JAX Mouse Strain Datasheet - 002020

C57BL/6J-Apc^Min/J

Stock No:: 002020 |; multiple intestinal neoplasia

Available Now

Overview

JAXTag^TM

Also Known As: Min, multiple intestinal neoplasia

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
	N79pN14 (05-AUG-14)

Apc^Min

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

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Research Applications

Cancer Research

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Base Price

Starting at:

$304.40 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):322-4. PubMed: 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):668-70. PubMed: 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)	AI047805; AU020952; AW124434; BTPS2; CC1; DP2; DP2.5; DP3; GS; Min; Min; PPP1R46; RATAPC; expressed sequence AI047805; expressed sequence AU020952; expressed sequence AW124434; multiple intestinal neoplasia
Strain of Origin	C57BL/6J
Chromosome	18
Molecular Note	A transversion point mutation that alters nucleotide 2549 from a T to an A. This converts codon 850 from one encoding a leucine to a stop codon, truncating the expected polypeptide.
Mutations Made By	Dr. William Dove, University of Wisconsin- Madison

Disease/Phenotype

Disease Terms

Research Areas By Genotype

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

Genotype: Apc^Min related

Cancer Research
- Increased Tumor Incidence
  - Adenomas
  - Adenomas: intestinal adenomas
  - Mammary Gland Tumors
  - Other Tissues/Organs
  - Other Tissues/Organs: GI tract (stomach, intestine, colon)

Mammalian Phenotype Terms by Genotype

Genotype: Apc^Min/Apc⁺
B6(AKR)-Apc^Min

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

hematopoietic system phenotype

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

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

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⁺
C57BL/6J-Apc^Min

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 colonic adenoma incidence
- tubular adenomas in the colon

increased intestinal adenoma incidence
- 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
- 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
- serotonergic cells were found in 18 of 18 adenomas
- tubular adenomas in the intestine

digestive/alimentary phenotype

increased intestinal adenoma incidence
- 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
- 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
- serotonergic cells were found in 18 of 18 adenomas
- tubular adenomas in the intestine

homeostasis/metabolism phenotype

increased circulating free fatty acid 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

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

liver/biliary system phenotype

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

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
- however, luminal IgA, IL-12, and TNF-alpha concentrations are normal

immune 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
- however, luminal IgA, IL-12, and TNF-alpha concentrations are normal

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

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 intestinal adenoma incidence
- mice develop intestinal adenomas and colorectal adenomas by 160-180 days of age
- small and large adenomas are seen throughout the intestine with more lesions found in the ileum compared to Apc^tm1Cip heterozygotes

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

digestive/alimentary phenotype

abnormal enterocyte proliferation
- 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 intestinal mucosa morphology
- ovariectomized mice exhibit abnormal submucosal with thickening of the muscularis mucosae and enrichment of stromal components compared with control 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
- mice develop intestinal adenomas and colorectal adenomas by 160-180 days of age
- small and large adenomas are seen throughout the intestine with more lesions found in the ileum compared to Apc^tm1Cip heterozygotes

intestinal obstruction
- due to tumors

intestine polyps

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

cellular phenotype

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

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

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

mortality/aging

premature death
- mice die at 169 days

digestive/alimentary phenotype

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

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

cellular phenotype

abnormal cell physiology
- cultured adenomatous tissue form highly clonogenic spheroids

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

Genotype: Apc^Min/Apc⁺
B6.Cg-Brca2^tm1Mbn Apc^Min

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

reproductive system phenotype

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

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

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

absent mature ovarian follicles

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

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

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

neoplasm

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

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
- invasion or metastases into the mammary lymph nodes was not observed during time course of study
- 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

endocrine/exocrine gland 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 nippleno nipple
- no differences are observed in branching of female mammary glands among genotypes or wild-type 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

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

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
- invasion or metastases into the mammary lymph nodes was not observed during time course of study
- 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

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

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 nippleno nipple
- no differences are observed in branching of female mammary glands among genotypes or wild-type females

absent 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
- invasion or metastases into the mammary lymph nodes was not observed during time course of study
- 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

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

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 incidence of tumors by chemical induction

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

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

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

cellular phenotype

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

homeostasis/metabolism phenotype

increased incidence of tumors by chemical induction

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

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

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

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

neoplasm

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

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

hematopoietic system phenotype

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

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

homeostasis/metabolism phenotype

hyperlipidemia

mortality/aging

premature death

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

neoplasm

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

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

digestive/alimentary phenotype

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

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

digestive/alimentary phenotype

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

hematopoietic system phenotype

decreased NK cell number
- 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 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

immune system phenotype

decreased NK cell number
- 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 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

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

embryo phenotype

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

abnormal embryo development

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

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

mortality/aging

embryonic lethality, complete penetrance
- at E10.5 histological analysis shows trophoblast giant cells and a small cluster of embryonic cells, source unknown
- at E13.5 decidual swellings were necrotic with remnants of trophoblast giant cells
- 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

