is filled with keratinous debris
- by 65 days after ENU treatment, 100% of females develop mammary tumors with a multiplicity of 6.7 +/- 2.8
- invasion or metastases into the mammary lymph nodes was not observed during time course of study

increased incidence of induced tumors
- multiple intestinal tumors are observed in ENU-treated mice, similar to Apc-heterozygous mice

reproductive system phenotype

absent corpus luteum
- absent in 26% of ENU-treated females

absent mature ovarian follicles

uterus atrophy
- observed in ENU-treated females displaying ovarian failure (atrophy); endometrium and myometrium appear immature

abnormal vagina epithelium morphology
- reduced in thickness and lined with vacuolated cells indicative of anestrus in ENU-treated females

abnormal ovarian follicle morphology
- remaining follicles are degenerating in ENU-treated females

abnormal ovarian folliculogenesis
- arrested follicular development is 6-fold more prevalent compared to ENU-treated Brca2-deficient mice

ovary atrophy
- complete loss of follicles (ovarian atrophy) is observed in about 25% of ENU-treated mutants, whereas almost no incidence is observed in ENU-treated wild-type or Brca2-mutant females

Genotype: Apc^Min/Apc⁺
involves: AKR/J * C57BL/6J

digestive/alimentary phenotype

increased intestinal adenocarcinoma incidence
- if mice are not anemic by 150 days of age, then tumors are not seen at 300 days of age
- locally invasive tumors seen in older animals but no metastasis
- sometimes small areas of carcinomas in anemic animals only

increased intestinal adenoma incidence
- either polyploid, papillary or sessile adenomas
- visible tumors of the large and small intestine

melena
- bloody feces

homeostasis/metabolism phenotype

hyperlipidemia

mortality/aging

premature death

neoplasm

increased intestinal adenoma incidence
- visible tumors of the large and small intestine
- either polyploid, papillary or sessile adenomas

increased intestinal adenocarcinoma incidence
- locally invasive tumors seen in older animals but no metastasis
- if mice are not anemic by 150 days of age, then tumors are not seen at 300 days of age
- sometimes small areas of carcinomas in anemic animals only

hematopoietic system phenotype

anemia
- progressive adult onset anemia beconming severe and chronic
- diagnosed in mutant mice by 60 days of age
- with few exceptions, likely the cause of lethality by 120 days of age

decreased hematocrit
- moribund animals with hematocrits around 10-20%

Genotype: Apc^Min/Apc⁺
involves: 129 * C57BL/6

digestive/alimentary phenotype

intestine polyps
- macroscopic lesions primarily within the proximal portion of the small intestine in mutant (n=22)

immune system phenotype

decreased splenocyte number
- reduction in splenic CD3+ T cells at 17 weeks old
- a less pronounced reduction in immature double positive CD4+,CD8+ cells in the spleen at 17 weeks old
- a strong reduction of mature single positive CD4+ and CD8+ cells in the spleen at 17 weeks old
- decreased DX5+, CD3- NK-cells in the spleen at 17 weeks old

decreased T cell number
- reduction in splenic CD3+ T cells at 17 weeks old

decreased NK cell number
- decreased DX5+, CD3- NK-cells in the spleen at 17 weeks old

hematopoietic system phenotype

decreased NK cell number
- decreased DX5+, CD3- NK-cells in the spleen at 17 weeks old

decreased splenocyte number
- a less pronounced reduction in immature double positive CD4+,CD8+ cells in the spleen at 17 weeks old
- a strong reduction of mature single positive CD4+ and CD8+ cells in the spleen at 17 weeks old
- decreased DX5+, CD3- NK-cells in the spleen at 17 weeks old
- reduction in splenic CD3+ T cells at 17 weeks old

decreased T cell number
- reduction in splenic CD3+ T cells at 17 weeks old

Genotype: Apc^Min/Apc^Min
involves: AKR/J * C57BL/6J

embryo phenotype

abnormal embryo size
- at E6.5 there is a range of abnormal development, underdeveloped embryonic tissue and associated maternal cells, with no obvious primitive ectoderm or proamniotic cavity to disorganized embryonic and extraembryonic tissue

abnormal egg cylinder morphology
- empty space is seen in the distal region where primitive ectoderm is expected

abnormal embryo development

growth/size/body region phenotype

abnormal embryo size
- at E6.5 there is a range of abnormal development, underdeveloped embryonic tissue and associated maternal cells, with no obvious primitive ectoderm or proamniotic cavity to disorganized embryonic and extraembryonic tissue

Genotype: Apc^Min/Apc^Min
involves: C57BL/6 * POMOD

embryo phenotype

abnormal embryo development
- at E7.5 embryos are disorganized,showing significant reduction in embryo growth and reduction of primitive ectoderm
- failure of primitive ectoderm development shortly after implantation

decreased embryo size
- embryos are small and embedded in maternal tissue

growth/size/body region phenotype

decreased embryo size
- embryos are small and embedded in maternal tissue

mortality/aging

embryonic lethality between implantation and placentation

embryonic lethality, complete penetrance

Genotype: Apc^Min/Apc⁺
involves: 129P2/OlaHsd * C57BL/6

digestive/alimentary phenotype

increased intestinal adenoma incidence
- loss of heterozygosity at 70 days of age is similar to heterozygous mice that are also homozygous for Foxl1^tm1Khk
- adenomas are present at 70 days of age

mammalian phenotype

neoplasm
- Normal - at 30 days, no colonic adenomas are found and normal colonic architecture and cellular morphology is observed
- Normal - no gastric adenomas are observed at 30 days of age

neoplasm

increased intestinal adenoma incidence
- loss of heterozygosity at 70 days of age is similar to heterozygous mice that are also homozygous for Foxl1^tm1Khk
- adenomas are present at 70 days of age

