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Type Chemically Induced Mutation; Coisogenic; Mutant Strain; Additional information on Genetically Engineered Mutant Mice. Mating System Inbred x Heterozygote (Female x Male) (C57BL/6J x Heterozygote) Species laboratory mouse Generation N65 (20-DEC-06) Donating Investigator Fang Jin, Univ of California, San Francisco ![]()
Appearance
black
Related Genotype: a/aDescription
The C57BL/6J-ApcMin/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-ApcMin 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-ApcMin 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-ApcMin heterozygous mice (Silverman et al., 2002).Development
The Min mutation was discovered in the progeny of a C57BL/6J male mutagenized by ethylnitrosourea. The founding (AKR x C57BL/6J)F1 female displayed circling behavior and was mated to a C57BL/6J male. Some progeny from this backcross developed adult onset anemia and intestinal adenomas. The circling behavior was determined to be a separate heritable trait and was eliminated through subsequent crosses to C57BL/6J. This strain was imported into The Jackson Laboratory in 1992.
| Control | ||
|---|---|---|
| Wild-type from the colony | ||
| 000664 C57BL/6J | ||
| Considerations for Choosing Controls | ||
Genetic Quality Control Annual Report
JAX® NOTES, Fall 1993; 455. The C57BL/6J-Min/+ Mouse.
View Related Disease (OMIM) Terms
Related Disease (OMIM) Terms
Adenomatous Polyposis of the Colon; APC - Models with phenotypic similarity to human disease where etiologies involve orthologs.1
1 Human genes are associated with this disease. Orthologs of those genes appear in the mouse genotype(s).
View Mammalian Phenotype Terms
Mammalian Phenotype Terms
assigned by genotype
ApcMin/Apc+
involves: C57BL/6 * C57BL/6J
- life span-post-weaning/aging
- premature death (MGI Ref ID J:134087)
- mice die at 169 days
- digestive/alimentary phenotype
- intestinal polyps (MGI Ref ID J:134087)
- mice develop more and bigger polyps than in ApcMin Myctm1Jlc heterozygotes
The following phenotype information may relate to a genetic background differing from this JAX® Mice strain.
ApcMin/Apc+
involves: AKR/J * C57BL/6J
- tumorigenesis
- intestinal adenocarcinoma (MGI Ref ID J:10209)
- locally invasive tumors seen in older animals but no metastasis
- sometimes small areas of carcinomas in anemic animals only
- intestinal adenoma (MGI Ref ID J:10209)
- visible tumors of the large and small intestine
- either polyploid, papillary or sessile adenomas
- digestive/alimentary phenotype
- melena (MGI Ref ID J:10209)
- bloody feces
- hematopoietic system phenotype
- anemia (MGI Ref ID J:10209)
- progressive adult onset anemia
- decreased hematocrit (MGI Ref ID J:10209)
- moribund animals with hematocrits around 10-20%
- homeostasis/metabolism phenotype
- hyperlipidemia (MGI Ref ID J:10209)
ApcMin/Apc+
involves: C57BL/6J
- life span-post-weaning/aging
- premature death (MGI Ref ID J:94108)
- heterozygotes begin to die at 7 months of age
- tumorigenesis
- intestinal adenoma (MGI Ref ID J:94108)
- small and large adenomas are seen throughout the intestine with more lesions found in the ileum compared to Apctm1Cip heterozygotes
- mammary adenocarcinoma (MGI Ref ID J:94108)
- 12% of heterozygotes developed mammary adenocanthomas
- digestive/alimentary phenotype
- rectal prolapse (MGI Ref ID J:94108)
- rectal prolapse is seen in 28% of surviving mutants at 7 months of age
ApcMin/Apc+
B6.Cg-Brca2tm1Mbn ApcMin
- growth/size phenotype
- decreased body weight (MGI Ref ID J:67445)
- 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
- *normal* reproductive system phenotype (MGI Ref ID J:67445)
- only observed in 1/9 ENU-treated males, similar to wild-type males (1/9)
- abnormal mammary gland development (MGI Ref ID J:67445)
- 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
- no differences are observed in branching of female mammary glands among genotypes or wild-type females