References

Moser AR; Pitot HC; Dove WF. 1990. A dominant mutation that predisposes to multiple intestinal neoplasia in the mouse. Science 247(4940):322-4. PubMed: 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):668-70. PubMed: 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):157-66. PubMed: 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):309-15. PubMed: 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):366-8. PubMed: 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):117-25. PubMed: 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):39-45. PubMed: 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):307-9. PubMed: 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):200-6. PubMed: 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):12970-7. PubMed: 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):5010-5. PubMed: 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):259-67. PubMed: 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):49-53. PubMed: 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):6944-51. PubMed: 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):245-7. PubMed: 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):199-207. PubMed: 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):403-8. PubMed: 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):309-13. PubMed: 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):3935-9. PubMed: 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):22-4. PubMed: 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):741-6. PubMed: 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):1307-17. PubMed: 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):51-60. PubMed: 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):6131-6. PubMed: 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):563-8. PubMed: 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):1184-93. PubMed: 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):107-16. PubMed: 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):1752-5. PubMed: 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):406-14. PubMed: 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):29-40. PubMed: 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):1167-73. PubMed: 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):6090-5. PubMed: 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):183-7. PubMed: 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):119-25. PubMed: 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):228-35. PubMed: 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):3281-4. PubMed: 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):534-9. PubMed: 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):535-40. PubMed: 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):617-21. PubMed: 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):19. PubMed: 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):1412-6. PubMed: 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):6723-9. PubMed: 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):5151-7. PubMed: 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):61-5. PubMed: 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):119-29. PubMed: 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):217-24. PubMed: 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):5434-40. PubMed: 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):8689-96. PubMed: 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):165-9. PubMed: 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):69-72. PubMed: 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):31-41. PubMed: 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):1157-1161. PubMed: 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):39-45. PubMed: 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):153. PubMed: 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):1445-52. PubMed: 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):285-95. PubMed: 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):2281-6. PubMed: 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):118-25. PubMed: 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):2547-51. PubMed: 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):895-901. PubMed: 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):6367-70. PubMed: 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):605-11. PubMed: 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):1367-80. PubMed: 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):5-10. PubMed: 14704285 MGI: J:88124

