Table 1.
A yearly chronological listing of selected apc mouse models and their phenotypes
| Year published | Alterations | Description of Genotypea | Phenotype | Reference |
|---|---|---|---|---|
| 1990 | Apc Min/+ | Nonsense mutation in codon 850 of the Apc gene (Armadillo repeats present). | Adenomas of small intestine upon loss of heterozygosity, high mortality with increasing age, is a result of intestinal obstruction and anemia, no progression to adenocarcinoma. | Moser et al.21 |
| 1994 | Apc 1638N | Truncation mutation at Exon 15 (1638 aa) made using cellular homologous recombination (Armadillo repeats present). | Adenomas of small intestine (fewer than Apc Min/+) often duodenal, occasionally in colon. Fibromatosis (desmoid tumors), gastric carcinoma, cutaneous cysts, occasional liver metastasis found. | Fodde et al.32 |
| 1995 | Apc Δ716/+ | Nonsense mutation in codon 716 of the Apc gene using cellular homologous recombination (Armadillo repeats disrupted, C57BL/6J background). | Adenomas of the small intestine, ten-fold increase over Apc Min/+. | Oshima et al.36 |
| 1995 | Apc Min/+ p53−/− |
Apc Min/+ mutation21 simultaneous with p53 mutation.37 | Adenomas of the small intestine, no difference to Apc Min/+ mutation alone. | Clarke et al.38 |
| 1996 | Apc Min/+/Msh2+/+ and Apc Min/+/Msh2+/− and Apc Min/+/Msh2−/− | Apc Min/+ mutation21 simultaneous with Msh2 null mutation.39 | Accelerated small intestinal tumor formation (MSH2-deficient mice develop lymphomas). | Reitmair et al.39 |
| 1997 | Apc 580S | Apc Exon 14 flanked by loxP, induction by Adenovirus-Cre (AxCANCre or AxSRaCre) causes exon fourteen deletion and introduces a frameshift mutation at codon 580 (Armadillo repeats disrupted). | Homozygotes develop adenomas of distal rectum attributed to the location of virus delivery. When mice were left to age over one year, approximately 50% progressed to invasive adenocarcinoma, no metastasis. | Shibata et al.40 |
| 1997 | Apc Min/+p53−/− and Apc Min/+ p53+/− | Apc Min mutation21 simultaneous with homozygous recessive and heterozygous p53 mutation.41 | Adenomas of the small intestine, no difference to Apc Min/+ mutation alone. | Fazeli et al.42 |
| 1998 | Apc 1309/+ | Nonsense mutation at codon 1309 (Armadillo repeats and beta-catenin sites present). | Adenomas of small intestine, fewer in number and more proximal than Apc Min/+. | Quesada et al.43 |
| 1998 | Apc 1638N p53−/− | Apc 1638N mutation32 simultaneous with p53 homozygous recessive mutation.41 | Seven-fold increase in desmoid multiplicity. | Smits et al.44 |
| 1998 | Apc +/Δ716/Dpc4/+ | Apc Δ716 mutation36 in combination with Dpc4 (known at present as SMAD4) inactivated in the study. | Dpc4 (SMAD4) and Apc D716 double heterozygous mice lead to adenomas that develop to adenocarcinomas in the small intestine and colon with submucosal infiltration. | Takaku et al.45 |
| 1999 | Apc 1638N/+/Mlh1 −/− | Apc 1638N32 mutation simultaneous with Mlh1 homozygous recessive mutation inactivated in the study. | Increased tumor incidence and multiplicity, 30% adenocarcinomas, significantly reduced lifespan, high number of tumors outside the intestine. | Edelmann et al.46 |
| 2000 | Apc Min/+ Mom1/+/ p53−/− |
Apc Min/+21 simultaneous with Mom1AKR,47 (known at present as PLA2G2A) heterozygotes and p53 homozygous recessive mutations.48 | In this study, contrary to earlier model implications, p53 deficiency increases intestinal adenoma multiplicity, and malignancy mutations were on congenic background (C57BL6/J). | Halberg et al.49 |
| 2000 | Apc Min/+ Msh2−/− Apc 1638N Msh2−/− | Apc Min/+21 or Apc1638N/+32 simultaneous with Msh2 null knockout (exon 7 deletion).50 | Rapid tumor formation in the small intestine, early death (2–3 months), more tumors in Apc Min/+ Msh2 −/− mice. | Smits et al.50 |