- abnormal ovarian follicle morphology (MGI Ref ID J:67445)
- remaining follicles are degenerating in ENU-treated females
- abnormal ovarian folliculogenesis (MGI Ref ID J:67445)
- arrested follicular development is 6-fold more prevalent compared to ENU-treated Brca2-deficient mice
- absent mature ovarian follicles (MGI Ref ID J:67445)
- abnormal vagina epithelium morphology (MGI Ref ID J:67445)
- reduced in thickness and lined with vacuolated cells indicative of anestrus in ENU-treated females
- absent corpus luteum (MGI Ref ID J:67445)
- absent in 26% of ENU-treated females
- ovary atrophy (MGI Ref ID J:67445)
- 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
- uterus atrophy (MGI Ref ID J:67445)
- observed in ENU-treated females displaying ovarian failure (atrophy); endometrium and myometrium appear immature
- tumorigenesis
- increased incidence of induced tumors (MGI Ref ID J:67445)
- multiple intestinal tumors are observed in ENU-treated mice, similar to Apc-heterozygous mice
- mammary gland tumor (MGI Ref ID J:67445)
- 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
- 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
- endocrine/exocrine gland phenotype
- abnormal adrenal gland morphology (MGI Ref ID J:67445)
- females exhibit some adrenal hyperplasia, while none is observed in males
- abnormal mammary gland development (MGI Ref ID J:67445)
- 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
- no differences are observed in branching of female mammary glands among genotypes or wild-type females
- abnormal ovarian follicle morphology (MGI Ref ID J:67445)
- remaining follicles are degenerating in ENU-treated females
- abnormal ovarian folliculogenesis (MGI Ref ID J:67445)
- arrested follicular development is 6-fold more prevalent compared to ENU-treated Brca2-deficient mice
- absent mature ovarian follicles (MGI Ref ID J:67445)
- absent corpus luteum (MGI Ref ID J:67445)
- absent in 26% of ENU-treated females
- ovary atrophy (MGI Ref ID J:67445)
- 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
View Research Applications
Research Applications
This mouse can be used to support research in many areas including:ApcMin related
Cancer Research
Increased Tumor Incidence (Adenomas: intestinal adenomas)
Increased Tumor Incidence (Mammary Gland Tumors)
Mouse/Human Gene Homologs
adenomatosis polyposis coli
| Allele Symbol | ApcMin | ||
|---|---|---|---|
| Allele Name | multiple intestinal neoplasia | ||
| Allele Type | Chemically induced (ENU) | ||
| Common Name(s) | ApcΔ850; Apc-; Apcdelta850; Min; Min-; | ||
| Mutation Made By | William Dove, University of Wisconsin | ||
| Strain of Origin | C57BL/6J | ||
| Gene Symbol and Name | Apc, adenomatosis polyposis coli | ||
| Chromosome | 18 | ||
| Gene Common Name(s) | AI047805; AU020952; AW124434; BTPS2; DP2; DP2.5; DP3; GS; Min; RATAPC; expressed sequence AI047805; expressed sequence AU020952; expressed sequence AW124434; multiple intestinal neoplasia; | ||
| General Note |
ApcMin, multiple intestinal neoplasia, dominant. A fully penetrant dominant mutation induced in a C57BL/6J mouse by ethylnitrosourea was designated Min because heterozygotes develop multiple adenomas throughout the intestine (J:10209). It was subsequently shown to be a base substitution mutation in the Apc gene which creates a stop codon truncating the polypeptide (J:830). ApcMin/+ mice develop an adult-onset progressive anemia characterized by a decreasing red cell countand an increasing proportion of reticulocytes, symptoms typical of anemia due to chronic blood loss. On the C57BL/6J genetic background on which ApcMin is maintained, this severe chronic anemia appears by 60 days of age and is probably the cause of death by 120 days of age in most affected mice. The anemia is presumably secondary to the development of multiple adenomas, which cause bleeding into the intestinal lumen (J:10209). In older