Additional - Apc^Min related

Ahn B; Ohshima H. 2001. Suppression of intestinal polyposis in Apc(Min/+) mice by inhibiting nitric oxide production. Cancer Res 61(23):8357-60. PubMed: 11731407 MGI: J:73152
Akeus P; Langenes V; Kristensen J; von Mentzer A; Sparwasser T; Raghavan S; Quiding-Jarbrink M. 2015. Treg-cell depletion promotes chemokine production and accumulation of CXCR3(+) conventional T cells in intestinal tumors. Eur J Immunol 45(6):1654-66. PubMed: 25754875 MGI: J:229714
Akitake-Kawano R; Seno H; Nakatsuji M; Kimura Y; Nakanishi Y; Yoshioka T; Kanda K; Kawada M; Kawada K; Sakai Y; Chiba T. 2013. Inhibitory role of Gas6 in intestinal tumorigenesis. Carcinogenesis 34(7):1567-74. PubMed: 23430954 MGI: J:199029
Akporiaye ET; Bradley-Dunlop D; Gendler SJ; Mukherjee P; Madsen CS; Hahn T; Besselsen DG; Dial SM; Cui H; Trevor K. 2007. Characterization of the MUC1.Tg/MIN transgenic mouse as a model for studying antigen-specific immunotherapy of adenomas. Vaccine 25(39-40):6965-74. PubMed: 17707958 MGI: J:128727
Alferez D; Wilkinson RW; Watkins J; Poulsom R; Mandir N; Wedge SR; Pyrah IT; Smith NR; Jackson L; Ryan AJ; Goodlad RA. 2008. Dual inhibition of VEGFR and EGFR signaling reduces the incidence and size of intestinal adenomas in Apc(Min/+) mice. Mol Cancer Ther 7(3):590-8. PubMed: 18347145 MGI: J:145378
Alferez DG; Ryan AJ; Goodlad RA; Wright NA; Wilkinson RW. 2010. Effects of vandetanib on adenoma formation in a dextran sodium sulphate enhanced Apc(MIN/+) mouse model. Int J Oncol 37(4):767-72. PubMed: 20811697 MGI: J:178668
Amos-Landgraf JM; Heijmans J; Wielenga MC; Dunkin E; Krentz KJ; Clipson L; Ederveen AG; Groothuis PG; Mosselman S; Muncan V; Hommes DW; Shedlovsky A; Dove WF; van den Brink GR. 2014. Sex disparity in colonic adenomagenesis involves promotion by male hormones, not protection by female hormones. Proc Natl Acad Sci U S A 111(46):16514-9. PubMed: 25368192 MGI: J:216744
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):157-66. PubMed: 12034317 MGI: J:77184
Andreassen A; Vikse R; Mikalsen A; Adamovic T; Steffensen IL; Hjertholm H; Levan G; Alexander J. 2006. 2-Amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) induces genetic changes in murine intestinal tumours and cells with Apc(Min) mutation. Mutat Res 604(1-2):60-70. PubMed: 16574467 MGI: J:107714
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):309-15. PubMed: 11420398 MGI: J:70642
Andres SF; Simmons JG; Mah AT; Santoro MA; Van Landeghem L; Lund PK. 2013. Insulin receptor isoform switching in intestinal stem cells, progenitors, differentiated lineages and tumors: evidence that IR-B limits proliferation. J Cell Sci 126(Pt 24):5645-56. PubMed: 24127567 MGI: J:211908
Angus-Hill ML; Elbert KM; Hidalgo J; Capecchi MR. 2011. T-cell factor 4 functions as a tumor suppressor whose disruption modulates colon cell proliferation and tumorigenesis. Proc Natl Acad Sci U S A 108(12):4914-9. PubMed: 21383188 MGI: J:170088
Aparicio T; Kotelevets L; Tsocas A; Laigneau JP; Sobhani I; Chastre E; Lehy T. 2005. Leptin stimulates the proliferation of human colon cancer cells in vitro but does not promote the growth of colon cancer xenografts in nude mice or intestinal tumorigenesis in Apc(Min/+) mice. Gut 54(8):1136-45. PubMed: 15857934 MGI: J:194729
Arenas RB; Fichera A; Mok P; Blanco MC; Michelassi F. 1996. Introduction of human adenomatous polyposis coli gene into Min mice via cationic liposomes. Surgery 120(4):712-7. PubMed: 8862382 MGI: J:36700
Babaei-Jadidi R; Li N; Saadeddin A; Spencer-Dene B; Jandke A; Muhammad B; Ibrahim EE; Muraleedharan R; Abuzinadah M; Davis H; Lewis A; Watson S; Behrens A; Tomlinson I; Nateri AS. 2011. FBXW7 influences murine intestinal homeostasis and cancer, targeting Notch, Jun, and DEK for degradation. J Exp Med 208(2):295-312. PubMed: 21282377 MGI: J:176848
Bacher JW; Abdel Megid WM; Kent-First MG; Halberg RB. 2005. Use of mononucleotide repeat markers for detection of microsatellite instability in mouse tumors. Mol Carcinog 44(4):285-92. PubMed: 16240453 MGI: J:107080
Backlund MG; Mann JR; Holla VR; Buchanan FG; Tai HH; Musiek ES; Milne GL; Katkuri S; DuBois RN. 2005. 15-Hydroxyprostaglandin dehydrogenase is down-regulated in colorectal cancer. J Biol Chem 280(5):3217-23. PubMed: 15542609 MGI: J:105183
Backlund MG; Mann JR; Holla VR; Shi Q; Daikoku T; Dey SK; DuBois RN. 2008. Repression of 15-hydroxyprostaglandin dehydrogenase involves histone deacetylase 2 and snail in colorectal cancer. Cancer Res 68(22):9331-7. PubMed: 19010907 MGI: J:141385