The following phenotype relates to a compound genotype created using this strain

Genotype: Apc^Min/Apc⁺
B6(AKR)-Apc

digestive/alimentary phenotype

increased intestinal adenocarcinoma incidence
- in N4-N8 backcross mice tumors are presesnt throughout the small and large intestines
- localization of tumors in the small and large intestines varies among mice

increased intestinal adenoma incidence

mortality/aging

premature death
- Background Sensitivity - average life-span has not decreased after N6 of backcrossing, suggesting genetic background influences effects of the mutation
- mutant mice do not a have a normal life-span, most rarely survive longer than 120 days of age

neoplasm

increased intestinal adenocarcinoma incidence
- in N4-N8 backcross mice tumors are presesnt throughout the small and large intestines
- localization of tumors in the small and large intestines varies among mice

increased intestinal adenoma incidence

increased mammary gland tumor incidence
- on this background colony maintenance data show that mammary tumors occasionally develop in heterozygous females but not in wild-type female siblings

reproductive system phenotype

abnormal pregnancy
- females are rarely able to maintain a pregnancy due to compromised health

endocrine/exocrine gland phenotype

increased mammary gland tumor incidence
- on this background colony maintenance data show that mammary tumors occasionally develop in heterozygous females but not in wild-type female siblings

mammary gland hyperplasia
- females of this genotype have an increased susceptibility to developing mammary neoplasia

hematopoietic system phenotype

anemia
- anemia is diagnosed by 60 days of age
- follows development of multiple adenomas which bleed into the intestinal lumen

integument phenotype

increased mammary gland tumor incidence
- on this background colony maintenance data show that mammary tumors occasionally develop in heterozygous females but not in wild-type female siblings

mammary gland hyperplasia
- females of this genotype have an increased susceptibility to developing mammary neoplasia

Genotype: Apc^Min/Apc⁺
involves: C57BL/6J

endocrine/exocrine gland phenotype

abnormal large intestine crypts of Lieberkuhn morphology
- ovariectomized mice exhibit reduced crypt length and distortion of surface epithelial cells in the colon compared with control mice

increased mammary adenocarcinoma incidence
- 12% of heterozygotes developed mammary adenocanthomas

hematopoietic system phenotype

anemia

integument phenotype

increased mammary adenocarcinoma incidence
- 12% of heterozygotes developed mammary adenocanthomas

mortality/aging

premature death
- heterozygotes begin to die at 7 months of age
- mice become moribound and die from anemia and intestinal obstruction by 160-180 days of age

neoplasm

increased mammary adenocarcinoma incidence
- 12% of heterozygotes developed mammary adenocanthomas

increased intestinal adenoma incidence
- small and large adenomas are seen throughout the intestine with more lesions found in the ileum compared to Apc^tm1Cip heterozygotes
- mice develop intestinal adenomas and colorectal adenomas by 160-180 days of age
- 50% of mice develop intestinal adenomas at 3 months of age, with 3 of 10 mice showing multiple tumors

cellular phenotype

abnormal intestinal goblet cell morphology
- the goblet cell ratio in ovariectomized mice is increased compared to in intact mice
- fewer mature goblet cells in the colon with prevelant pregoblet cells in ovariectomized mcie treated with 17beta-estradiol

abnormal enterocyte proliferation
- reduced proliferation of cells in the colon in ovariectomized
- Normal - however, 17beta-estradiol replacement increases colonocyte proliferation 2-fold

digestive/alimentary phenotype

abnormal enterocyte proliferation
- Normal - however, 17beta-estradiol replacement increases colonocyte proliferation 2-fold
- reduced proliferation of cells in the colon in ovariectomized

abnormal intestinal goblet cell morphology
- fewer mature goblet cells in the colon with prevelant pregoblet cells in ovariectomized mcie treated with 17beta-estradiol
- the goblet cell ratio in ovariectomized mice is increased compared to in intact mice

abnormal large intestine crypts of Lieberkuhn morphology
- ovariectomized mice exhibit reduced crypt length and distortion of surface epithelial cells in the colon compared with control mice

increased intestinal adenoma incidence
- small and large adenomas are seen throughout the intestine with more lesions found in the ileum compared to Apc^tm1Cip heterozygotes
- mice develop intestinal adenomas and colorectal adenomas by 160-180 days of age
- 50% of mice develop intestinal adenomas at 3 months of age, with 3 of 10 mice showing multiple tumors

intestinal obstruction
- due to tumors

abnormal intestinal mucosa morphology
- ovariectomized mice exhibit abnormal submucosal with thickening of the muscularis mucosae and enrichment of stromal components compared with control mice