| 2000 | Apc Δ474 | Mutant form of mRNA encoding only 474 aa of the Apc gene, created by exon duplication using homologous recombination. | Adenomas of the small intestine are present in duodenum, stomach, colon, and mammary gland. Mice treated with COX-2 inhibitor reduced the number of polyps. | Sasai et al.51 |
| 2002 | Apc Min/+ treated with azoxymethane (AOM) | Apc Min/+21 simultaneous with random unidentified mutations. | Significantly increased incidence of colonic adenocarcinomas. | Møllersen, Suzui et al.52,53 |
| 2002 | Apc Δ716/+ SMAD2/+ | Nonsense mutation in codon 716 of the Apc gene36 and heterozygous mutation of SMAD2 inactivated in the study. | Combination of Apc mutation and loss of SMAD2 leads to no changes in tumor size or properties compared to Apc Δ716/+ mice. | Takaku et al.54 |
| 2002 | Apc Δ580/+ SMAD2/+ | Nonsense mutation in codon 580 of the Apc gene40 and heterozygous mutation of SMAD2 inactivated in study. | Combination of Apc mutation and loss of SMAD2 leads to larger tumors, higher incidence of malignant phenotype compared to Apc Δ580/+ mice. | Hamamoto et al.55 |
| 2002 | Apc 1638N/+ Fen1/+ | Apc 1638N/+32 and Fen1/+ double heterozygous mice inactivated in study. | Increased malignancy of intestinal tumors compared to Apc1638N mice, Fen1 heterozygosity led to microsatellite instability in tumors. | Kucherlapati et al.56 |
| 2002 | Apc Δ716/+ Smad4 Apc Δ716/+ PTGS2(COX-2) Apc Δ716/+ PTGER2 |
Nonsense mutation in codon 716 of the Apc gene36 with Smad4,45 PTGS2(COX-2),57 or PTGER258 alterations. | Micro-vessel density (MVD) is determined in tumors. Apc Δ716 alone produced polyps, with Smad4 polyps progress to adenocarcinomas, MVD was size dependent; with PTGS and PTGER2, adenoma growth was suppressed, MVD did not increase. | Seno et al.59 |
| 2003 | Apc Δ716/+ CDX2/+ | Apc Δ716/+36 and CDX2/+ inactivated in the study, double heterozygous mice. | Increased adenoma formation in the colon reported, reduced number of polyps in the small intestine. | Aoki et al.60 |
| 2004 | Apc Δ14/+ | Heterozygotes have Apc Exon 14 deletion (Armadillo repeats deleted), Cre-loxP strategy (MeuCre40 transgene). | Reported shift of tumors to distal colon and rectum associated with rectal prolapse. | Colnot et al.61 |
| 2004 | Apc Min/+ treated with PhIP | PHIP (2-amino-1-methyl-6 phenylimidazo[4,5-b] pyridine) treatment of Apc Min/+21 mice leads to APC LOH. | Increased tumor initiation two- to three-fold compared to Apc Min/+ mice. | Møllersen et al.62 |
| 2005 | Apc Min/+ BubR1/+ | Apc Min/+21 BubR1/+ double heterozygous mice. | Increased colonic tumor initiation compared to Apc Min/+ (ten-fold) and progression by chromosomal instability. | Rao et al.63 |
| 2005 | Apc Min/+ EphB2 −/+ Apc Min/+ EphB3 −/+ Apc Min/+ EphB3 −/− | Apc Min/+21 mutation simultaneous with homozygous recessive and heterozygous EphB364 and heterozygous EphB2 mutation65 (dominant negative, transgenic). | Reduced adenomas of the small intestine, increased adenocarcinomas of the colorectum. | Batlle et al.66 |
| 2005 | Apc Min/+ MIF −/− | Apc Min/+ mutations simultaneous with homozygous MIF (cytokine macrophage migratory inhibitory factor) | MIF expression and “tautomerase” activity were higher in Apc Min/+ tumors (epithelial and stromal cells) over normal mucosa, increasing with higher grade tumors. Loss of MIF associated with reduction in the number of adenomas and angiogenesis suggesting MIF drives tumorigenesis. | Wilson et al.67 |
| 2006 | Apc CKO/FRT | Exon 14 of Apc flanked by loxP and FRT sites, “FLP e-deleter” used to make Apc CKO/+ mice. | Hung et al. used this conditional knockout to create sporadic colon tumors with metastasis by laparoscopy. | Kuraguchi et al.68, Hung et al.14 |