Baek SJ; Okazaki R; Lee SH; Martinez J; Kim JS; Yamaguchi K; Mishina Y; Martin DW; Shoieb A; McEntee MF; Eling TE. 2006. Nonsteroidal anti-inflammatory drug-activated gene-1 over expression in transgenic mice suppresses intestinal neoplasia. Gastroenterology 131(5):1553-60. PubMed: 17101328 MGI: J:120981
Baker DJ; Jin F; Jeganathan KB; van Deursen JM. 2009. Whole chromosome instability caused by Bub1 insufficiency drives tumorigenesis through tumor suppressor gene loss of heterozygosity. Cancer Cell 16(6):475-86. PubMed: 19962666 MGI: J:155824
Baker SM; Harris AC; Tsao JL; Flath TJ; Bronner CE; Gordon M ; Shibata D ; Liskay RM. 1998. Enhanced intestinal adenomatous polyp formation in Pms2-/-;Min mice. Cancer Res 58(6):1087-9. PubMed: 9515784 MGI: J:46419
Baltgalvis KA; Berger FG; Pena MM; Davis JM; Carson JA. 2008. Effect of exercise on biological pathways in ApcMin/+ mouse intestinal polyps. J Appl Physiol 104(4):1137-43. PubMed: 18239078 MGI: J:147321
Baltgalvis KA; Berger FG; Pena MM; Davis JM; Muga SJ; Carson JA. 2008. Interleukin-6 and cachexia in ApcMin/+ mice. Am J Physiol Regul Integr Comp Physiol 294(2):R393-401. PubMed: 18056981 MGI: J:130429
Baltgalvis KA; Berger FG; Pena MM; Mark Davis J; White JP; Carson JA. 2010. Activity level, apoptosis, and development of cachexia in Apc(Min/+) mice. J Appl Physiol 109(4):1155-61. PubMed: 20651218 MGI: J:185914
Barak Y; Liao D; He W; Ong ES; Nelson MC; Olefsky JM; Boland R; Evans RM. 2002. Effects of peroxisome proliferator-activated receptor delta on placentation, adiposity, and colorectal cancer. Proc Natl Acad Sci U S A 99(1):303-8. PubMed: 11756685 MGI: J:73557
Baran AA; Silverman KA; Zeskand J; Koratkar R; Palmer A; McCullen K; Curran WJ Jr; Edmonston TB; Siracusa LD; Buchberg AM. 2007. The modifier of Min 2 (Mom2) locus: embryonic lethality of a mutation in the Atp5a1 gene suggests a novel mechanism of polyp suppression. Genome Res 17(5):566-76. PubMed: 17387143 MGI: J:122207
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):366-8. PubMed: 11865977 MGI: J:75249
Barker N; van Es JH; Kuipers J; Kujala P; van den Born M; Cozijnsen M; Haegebarth A; Korving J; Begthel H; Peters PJ; Clevers H. 2007. Identification of stem cells in small intestine and colon by marker gene Lgr5. Nature 449(7165):1003-7. PubMed: 17934449 MGI: J:127123
Barnes CJ; Lee M. 1998. Chemoprevention of spontaneous intestinal adenomas in the adenomatous polyposis coli Min mouse model with aspirin. Gastroenterology 114(5):873-7. PubMed: 9558273 MGI: J:48008
Barone M; Notarnicola M; Caruso MG; Scavo MP; Viggiani MT; Tutino V; Polimeno L; Pesetti B; Di Leo A; Francavilla A. 2014. Olive oil and omega-3 polyunsaturated fatty acids suppress intestinal polyp growth by modulating the apoptotic process in ApcMin/+ mice. Carcinogenesis 35(7):1613-9. PubMed: 24632492 MGI: J:211552
Barone M; Tanzi S; Lofano K; Scavo MP; Pricci M; Demarinis L; Papagni S; Guido R; Maiorano E; Ingravallo G; Comelli MC; Francavilla A; Di Leo A. 2010. Dietary-induced ERbeta upregulation counteracts intestinal neoplasia development in intact male ApcMin/+ mice. Carcinogenesis 31(2):269-74. PubMed: 19945967 MGI: J:156778
Bashir O; FitzGerald AJ; Goodlad RA. 2004. Both suboptimal and elevated vitamin intake increase intestinal neoplasia and alter crypt fission in the ApcMin/+ mouse. Carcinogenesis 25(8):1507-15. PubMed: 15016659 MGI: J:91525
Bashir O; Fitzgerald AJ; Berlanga-Acosta J; Playford RJ; Goodlad RA. 2003. Effect of epidermal growth factor administration on intestinal cell proliferation, crypt fission and polyp formation in multiple intestinal neoplasia (Min) mice. Clin Sci (Lond) 105(3):323-330. PubMed: 12749762 MGI: J:84232
Bastide NM; Chenni F; Audebert M; Santarelli RL; Tache S; Naud N; Baradat M; Jouanin I; Surya R; Hobbs DA; Kuhnle GG; Raymond-Letron I; Gueraud F; Corpet DE; Pierre FH. 2015. A central role for heme iron in colon carcinogenesis associated with red meat intake. Cancer Res 75(5):870-9. PubMed: 25592152 MGI: J:219805
Batlle E; Bacani J; Begthel H; Jonkeer S; Gregorieff A; van de Born M; Malats N; Sancho E; Boon E; Pawson T; Gallinger S; Pals S; Clevers H. 2005. EphB receptor activity suppresses colorectal cancer progression. Nature 435(7045):1126-30. PubMed: 15973414 MGI: J:99366
Beazer-Barclay Y; Levy DB; Moser AR; Dove WF; Hamilton SR; Vogelstein B; Kinzler KW. 1996. Sulindac suppresses tumorigenesis in the Min mouse. Carcinogenesis 17(8):1757-60. PubMed: 8761438 MGI: J:101582