rectal prolapse
- rectal prolapse is seen in 28% of surviving mutants at 7 months of age

intestine polyps

Genotype: Apc^Min/Apc⁺
C57BL/6J-Apc

digestive/alimentary phenotype

increased colon adenoma incidence
- tubular adenomas in the colon

increased intestinal adenoma incidence
- serotonergic cells were found in 18 of 18 adenomas
- at 8 and 15 weeks of age, females have proportionally more small adenomas and fewer medium-sized adenomas than males
- develop adenomatous polyps with moderate dysplasia, mild nuclear atypia and frequent mitotic figures throughout the duodenal-to-colonic axis
- mean diameter of adenomas and adenoma burden increases significantly between weeks 5 and 8 and between weeks 8 and 15
- mice fed a beef or inulin diet develop a similar number of adenomas as mice fed the rodent chow diet
- Normal - mice treated with a novel TNIK inhibitor NCB-0846 show reduced multiplicity and size of tumors that develop in the small intestine
- most mutants exhibit a few small or medium-sized adenomas at 5 weeks of age, with numbers increasing significantly between 5 and 8 weeks and then staying at the same level thereafter
- tubular adenomas in the intestine

growth/size/body region phenotype

postnatal growth retardation
- regular chow-fed males stop gaining weight, lose more weight, and are smaller at 15 weeks than beef-fed males

hematopoietic system phenotype

decreased macrophage cell number
- fewer Mac-1+ (macrophages) cells in ileal mucosa at 5 weeks of age, however numbers are normal at later time points and in all dietary treatments
- Normal - however, luminal IgA, IL-12, and TNF-alpha concentrations are normal

homeostasis/metabolism phenotype

increased prostaglandin level
- increase in luminal prostaglandin E2 at 15 weeks of age

increased circulating free fatty acids level
- females exhibit increased free fatty acid levels at 15 weeks of age

increased circulating triglyceride level
- females show increased triglyceride levels at 15 weeks of age

immune system phenotype

decreased macrophage cell number
- Normal - however, luminal IgA, IL-12, and TNF-alpha concentrations are normal
- fewer Mac-1+ (macrophages) cells in ileal mucosa at 5 weeks of age, however numbers are normal at later time points and in all dietary treatments

liver/biliary system phenotype

hepatic steatosis
- centrilobular-restricted steatosis is seen in the livers of mutants at 15 weeks of age

mortality/aging

premature death
- Background Sensitivity - life span is reduced compared to mice on an (MA/MyJ x C57BL/6J-Apc)F1 or (AKR/J x C57BL/6J-Apc)F1 background
- average lifespan is 118 +/- 26 days

neoplasm

increased intestinal adenoma incidence
- mean diameter of adenomas and adenoma burden increases significantly between weeks 5 and 8 and between weeks 8 and 15
- Normal - mice treated with a novel TNIK inhibitor NCB-0846 show reduced multiplicity and size of tumors that develop in the small intestine
- tubular adenomas in the intestine
- most mutants exhibit a few small or medium-sized adenomas at 5 weeks of age, with numbers increasing significantly between 5 and 8 weeks and then staying at the same level thereafter
- develop adenomatous polyps with moderate dysplasia, mild nuclear atypia and frequent mitotic figures throughout the duodenal-to-colonic axis
- mice fed a beef or inulin diet develop a similar number of adenomas as mice fed the rodent chow diet
- serotonergic cells were found in 18 of 18 adenomas
- at 8 and 15 weeks of age, females have proportionally more small adenomas and fewer medium-sized adenomas than males

increased colon adenoma incidence
- tubular adenomas in the colon

Genotype: Apc^Min/Apc^Min
involves: C57BL/6J

cellular phenotype

abnormal cell physiology
- cultured adenomatous tissue form highly clonogenic spheroids

Genotype: Apc^Min/Apc⁺
involves: C57BL/6 * C57BL/6J

digestive/alimentary phenotype

intestine polyps
- mice develop more and bigger polyps than in Apc^Min Myc^tm1Jlc heterozygotes

mortality/aging

premature death
- mice die at 169 days

References

Moser AR; Pitot HC; Dove WF. 1990. A dominant mutation that predisposes to multiple intestinal neoplasia in the mouse. Science 247(4940):322-4PubMed: 2296722 MGI: J:10209
Su LK; Kinzler KW; Vogelstein B; Preisinger AC; Moser AR; Luongo C; Gould KA; Dove WF. 1992. Multiple intestinal neoplasia caused by a mutation in the murine homolog of the APC gene [published erratum appears in Science 1992 May 22;256(5060):1114] Science 256(5057):668-70PubMed: 1350108 MGI: J:830