mice, the adenomas may progress into intestinal adenocarcinomas (J:10209). ApcMin/+ female mice are prone to develop mammary cancer, and their mammary glands are more sensitive to chemical carcinogens than those of wild-type females. Tissue transplants into wild-type hosts show that the propensity to develop mammary tumors is intrinsic to the ApcMin/+ mammary tissue. Focal alveolar hypoplasias also arise in long-term grafts of ApcMin mammary glands (J:15101). ApcMin/+ males are fertile but females are rarely healthy enough to maintain a pregnancy (J:10209). Homozygous mice for Min fail to survive beyond day 7 of gestation (J:27993). In F1 hybrids, ApcMin/+ mice have a reduced number of tumors and may survive up to 300 days (J:10209). Tumors in C57BL/6J-ApcMin/+ mice are not invasive, but those in hybrid mice can become invasive. A single major modifying locus unlinked to Apc called Mom1 controls tumor number and growth rate (see Pla2g2a) (J:15703, J:37224). ApcMin/+ mutants provide a model for studying development of intestinal neoplasias. Intestinal adenomas from ApcMin/+ homozygotes tend to lose the chromosome carrying the wild-type allele (J:21369). Treatment of the heterozygotes with ethylnitrosourea (ENU) tends to increase formation of neoplasms, presumably by eliminating the normal allele. The type of neoplasm initiated is dependent on the age at mutagen treatment (J:29099). Human tumors from APC mutant heterozygotes also tend to show inactivation of the normal APC allele (J:21856). Mouse strains homozygous null for Trp53 and heterozygous ApcMin/+ show increased pancreatic neoplasia, with loss of the Apc+ allele in the neoplasms. These mice do not, however, develop increased intestinal malignancy (J:29664). A targeted chain-termination mutation in the Apc gene causes development of multiple intestinal neoplasms in a manner similar to that of the spontaneous ApcMin mutation (J:20443). It was noted that intestinal polyps in mice heterozygous for another targeted truncation mutation lose the normal Apc gene, like those from heterozygotes for the spontaneous mutation (J:25200). On the C57BL/6J genetic background on which ApcMin is maintained, severe chronic anemia appears by 60 days of age and is probably the cause of death by 120 days of age in most affected mice. The anemia is presumably secondary to the development of multiple adenomas, which cause bleeding into the intestinal lumen (J:10209). In older mice, the adenomas may progress into intestinal adenocarcinomas (J:10209). ApcMin/+ female mice are prone to develop mammary cancer, and their mammary glands are more sensitive to chemical carcinogens than those of wild-type females. ApcMin/+ males are fertile but females are rarely healthy enough to maintain a pregnancy (J:10209). Homozygotes fail to survive beyond day 7 of gestation (J:27993). In F1 hybrids ApcMin/+ mice have a reduced number of tumors and may survive up to 300 days (J:10209). Tumors in C57BL/6J-ApcMin/+ mice are not invasive, but those in hybrid mice can become invasive. A major modifying locus to Apc is Pla2g2a (formerly, Mom1), which controls tumor number and growth rate (J:15703, J:37224). Intestinal adenomas from ApcMin/+ homozygotes tend to lose the chromosome carrying the wild-type allele (J:21369). Human tumors from APC mutant heterozygotes also tend to show inactivation of the normal APC allele (J:21856). | ||
| 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. [MGI Ref ID J:830] | ||
Genotyping Protocols
ApcMin, EP, vers. 4
ApcMin, STD PCR, vers. 3
Helpful Links
Optimizing PCR Protocols
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 Ref ID 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 Ref ID J:830]
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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID 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 Ref ID J:90679]
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