Belcheva A; Green B; Weiss A; Streutker C; Martin A. 2013. Elevated incidence of polyp formation in APC(Min/(+))Msh2(-)/(-) mice is independent of nitric oxide-induced DNA mutations. PLoS One 8(5):e65204. PubMed: 23741483 MGI: J:200824
Belcheva A; Irrazabal T; Robertson SJ; Streutker C; Maughan H; Rubino S; Moriyama EH; Copeland JK; Kumar S; Green B; Geddes K; Pezo RC; Navarre WW; Milosevic M; Wilson BC; Girardin SE; Wolever TM; Edelmann W; Guttman DS; Philpott DJ; Martin A. 2014. Gut microbial metabolism drives transformation of MSH2-deficient colon epithelial cells. Cell 158(2):288-99. PubMed: 25036629 MGI: J:214622
Bellafante E; Morgano A; Salvatore L; Murzilli S; Di Tullio G; D'Orazio A; Latorre D; Villani G; Moschetta A. 2014. PGC-1beta promotes enterocyte lifespan and tumorigenesis in the intestine. Proc Natl Acad Sci U S A 111(42):E4523-31. PubMed: 25288742 MGI: J:216428
Bellis J; Duluc I; Romagnolo B; Perret C; Faux MC; Dujardin D; Formstone C; Lightowler S; Ramsay RG; Freund JN; De Mey JR. 2012. The tumor suppressor Apc controls planar cell polarities central to gut homeostasis. J Cell Biol 198(3):331-41. PubMed: 22851318 MGI: J:191316
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):117-25. PubMed: 11215675 MGI: J:67445
Berger FG; Kramer DL; Porter CW. 2007. Polyamine metabolism and tumorigenesis in the Apc(Min/+) mouse. Biochem Soc Trans 35(Pt 2):336-9. PubMed: 17371273 MGI: J:122673
Bhandaru M; Kempe DS; Rotte A; Rexhepaj R; Kuhl D; Lang F. 2009. Hyperaldosteronism, hypervolemia, and increased blood pressure in mice expressing defective APC. Am J Physiol Regul Integr Comp Physiol 297(3):R571-5. PubMed: 19494170 MGI: J:152204
Bilger A; Shoemaker AR; Gould KA; Dove WF. 1996. Manipulation of the mouse germline in the study of Min-induced neoplasia. Semin Cancer Biol 7(5):249-60. PubMed: 9110402 MGI: J:40100
Bilger A; Sullivan R; Prunuske AJ; Clipson L; Drinkwater NR; Dove WF. 2008. Widespread hyperplasia induced by transgenic TGFalpha in ApcMin mice is associated with only regional effects on tumorigenesis. Carcinogenesis 29(9):1825-30. PubMed: 18310091 MGI: J:139925
Bjerknes M; Cheng H. 1999. Colossal crypts bordering colon adenomas in Apc(Min) mice express full-length Apc. Am J Pathol 154(6):1831-4. PubMed: 10362808 MGI: J:55509
Blanc V; Henderson JO; Newberry RD; Xie Y; Cho SJ; Newberry EP; Kennedy S; Rubin DC; Wang HL; Luo J; Davidson NO. 2007. Deletion of the AU-Rich RNA Binding Protein Apobec-1 Reduces Intestinal Tumor Burden in Apcmin Mice. Cancer Res 67(18):8565-73. PubMed: 17875695 MGI: J:124876
Bobe G; Wang B; Seeram NP; Nair MG; Bourquin LD. 2006. Dietary anthocyanin-rich tart cherry extract inhibits intestinal tumorigenesis in APC(Min) mice fed suboptimal levels of sulindac. J Agric Food Chem 54(25):9322-8. PubMed: 17147414 MGI: J:121119
Bogan C; Chen J; O'Sullivan MG; Cormier RT. 2009. Loss of EphA2 receptor tyrosine kinase reduces ApcMin/+ tumorigenesis. Int J Cancer 124(6):1366-71. PubMed: 19089910 MGI: J:147511
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Wood PA; Yang X; Taber A; Oh EY; Ansell C; Ayers SE; Al-Assaad Z; Carnevale K; Berger FG; Pena MM; Hrushesky WJ. 2008. Period 2 mutation accelerates ApcMin/+ tumorigenesis. Mol Cancer Res 6(11):1786-93. PubMed: 19010825 MGI: J:224283
Xia D; Wang D; Kim SH; Katoh H; DuBois RN. 2012. Prostaglandin E2 promotes intestinal tumor growth via DNA methylation. Nat Med 18(2):224-6. PubMed: 22270723 MGI: J:181279
Xia F; Altieri DC. 2006. Mitosis-independent survivin gene expression in vivo and regulation by p53. Cancer Res 66(7):3392-5. PubMed: 16585159 MGI: J:108219
Xu C; Reichert EC; Nakano T; Lohse M; Gardner AA; Revelo MP; Topham MK; Stafforini DM. 2013. Deficiency of Phospholipase A2 Group 7 Decreases Intestinal Polyposis and Colon Tumorigenesis in ApcMin/+ Mice. Cancer Res 73(9):2806-16. PubMed: 23361301 MGI: J:196880
Xu H; Posner GH; Stevenson M; Campbell FC. 2010. Apc(MIN) modulation of vitamin D secosteroid growth control. Carcinogenesis 31(8):1434-41. PubMed: 20488884 MGI: J:162653
Xu H; Zhang Y; Pena MM; Pirisi L; Creek KE. 2017. Six1 promotes colorectal cancer growth and metastasis by stimulating angiogenesis and recruiting tumor-associated macrophages. Carcinogenesis 38(3):281-292. PubMed: 28199476 MGI: J:241877
Xue X; Ramakrishnan SK; Shah YM. 2014. Activation of HIF-1alpha does not increase intestinal tumorigenesis. Am J Physiol Gastrointest Liver Physiol 307(2):G187-95. PubMed: 24875099 MGI: J:221716
Xue X; Shah YM. 2013. Hypoxia-inducible factor-2alpha is essential in activating the COX2/mPGES-1/PGE2 signaling axis in colon cancer. Carcinogenesis 34(1):163-9. PubMed: 23042097 MGI: J:193648