Additional References

Andreassen A; Mollersen L; Vikse R; Steffensen IL; Mikalsen A; Paulsen JE; Alexander J. 2002. One dose of 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) or 2-amino-3-methylimidazo[4,5-f]quinoline (IQ) induces tumours in Min/+ mice by truncation mutations or LOH in the Apc gene. Mutat Res 517(1-2):157-66PubMed: 12034317 MGI: J:77184
Andreassen A; Vikse R; Steffensen IL; Paulsen JE; Alexander J. 2001. Intestinal tumours induced by the food carcinogen 2-amino-1-methyl-6-phenylimidazo. Mutagenesis 16(4):309-15PubMed: 11420398 MGI: J:70642
Barbour K W; Davis T; White A; Baumann H; Berger F G. 2001. Haptoglobin, inflammation, and tumorigenesis in the MIN mouse. Redox Rep 6(6):366-8PubMed: 11865977 MGI: J:75249
Bennett LM; McAllister KA; Ward T; Malphurs J; Collins NK; Seely JC; Davis BJ; Wiseman RW. 2001. Mammary tumor induction and premature ovarian failure in ApcMin mice are not enhanced by Brca2 deficiency. Toxicol Pathol 29(1):117-25PubMed: 11215675 MGI: J:67445
Cooper AM; Magram J; Ferrante J; Orme IM. 1997. Interleukin 12 (IL-12) is crucial to the development of protective immunity in mice intravenously infected with mycobacterium tuberculosis. J Exp Med 186(1):39-45PubMed: 9206995 MGI: J:41494
Davis CD; Zeng H; Finley JW. 2002. Selenium-enriched broccoli decreases intestinal tumorigenesis in multiple intestinal neoplasia mice. J Nutr 132(2):307-9PubMed: 11823596 MGI: J:74364
De Giovanni C; Landuzzi L; Nicoletti G; Astolfi A; Croci S; Micaroni M; Nanni P; Lollini PL. 2004. Apc10.1: an ApcMin/+ intestinal cell line with retention of heterozygosity. Int J Cancer 109(2):200-6PubMed: 14750170 MGI: J:88314
Dinchuk JE; Focht RJ; Kelley JA; Henderson NL; Zolotarjova NI; Wynn R; Neff NT; Link J; Huber RM; Burn TC; Rupar MJ; Cunningham MR; Selling BH; Ma J; Stern AA; Hollis GF; Stein RB; Friedman PA. 2002. Absence of Post-translational Aspartyl beta -Hydroxylation of Epidermal Growth Factor Domains in Mice Leads to Developmental Defects and an Increased Incidence of Intestinal Neoplasia. J Biol Chem 277(15):12970-7PubMed: 11773073 MGI: J:75888
Erik Paulsen J; Steffensen IL; Loberg EM; Husoy T; Namork E; Alexander J. 2001. Qualitative and Quantitative Relationship between Dysplastic Aberrant Crypt Foci and Tumorigenesis in the Min/+ Mouse Colon. Cancer Res 61(13):5010-5PubMed: 11431334 MGI: J:70170
Ernest S; Christensen B; Gilfix BM; Mamer OA; Hosack A; Rodier M; Colmenares C; McGrath J; Bale A; Balling R; Sankoff D; Rosenblatt DS; Nadeau JH. 2002. Genetic and molecular control of folate-homocysteine metabolism in mutant mice. Mamm Genome 13(5):259-67PubMed: 12016514 MGI: J:76559
Gould TD; Gray NA; Manji HK. 2003. Effects of a glycogen synthase kinase-3 inhibitor, lithium, in adenomatous polyposis coli mutant mice. Pharmacol Res 48(1):49-53PubMed: 12770514 MGI: J:84200
Greiner JW; Zeytin H; Anver MR; Schlom J. 2002. Vaccine-based therapy directed against carcinoembryonic antigen demonstrates antitumor activity on spontaneous intestinal tumors in the absence of autoimmunity. Cancer Res 62(23):6944-51PubMed: 12460911 MGI: J:80324
Gupta RA; Wang D; Katkuri S; Wang H; Dey SK; DuBois RN. 2004. Activation of nuclear hormone receptor peroxisome proliferator-activated receptor-delta accelerates intestinal adenoma growth. Nat Med 10(3):245-7PubMed: 14758356 MGI: J:88127
Gutierrez LS; Suckow M; Lawler J; Ploplis VA; Castellino FJ. 2003. Thrombospondin 1--a regulator of adenoma growth and carcinoma progression in the APC(Min/+) mouse model. Carcinogenesis 24(2):199-207PubMed: 12584168 MGI: J:79641
Hansen-Petrik MB; McEntee MF; Jull B; Shi H; Zemel MB; Whelan J. 2002. Prostaglandin E(2) protects intestinal tumors from nonsteroidal anti-inflammatory drug-induced regression in Apc(Min/+) mice. Cancer Res 62(2):403-8PubMed: 11809688 MGI: J:74005
