Identification ofMom12andMom13, two novel modifier loci ofApcMin-mediated intestinal tumorigenesis

Crist, Richard C.; Roth, Jeffrey; Lisanti, Michael P.; Siracusa, Linda D.; Buchberg, Arthur M.

doi:10.4161/cc.10.7.15089

Cited by 18 publications

(11 citation statements)

References 41 publications

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“…Some Mom genes are found on chromosome 18. Some modifiers are single genes, others are thought to represent contiguous genes, and some remain less well-defined [50–54]. The modifiers appear to function as recessive, dominant, or semi-dominant loci.…”

Section: Apcmin/+mentioning

confidence: 99%

More than two decades of Apc modeling in rodents

Zeineldin

Neufeld

2013

Biochimica et Biophysica Acta (BBA) - Reviews on Cancer

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Section: Apcmin/+mentioning

confidence: 99%

More than two decades of Apc modeling in rodents

Zeineldin

Neufeld

2013

Biochimica et Biophysica Acta (BBA) - Reviews on Cancer

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“…The Mom-2 ( Atp5a1 ) allele is on the same chromosome as Apc (chromosome 18) and appears to inhibit loss of the wild-type Apc allele (48, 51). The mechanisms of action of other modifiers such as Mom-3 , Mom-7 , Mom-12 and Mom-13 are not understood (52–54). …”

Section: Introductionmentioning

confidence: 99%

Understanding Phenotypic Variation in Rodent Models with Germline Apc Mutations

Zeineldin

Neufeld

2013

Cancer Research

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Adenomatous Polyposis Coli (APC) is best known for its crucial role in colorectal cancer suppression. Rodent models with various Apc mutations have enabled experimental validation of different Apc functions in tumors and normal tissues. Since the development of the first mouse model with a germline Apc mutation in the early 1990s, twenty other Apc mouse and rat models have been generated. This article compares and contrasts currently available Apc rodent models with particular emphasis on providing potential explanations for their reported variation in three areas: 1) intestinal polyp multiplicity, 2) intestinal polyp distribution, and 3) extra intestinal phenotypes.

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“…27,28 Breeding of penetrant C57Bl/6J-derived Apc Min mutation onto different genetic backgrounds (A/J, AKR/J, BTBr, 129P2/OlaHsd) identified modifier loci Mom1-Mom13. [29][30][31][32][33][34][35][36] Human chromosomal regions (Chr. 1p35-36) showing conserved synteny with mouse Mom1 and Mom4 have been associated with familial and sporadic cases of CRC.…”

Section: Resultsmentioning

confidence: 99%