Xue X; Taylor M; Anderson E; Hao C; Qu A; Greenson JK; Zimmermann EM; Gonzalez FJ; Shah YM. 2012. Hypoxia-inducible factor-2alpha activation promotes colorectal cancer progression by dysregulating iron homeostasis. Cancer Res 72(9):2285-93. PubMed: 22419665 MGI: J:185744
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):895-901. PubMed: 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):6367-70. PubMed: 12438216 MGI: J:80301
Yamada Y; Jackson-Grusby L; Linhart H; Meissner A; Eden A; Lin H; Jaenisch R. 2005. Opposing effects of DNA hypomethylation on intestinal and liver carcinogenesis. Proc Natl Acad Sci U S A 102(38):13580-5. PubMed: 16174748 MGI: J:101415
Yamada Y; Mori H. 2007. Multistep carcinogenesis of the colon in Apc(Min/+) mouse. Cancer Sci 98(1):6-10. PubMed: 17052257 MGI: J:120998
Yamaguchi K; Cekanova M; McEntee MF; Yoon JH; Fischer SM; Renes IB; Van Seuningen I; Baek SJ. 2008. Peroxisome proliferator-activated receptor ligand MCC-555 suppresses intestinal polyps in ApcMin/+ mice via extracellular signal-regulated kinase and peroxisome proliferator-activated receptor-dependent pathways. Mol Cancer Ther 7(9):2779-87. PubMed: 18790758 MGI: J:152123
Yang K; Fan KH; Lamprecht SA; Edelmann W; Kopelovich L; Kucherlapati R; Lipkin M. 2005. Peroxisome proliferator-activated receptor gamma agonist troglitazone induces colon tumors in normal C57BL/6J mice and enhances colonic carcinogenesis in Apc(1638 N/+) Mlh1(+/-) double mutant mice. Int J Cancer 116(4):495-9. PubMed: 15818612 MGI: J:99671
Yang K; Popova NV; Yang WC; Lozonschi I; Tadesse S; Kent S; Bancroft L; Matise I; Cormier RT; Scherer SJ; Edelmann W; Lipkin M; Augenlicht L; Velcich A. 2008. Interaction of Muc2 and Apc on Wnt signaling and in intestinal tumorigenesis: potential role of chronic inflammation. Cancer Res 68(18):7313-22. PubMed: 18794118 MGI: J:141219
Yang X; Wood PA; Ansell CM; Ohmori M; Oh EY; Xiong Y; Berger FG; Pena MM; Hrushesky WJ. 2009. Beta-catenin induces beta-TrCP-mediated PER2 degradation altering circadian clock gene expression in intestinal mucosa of ApcMin/+ mice. J Biochem 145(3):289-97. PubMed: 19106159 MGI: J:149073
Yao LM; He JP; Chen HZ; Wang Y; Wang WJ; Wu R; Yu CD; Wu Q. 2012. Orphan receptor TR3 participates in cisplatin-induced apoptosis via Chk2 phosphorylation to repress intestinal tumorigenesis. Carcinogenesis 33(2):301-11. PubMed: 22159226 MGI: J:181110
Yekkala K; Baudino TA. 2007. Inhibition of intestinal polyposis with reduced angiogenesis in ApcMin/+ mice due to decreases in c-Myc expression. Mol Cancer Res 5(12):1296-303. PubMed: 18171987 MGI: J:134087
Yerushalmi HF; Besselsen DG; Ignatenko NA; Blohm-Mangone KA; Padilla-Torres JL; Stringer DE; Cui H; Holubec H; Payne CM; Gerner EW. 2006. The role of NO synthases in arginine-dependent small intestinal and colonic carcinogenesis. Mol Carcinog 45(2):93-105. PubMed: 16329147 MGI: J:107079
Yerushalmi HF; Besselsen DG; Ignatenko NA; Blohm-Mangone KA; Padilla-Torres JL; Stringer DE; Guillen JM; Holubec H; Payne CM; Gerner EW. 2006. Role of polyamines in arginine-dependent colon carcinogenesis in Apc(Min) (/+) mice. Mol Carcinog 45(10):764-73. PubMed: 16705737 MGI: J:115819
Yokomine K; Nakatsura T; Senju S; Nakagata N; Minohara M; Kira J; Motomura Y; Kubo T; Sasaki Y; Nishimura Y. 2007. Regression of intestinal adenomas by vaccination with heat shock protein 105-pulsed bone marrow-derived dendritic cells in Apc(Min/+) mice. Cancer Sci 98(12):1930-5. PubMed: 17892515 MGI: J:129988
Yoshida M; Zhao L; Grigoryan G; Shim H; He P; Yun CC. 2016. Deletion of Na+/H+ exchanger regulatory factor 2 represses colon cancer progress by suppression of Stat3 and CD24. Am J Physiol Gastrointest Liver Physiol 310(8):G586-98. PubMed: 26867566 MGI: J:234305
You S; Ohmori M; Pena MM; Nassri B; Quiton J; Al-Assad ZA; Liu L; Wood PA; Berger SH; Liu Z; Wyatt MD; Price RL; Berger FG; Hrushesky WJ. 2006. Developmental abnormalities in multiple proliferative tissues of Apc(Min/+) mice. Int J Exp Pathol 87(3):227-36. PubMed: 16709231 MGI: J:122752
Young LE; Moore AE; Sokol L; Meisner-Kober N; Dixon DA. 2012. The mRNA stability factor HuR inhibits microRNA-16 targeting of COX-2. Mol Cancer Res 10(1):167-80. PubMed: 22049153 MGI: J:205397
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):1367-80. PubMed: 11478486 MGI: J:70920
Yue HH; Diehl GE; Winoto A. 2005. Loss of TRAIL-R does not affect thymic or intestinal tumor development in p53 and adenomatous polyposis coli mutant mice. Cell Death Differ 12(1):94-7. PubMed: 15514675 MGI: J:94118