Hertervig E; Nilsson A; Nilbert M; Duan RD. 2003. Reduction in alkaline sphingomyelinase in colorectal tumorigenesis is not related to the APC gene mutation. Int J Colorectal Dis 18(4):309-13PubMed: 12774245 MGI: J:84197
Hong KH; Bonventre JC; O'Leary E; Bonventre JV; Lander ES. 2001. Deletion of cytosolic phospholipase A(2) suppresses Apc(Min)-induced tumorigenesis. Proc Natl Acad Sci U S A 98(7):3935-9PubMed: 11274413 MGI: J:68495
Huang EH; Carter JJ; Whelan RL; Liu YH; Rosenberg JO; Rotterdam H; Schmidt AM; Stern DM; Forde KA. 2002. Colonoscopy in mice. Surg Endosc 16(1):22-4PubMed: 11961598 MGI: J:77864
Huerta S; Irwin RW; Heber D; Go VL; Koeffler HP; Uskokovic MR; Harris DM. 2002. 1alpha,25-(OH)(2)-D(3) and its synthetic analogue decrease tumor load in the Apc(min) Mouse. Cancer Res 62(3):741-6PubMed: 11830528 MGI: J:74361
Iinuma T; Homma S; Noda T; Kufe D; Ohno T; Toda G. 2004. Prevention of gastrointestinal tumors based on adenomatous polyposis coli gene mutation by dendritic cell vaccine. J Clin Invest 113(9):1307-17PubMed: 15124022 MGI: J:90168
Kawajiri H; Hsi LC; Kamitani H; Ikawa H; Geller M; Ward T; Eling TE; Glasgow WC. 2002. Arachidonic and linoleic acid metabolism in mouse intestinal tissue: evidence for novel lipoxygenase activity. Arch Biochem Biophys 398(1):51-60PubMed: 11811948 MGI: J:74371
Lal G; Ash C; Hay K; Redston M; Kwong E; Hancock B; Mak T; Kargman S; Evans JF; Gallinger S. 2001. Suppression of intestinal polyps in msh2-deficient and non-msh2-deficient multiple intestinal neoplasia mice by a specific cyclooxygenase-2 inhibitor and by a dual cyclooxygenase-1/2 inhibitor. Cancer Res 61(16):6131-6PubMed: 11507063 MGI: J:70902
Lew JI; Guo Y; Kim RK; Vargish L; Michelassi F; Arenas RB. 2002. Reduction of Intestinal Neoplasia With Adenomatous Polyposis Coli Gene Replacement and COX-2 Inhibition Is Additive. J Gastrointest Surg 6(4):563-8PubMed: 12127122 MGI: J:77954
Lustig B; Jerchow B; Sachs M; Weiler S; Pietsch T; Karsten U; van de Wetering M; Clevers H; Schlag PM; Birchmeier W; Behrens J. 2002. Negative feedback loop of Wnt signaling through upregulation of conductin/axin2 in colorectal and liver tumors. Mol Cell Biol 22(4):1184-93PubMed: 11809809 MGI: J:74286
Mabley JG; Pacher P; Bai P; Wallace R; Goonesekera S; Virag L; Southan GJ; Szabo C. 2004. Suppression of intestinal polyposis in Apcmin/+ mice by targeting the nitric oxide or poly(ADP-ribose) pathways. Mutat Res 548(1-2):107-16PubMed: 15063141 MGI: J:89155
Mai V; Colbert LH; Berrigan D; Perkins SN; Pfeiffer R; Lavigne JA; Lanza E; Haines DC; Schatzkin A; Hursting SD. 2003. Calorie restriction and diet composition modulate spontaneous intestinal tumorigenesis in Apc(Min) mice through different mechanisms. Cancer Res 63(8):1752-5PubMed: 12702556 MGI: J:82980
Marten K; Bremer C; Khazaie K; Sameni M; Sloane B; Tung CH; Weissleder R. 2002. Detection of dysplastic intestinal adenomas using enzyme-sensing molecular beacons in mice. Gastroenterology 122(2):406-14PubMed: 11832455 MGI: J:74358
Mollersen L; Vikse R; Andreassen A; Steffensen IL; Mikalsen A; Paulsen JE; Alexander J. 2004. Adenomatous polyposis coli truncation mutations in 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP)-induced intestinal tumours of multiple intestinal neoplasia mice. Mutat Res 557(1):29-40PubMed: 14706516 MGI: J:87470
Mutanen M; Pajari AM; Oikarinen SI. 2000. Beef induces and rye bran prevents the formation of intestinal polyps in Apc(Min) mice: relation to beta-catenin and PKC isozymes. Carcinogenesis 21(6):1167-73PubMed: 10837006 MGI: J:62978
Niho N; Takahashi M; Kitamura T; Shoji Y; Itoh M; Noda T; Sugimura T; Wakabayashi K. 2003. Concomitant suppression of hyperlipidemia and intestinal polyp formation in Apc-deficient mice by peroxisome proliferator-activated receptor ligands. Cancer Res 63(18):6090-5PubMed: 14522940 MGI: J:86036
Oikannen SI; Pajari A; Mutanen M. 2000. Chemopreventive activity of hydroksymatairesinol in adenomatous polyposis colimultiple intestinal neoplasia (Apc)(Min) mice Cancer Lett 159(2):183-7PubMed: 10996730 MGI: J:64666
Oikarinen S; Heinonen S; Karppinen S; Matto J; Adlercreutz H; Poutanen K; Mutanen M. 2003. Plasma enterolactone or intestinal Bifidobacterium levels do not explain adenoma formation in multiple intestinal neoplasia (Min) mice fed with two different types of rye-bran fractions. Br J Nutr 90(1):119-25PubMed: 12844383 MGI: J:85024
Paoni NF; Feldman MW; Gutierrez LS; Ploplis VA; Castellino FJ. 2003. Transcriptional profiling of the transition from normal intestinal epithelia to adenomas and carcinomas in the APCMin/+ mouse. Physiol Genomics 15(3):228-35PubMed: 13130079 MGI: J:86113
Paulsen JE; Alexander J. 2001. Growth stimulation of intestinal tumours in Apc(Min/+) mice by dietary L-methionine supplementation. Anticancer Res 21(5):3281-4PubMed: 11848484 MGI: J:75262
Paulsen JE; Namork E; Steffensen IL; Eide TJ; Alexander J. 2000. Identification and quantification of aberrant crypt foci in the colon of Min mice--a murine model of familial adenomatous polyposis Scand J Gastroenterol 35(5):534-9PubMed: 10868458 MGI: J:62966
Perkins S; Verschoyle RD; Hill K; Parveen I; Threadgill MD; Sharma RA; Williams ML; Steward WP; Gescher AJ. 2002. Chemopreventive efficacy and pharmacokinetics of curcumin in the min/+ mouse, a model of familial adenomatous polyposis. Cancer Epidemiol Biomarkers Prev 11(6):535-40PubMed: 12050094 MGI: J:77168
Rao CV; Cooma I; Rodriguez JG; Simi B; El-Bayoumy K; Reddy BS. 2000. Chemoprevention of familial adenomatous polyposis development in the APC(min) mouse model by 1,4-phenylene bis(methylene)selenocyanate. Carcinogenesis 21(4):617-21PubMed: 10753194 MGI: J:61783
Reuter BK; Zhang XJ; Miller MJ. 2002. Therapeutic utility of aspirin in the ApcMin/+ murine model of colon carcinogenesis. BMC Cancer 2(1):19PubMed: 12171603 MGI: J:78510
Roy HK; Karoski WJ; Ratashak A; Smyrk TC. 2001. Chemoprevention of intestinal tumorigenesis by nabumetone: induction of apoptosis and Bcl-2 downregulation. Br J Cancer 84(10):1412-6PubMed: 11355956 MGI: J:69899
Schmelz EM; Roberts PC; Kustin EM; Lemonnier LA; Sullards MC; Dillehay DL; Merrill AH Jr. 2001. Modulation of intracellular beta-catenin localization and intestinal tumorigenesis in vivo and in vitro by sphingolipids. Cancer Res 61(18):6723-9PubMed: 11559543 MGI: J:71590
Shailubhai K; Yu HH; Karunanandaa K; Wang JY; Eber SL; Wang Y; Joo NS; Kim HD; Miedema BW; Abbas SZ; Boddupalli SS; Currie MG; Forte LR. 2000. Uroguanylin treatment suppresses polyp formation in the Apc(Min/+) mouse and induces apoptosis in human colon adenocarcinoma cells via cyclic GMP. Cancer Res 60(18):5151-7PubMed: 11016642 MGI: J:64784
Sibani S; Melnyk S; Pogribny IP; Wang W; Hiou-Tim F; Deng L; Trasler J; James SJ; Rozen R. 2002. Studies of methionine cycle intermediates (SAM, SAH), DNA methylation and the impact of folate deficiency on tumor numbers in Min mice. Carcinogenesis 23(1):61-5PubMed: 11756224 MGI: J:73559
Silverman KA; Koratkar RA; Siracusa LD; Buchberg AM. 2003. Exclusion of Madh2, Madh4, and Madh7 as candidates for the modifier of Min 2 ( Mom2) locus. Mamm Genome 14(2):119-29PubMed: 12584607 MGI: J:81868
Sohn KJ; Choi M; Song J; Chan S; Medline A; Gallinger S; Kim YI. 2003. Msh2 deficiency enhances somatic Apc and p53 mutations in Apc+/-Msh2-/- mice. Carcinogenesis 24(2):217-24PubMed: 12584170 MGI: J:79407
Song J; Medline A; Mason JB; Gallinger S; Kim YI. 2000. Effects of dietary folate on intestinal tumorigenesis in the apcMin mouse Cancer Res 60(19):5434-40PubMed: 11034085 MGI: J:65027
Steffensen IL; Schut HA; Paulsen JE; Andreassen A; Alexander J. 2001. Intestinal tumorigenesis in multiple intestinal neoplasia mice induced by the food mutagen 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine: perinatal susceptibility, regional variation, and correlation with DNA adducts. Cancer Res 61(24):8689-96PubMed: 11751386 MGI: J:73361