Yum MK; Kang JS; Lee AE; Jo YW; Seo JY; Kim HA; Kim YY; Seong J; Lee EB; Kim JH; Han JM; Kim S; Kong YY. 2016. AIMP2 Controls Intestinal Stem Cell Compartments and Tumorigenesis by Modulating Wnt/beta-Catenin Signaling. Cancer Res 76(15):4559-68. PubMed: 27262173 MGI: J:234840
Yusta B; Holland D; Waschek JA; Drucker DJ. 2012. Intestinotrophic glucagon-like peptide-2 (GLP-2) activates intestinal gene expression and growth factor-dependent pathways independent of the vasoactive intestinal peptide gene in mice. Endocrinology 153(6):2623-32. PubMed: 22535770 MGI: J:188646
Zechel JL; Doerner SK; Lager A; Tesar PJ; Heaney JD; Nadeau JH. 2013. Contrasting effects of Deadend1 (Dnd1) gain and loss of function mutations on allelic inheritance, testicular cancer, and intestinal polyposis. BMC Genet 14:54. PubMed: 23773267 MGI: J:221231
Zeilstra J; Joosten SP; Dokter M; Verwiel E; Spaargaren M; Pals ST. 2008. Deletion of the WNT target and cancer stem cell marker CD44 in Apc(Min/+) mice attenuates intestinal tumorigenesis. Cancer Res 68(10):3655-61. PubMed: 18483247 MGI: J:135025
Zeilstra J; Joosten SP; van Andel H; Tolg C; Berns A; Snoek M; van de Wetering M; Spaargaren M; Clevers H; Pals ST. 2014. Stem cell CD44v isoforms promote intestinal cancer formation in Apc(min) mice downstream of Wnt signaling. Oncogene 33(5):665-70. PubMed: 23318432 MGI: J:204874
Zeineldin M; Cunningham J; McGuinness W; Alltizer P; Cowley B; Blanchat B; Xu W; Pinson D; Neufeld KL. 2012. A knock-in mouse model reveals roles for nuclear Apc in cell proliferation, Wnt signal inhibition and tumor suppression. Oncogene 31(19):2423-37. PubMed: 21996741 MGI: J:186132
Zeineldin M; Jensen D; Paranjape SR; Parelkar NK; Jokar I; Vielhauer GA; Neufeld KL. 2014. Human cancer xenografts in outbred nude mice can be confounded by polymorphisms in a modifier of tumorigenesis. Genetics 197(4):1365-76. PubMed: 24913681 MGI: J:216876
Zeineldin M; Neufeld KL. 2013. Understanding phenotypic variation in rodent models with germline Apc mutations. Cancer Res 73(8):2389-99. PubMed: 23580574 MGI: J:197040
Zeitels LR; Acharya A; Shi G; Chivukula D; Chivukula RR; Anandam JL; Abdelnaby AA; Balch GC; Mansour JC; Yopp AC; Richardson JA; Mendell JT. 2014. Tumor suppression by miR-26 overrides potential oncogenic activity in intestinal tumorigenesis. Genes Dev 28(23):2585-90. PubMed: 25395662 MGI: J:217396
Zell JA; Ignatenko NA; Yerushalmi HF; Ziogas A; Besselsen DG; Gerner EW; Anton-Culver H. 2007. Risk and risk reduction involving arginine intake and meat consumption in colorectal tumorigenesis and survival. Int J Cancer 120(3):459-68. PubMed: 17096347 MGI: J:117825
Zeng Q; Phukan S; Xu Y; Sadim M; Rosman DS; Pennison M; Liao J; Yang GY; Huang CC; Valle L; Di Cristofano A; de la Chapelle A; Pasche B. 2009. Tgfbr1 haploinsufficiency is a potent modifier of colorectal cancer development. Cancer Res 69(2):678-86. PubMed: 19147584 MGI: J:143706
Zeytin HE; Patel AC; Rogers CJ; Canter D; Hursting SD; Schlom J; Greiner JW. 2004. Combination of a poxvirus-based vaccine with a cyclooxygenase-2 inhibitor (celecoxib) elicits antitumor immunity and long-term survival in CEA.Tg/MIN mice. Cancer Res 64(10):3668-78. PubMed: 15150127 MGI: J:90258
Zhang S; Li L; Kendrick SL; Gerard RD; Zhu H. 2014. TALEN-mediated somatic mutagenesis in murine models of cancer. Cancer Res 74(18):5311-21. PubMed: 25070752 MGI: J:215988
Zhang T; Nanney LB; Luongo C; Lamps L; Heppner KJ; DuBois RN ; Beauchamp RD. 1997. Concurrent overexpression of cyclin D1 and cyclin-dependent kinase 4 (Cdk4) in intestinal adenomas from multiple intestinal neoplasia (Min) mice and human familial adenomatous polyposis patients. Cancer Res 57(1):169-75. PubMed: 8988060 MGI: J:37447
Zhang T; Nanney LB; Peeler MO; Williams CS; Lamps L; Heppner KJ; DuBois RN; Beauchamp RD. 1997. Decreased transforming growth factor beta type II receptor expression in intestinal adenomas from Min/+ mice is associated with increased cyclin D1 and cyclin-dependent kinase 4 expression. Cancer Res 57(9):1638-43. PubMed: 9134999 MGI: J:40133
Zheng W; Wong KE; Zhang Z; Dougherty U; Mustafi R; Kong J; Deb DK; Zheng H; Bissonnette M; Li YC. 2012. Inactivation of the vitamin D receptor in APC(min/+) mice reveals a critical role for the vitamin D receptor in intestinal tumor growth. Int J Cancer 130(1):10-9. PubMed: 21328347 MGI: J:178583
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Also Known As: Min, multiple intestinal neoplasia