Suckow MA; Gutierrez LS; Risatti CA; Wolter WR; Taylor RE; Pollard M; Navari RM; Castellino FJ; Paoni NF. 2004. The anti-ischemia agent ranolazine promotes the development of intestinal tumors in APC(Min/+) mice. Cancer Lett 209(2):165-9PubMed: 15159018 MGI: J:90679
Suganuma M; Ohkura Y; Okabe S; Fujiki H. 2001. Combination cancer chemoprevention with green tea extract and sulindac shown in intestinal tumor formation in Min mice. J Cancer Res Clin Oncol 127(1):69-72PubMed: 11206275 MGI: J:67939
Suzui M; Okuno M; Tanaka T; Nakagama H; Moriwaki H. 2002. Enhanced colon carcinogenesis induced by azoxymethane in min mice occurs via a mechanism independent of beta-catenin mutation. Cancer Lett 183(1):31-41PubMed: 12049812 MGI: J:77169
Symolon H; Schmelz EM; Dillehay DL; Merrill AH Jr. 2004. Dietary Soy Sphingolipids Suppress Tumorigenesis and Gene Expression in 1,2-Dimethylhydrazine-Treated CF1 Mice and Apc(Min/+) Mice. J Nutr 134(5):1157-1161PubMed: 15113963 MGI: J:90172
Trasler J; Deng L; Melnyk S; Pogribny I; Hiou-Tim F; Sibani S; Oakes C; Li E; James SJ; Rozen R. 2003. Impact of Dnmt1 deficiency, with and without low folate diets, on tumor numbers and DNA methylation in Min mice. Carcinogenesis 24(1):39-45PubMed: 12538347 MGI: J:81577
Tucker J; Davis C; Kitchens M; Bunni M; Priest D; Spencer H; Berger F. 2002. Response to 5-fluorouracil chemotherapy is modified by dietary folic acid deficiency in Apc(Min/+) mice. Cancer Lett 187(1-2):153PubMed: 12359363 MGI: J:79692
Wagenaar-Miller RA; Hanley G; Shattuck-Brandt R; DuBois RN; Bell RL; Matrisian LM; Morgan DW. 2003. Cooperative effects of matrix metalloproteinase and cyclooxygenase-2 inhibition on intestinal adenoma reduction. Br J Cancer 88(9):1445-52PubMed: 12778076 MGI: J:83488
Wang D; Wang H; Shi Q; Katkuri S; Walhi W; Desvergne B; Das SK; Dey SK; DuBois RN. 2004. Prostaglandin E(2) promotes colorectal adenoma growth via transactivation of the nuclear peroxisome proliferator-activated receptor delta. Cancer Cell 6(3):285-95PubMed: 15380519 MGI: J:93551
Weber GF; Bronson RT; Ilagan J; Cantor H; Schmits R; Mak TW. 2002. Absence of the CD44 gene prevents sarcoma metastasis. Cancer Res 62(8):2281-6PubMed: 11956084 MGI: J:76201
Weyant MJ; Carothers AM; Dannenberg AJ; Bertagnolli MM. 2001. (+)-Catechin inhibits intestinal tumor formation and suppresses focal adhesion kinase activation in the min/+ mouse. Cancer Res 61(1):118-25PubMed: 11196148 MGI: J:67060
Weyant MJ; Carothers AM; Mahmoud NN; Bradlow HL; Remotti H; Bilinski RT; Bertagnolli MM. 2001. Reciprocal expression of ERalpha and ERbeta is associated with estrogen-mediated modulation of intestinal tumorigenesis. Cancer Res 61(6):2547-51PubMed: 11289129 MGI: J:68469
Yamada T; Mori Y; Hayashi R; Takada M; Ino Y; Naishiro Y; Kondo T; Hirohashi S. 2003. Suppression of intestinal polyposis in Mdr1-deficient ApcMin/+ mice. Cancer Res 63(5):895-901PubMed: 12615699 MGI: J:82288
Yamada Y; Hata K; Hirose Y; Hara A; Sugie S; Kuno T; Yoshimi N; Tanaka T; Mori H. 2002. Microadenomatous lesions involving loss of apc heterozygosity in the colon of adult apc(min/+) mice. Cancer Res 62(22):6367-70PubMed: 12438216 MGI: J:80301
Yang K; Fan K; Kurihara N; Shinozaki H; Rigas B; Augenlicht L; Kopelovich L; Edelmann W; Kucherlapati R; Lipkin M. 2003. Regional response leading to tumorigenesis after sulindac in small and large intestine of mice with Apc mutations. Carcinogenesis 24(3):605-11PubMed: 12663524 MGI: J:82832
Yu CF; Whiteley L; Carryl O; Basson MD. 2001. Differential dietary effects on colonic and small bowel neoplasia in C57BL/6J Apc Min/+ mice. Dig Dis Sci 46(7):1367-80PubMed: 11478486 MGI: J:70920
Ziegler CC; Rainwater L; Whelan J; McEntee MF. 2004. Dietary resveratrol does not affect intestinal tumorigenesis in Apc(Min/+) mice. J Nutr 134(1):5-10PubMed: 14704285 MGI: J:88124