Donating Investigator

Genetic overview

Research Applications

Base Price

Detailed Description

Development

Control Suggestions

Additional Information

Selected References

ApcMin

Allele Symbol: ApcMin

Disease Terms

Research Areas By Genotype

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

Genotype: ApcMin related

Mammalian Phenotype Terms by Genotype

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

digestive/alimentary phenotype

mortality/aging

neoplasm

reproductive system phenotype

hematopoietic system phenotype

endocrine/exocrine gland phenotype

integument phenotype

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

mortality/aging

neoplasm

digestive/alimentary phenotype

homeostasis/metabolism phenotype

liver/biliary system phenotype

growth/size/body region phenotype

hematopoietic system phenotype

immune system phenotype

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

integument phenotype

mortality/aging

neoplasm

digestive/alimentary phenotype

cellular phenotype

endocrine/exocrine gland phenotype

hematopoietic system phenotype

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

mortality/aging

digestive/alimentary phenotype

Genotype: ApcMin/ApcMininvolves: C57BL/6J

cellular phenotype

Genotype: ApcMin/Apc+B6.Cg-Brca2tm1Mbn ApcMin

growth/size/body region phenotype

reproductive system phenotype

neoplasm

endocrine/exocrine gland phenotype

integument phenotype

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

mortality/aging

neoplasm

digestive/alimentary phenotype

cellular phenotype

homeostasis/metabolism phenotype

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

mortality/aging

neoplasm

digestive/alimentary phenotype

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

neoplasm

digestive/alimentary phenotype

hematopoietic system phenotype

homeostasis/metabolism phenotype

mortality/aging

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

neoplasm

digestive/alimentary phenotype

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

digestive/alimentary phenotype

hematopoietic system phenotype

immune system phenotype

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

embryo phenotype

growth/size/body region phenotype

Genotype: ApcMin/ApcMininvolves: C57BL/6 * POMOD

Apc^Min

Allele Symbol: Apc^Min

Genotype: Apc^Min related

Genotype: Apc^Min/Apc⁺
B6(AKR)-Apc^Min

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

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

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

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

Genotype: Apc^Min/Apc⁺
B6.Cg-Brca2^tm1Mbn Apc^Min

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

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

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

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

Genotype: Apc^Min/Apc⁺
involves: 129/Sv * 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^Min
involves: C57BL/6J * CAST/EiJ

Additional - Apc^Min related