Additional - Apc^Min related

Technical Support

CONTACT TECHNICAL SUPPORT

Genotyping Protocols
- End Point Analysis:Apcalternate1
- Genotyping resources and troubleshooting
Breeding Considerations

This strain is a good breeder.

This strain is maintained by breeding heterozygote males to C57BL/6J females. Female heterozygotes are not recommended because anemia and intestinal adenomas interfere with pregnancy. Breeding performance in heterozygote males declines as anemia and tumors develop.
- Additional Breeding and Husbandry Support
Mating System
- Inbred x Heterozygote
- (C57BL/6J x Heterozygote
Appearance
- black
  Related Genotype: a/a
Citation
When using the multiple intestinal neoplasia mouse strain in a publication, please cite the originating article(s) and include JAX stock #002020 in your Materials and Methods section.

Animal Health Reports

Facility Barrier Level Descriptions

AX4 (Standard)

Pricing & Availability

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Genotype

Price

weeks

Cryorecovery - Pricing

Service/Product	Description	Price
	Heterozygous or Wild-type for Apc<Min>

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The Jackson Laboratory has rigorous genetic quality control and mutant gene genotyping programs to ensure the genetic background of JAX® Mice strains as well as the genotypes of strains with identified molecular mutations. JAX® Mice strains are only made available to researchers after meeting our standards. However, the phenotype of each strain may not be fully characterized and/or captured in the strain data sheets. Therefore, we cannot guarantee a strain's phenotype will meet all expectations. To ensure that JAX® Mice will meet the needs of individual research projects or when requesting a strain that is new to your research, we suggest ordering and performing tests on a small number of mice to determine suitability for your particular project. We do not guarantee breeding performance and therefore suggest that investigators order more than one breeding pair to avoid delays in their research.

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Also Known As:multiple intestinal neoplasia, Min

Donating Investigator

Genetic overview

Research Applications

Base Price

Detailed Description

Development

Control Suggestions

Additional Information

Selected References

ApcMin

Allele Symbol: ApcMin

Disease Terms

Model with phenotypic similarity to human disease where etiologies involve orthologs. Human genes are associated with this disease. Orthologs of those genes appear in the mouse genotype(s).

Research Areas By Phenotype

This mouse can be used to support research in many areas including:

Genotype: ApcMin related

Mammalian Phenotype Terms by Genotype

Genotype: ApcMin/Apc+(MA/MyJ x C57BL/6J-Apc)F1

digestive/alimentary phenotype

mortality/aging

neoplasm

Genotype: ApcMin/ApcMininvolves: C57BL/6J * CAST/EiJ

mortality/aging

Genotype: ApcMin/Apc+(AKR/J x C57BL/6J-Apc)F1

cellular phenotype

digestive/alimentary phenotype

homeostasis/metabolism phenotype

mortality/aging

neoplasm

Genotype: ApcMin/Apc+B6.Cg-Brca2 Apc

endocrine/exocrine gland phenotype

growth/size/body region phenotype

integument phenotype

mammalian phenotype

neoplasm

reproductive system phenotype

Genotype: ApcMin/Apc+involves: AKR/J * C57BL/6J

digestive/alimentary phenotype

homeostasis/metabolism phenotype

mortality/aging

neoplasm

hematopoietic system phenotype

Genotype: ApcMin/Apc+involves: 129 * C57BL/6

digestive/alimentary phenotype

immune system phenotype

hematopoietic system phenotype

Genotype: ApcMin/ApcMininvolves: AKR/J * C57BL/6J

embryo phenotype

growth/size/body region phenotype

Genotype: ApcMin/ApcMininvolves: C57BL/6 * POMOD

embryo phenotype

growth/size/body region phenotype

mortality/aging

Genotype: ApcMin/Apc+involves: 129P2/OlaHsd * C57BL/6

digestive/alimentary phenotype

mammalian phenotype

neoplasm

Genotype: ApcMin/Apc+B6(AKR)-Apc

digestive/alimentary phenotype

mortality/aging

neoplasm

reproductive system phenotype

endocrine/exocrine gland phenotype

hematopoietic system phenotype

integument phenotype

Genotype: ApcMin/Apc+involves: C57BL/6J

endocrine/exocrine gland phenotype

hematopoietic system phenotype

integument phenotype

mortality/aging

neoplasm

cellular phenotype

digestive/alimentary phenotype

Genotype: ApcMin/Apc+C57BL/6J-Apc

digestive/alimentary phenotype

growth/size/body region phenotype

hematopoietic system phenotype

homeostasis/metabolism phenotype

immune system phenotype

Apc^Min

Allele Symbol: Apc^Min

Genotype: Apc^Min related

Genotype: Apc^Min/Apc⁺
(MA/MyJ x C57BL/6J-Apc)F1

Genotype: Apc^Min/Apc^Min
involves: C57BL/6J * CAST/EiJ

Genotype: Apc^Min/Apc⁺
(AKR/J x C57BL/6J-Apc)F1

Genotype: Apc^Min/Apc⁺
B6.Cg-Brca2 Apc

Genotype: Apc^Min/Apc⁺
involves: AKR/J * C57BL/6J

Genotype: Apc^Min/Apc⁺
involves: 129 * C57BL/6

Genotype: Apc^Min/Apc^Min
involves: AKR/J * C57BL/6J

Genotype: Apc^Min/Apc^Min
involves: C57BL/6 * POMOD

Genotype: Apc^Min/Apc⁺
involves: 129P2/OlaHsd * C57BL/6

Genotype: Apc^Min/Apc⁺
B6(AKR)-Apc

Genotype: Apc^Min/Apc⁺
involves: C57BL/6J

Genotype: Apc^Min/Apc⁺
C57BL/6J-Apc

Genotype: Apc^Min/Apc^Min
involves: C57BL/6J

Genotype: Apc^Min/Apc⁺
involves: C57BL/6 * C57BL/6J

Additional - Apc^Min related