| 2006 | Apc Min/+ treated with dextran sulfate sodium salt (DSS) | Apc Min/+ mutation21 in the presence of inflammation and disruption of the intestinal epithelial lining caused by DSS. | High incidence of well-differentiated colonic carcinomas. | Tanaka et al.69 |
| 2006 | Apc 580S AhCreT/+ Kras/LSLV12/+ | Apc Exon 14 flanked by loxP,40 induction and deletion by AhCre, and Kras V12 mutation. (Cre induction in liver and intestine by napthoflavone treatment). | Kras V12 mutation has no effect on intestinal epithelium, APC loss in the presence of activated Kras increases tumor progression, 17% are invasive adenocarcinomas. | Sansom et al.70 |
| 2006 | Apc 1638N/TGFBR2flx/flx Villin-Cre | Apc1638N/+32 simultaneous with TGFRB2 −/− predominantly in intestine and colon | Tumor incidence unchanged, tumor progression to invasive adenocarcinoma | Muñoz et al.71 |
| 2006 | Apc Min/+ SMAD3−/− | Apc Min/+ mutation21 simultaneous with SMAD3 homozygous recessive mutation | Tumor progression in distal colon with mixed histology reduces lifespan, no metastases | Sodir et al.72 |
| 2006 | Apc 1638N SMAD4/+ | Apc +/1638N32 mutation simultaneous with SMAD4/DPC4 (SMAD4 E6sad, single nucleotide deletion in the exon 6 splice acceptor site results in unstable mRNA). Genes map to the same chromosome and are therefore analyzed "in cis" and "intrans" to each other. | Increased tumor multiplicity for double heterozygotes both "incis" and "intrans" LOH of SMAD4 occurs at later stages of tumor progression | Alberici et al.73 |
| 2007 | Apc 1638N/+ Exo1 +/− Fen1+/− | Double and triple heterozygous mice combinations for Apc 1638N,32 Exonuclease 1,74 and Flap endonuclease 1.56 | Increased tumor incidence, higher progression to malignancy, high incidence of hematopoietic cancers. | Kucherlapati et al.75 |
| 2007 | Apc Min/+ MYD88 −/− |
Apc Min/+21 MYD88−/− (innate immune signal transduction adaptor) |
MYD88 reduced the number of polyps, mortality decreased. | Rakoff-Nahoum et al.76 |
| 2008 | Apc 2lox14/+ Kras LSL-G12D/+ Apc 2lox14/+ Nras LSL-G12D/+ Fapbl-Cre (or) Villin-Cre |
APC Exon 14 flanked by loxP Kras and Nras flanked by loxP. Induction and deletion by Fapbl-Cre77 (or) Villin-Cre78 |
Kras G12D, but not NrasG12D, drives colon cancer progression. | Haigis et al.79 |
| 2008 | Apc1638N Rb1−/− Villin-Cre |
Apc1638N32 Rbtm2Brn80 Rb1 exon 19(20) flanked by loxP Villin-Cre78 |
Tumors of the small and large intestine. The small intestinal tumors are a mixture of adenomas and adenocarcinomas. Tumors of the cecum and proximal colon are mostly adenomas. | Kucherlapati et al.81 |
| 2009 | Apc Min/+ (C57BL/6) Apc Min/+ (SWR/J) Apc Min/+ (C57BR/cdcJ Apc Min/+ (Nbs1DB) |
C57BL/6J Apc Min/+21 bred with mice of different backgrounds to make hybrids (SWR/J or C57BR/cdcJ); APC Min/+ also bred with Nbs1DB (Nijmegen breakage syndrome alteration) | Hybrid Apc Min/+ mice had decreased adenoma frequency, longer survival, increased adenocarcinomas with occasional metastasis to the lymph nodes. The presence Nbs1 DB alteration created MSI that did not affect tumor multiplicity, mouse lifespan, or tumor progression |
Halberg et al.82 |
| 2009 | cis-ApcΔ716/+Smad4/+ Mmp7−/− | Apc truncated at codon 716 heterozygote,36 Smad4 heterozygote,45 with metalloproteinase (MMP7−/−)83 homozygous recessive | MMP7 knockout reduces tumor frequency and size but not invasiveness | Kitamura et al.84 |
| 2009 | Apc 1638N/+ Notch1 | Apc 1638N32 mutation simultaneous with a constitutively activated NOTCH1 receptor | Notch1 activation reported to result in increased adenoma formation at an earlier age, decreased survival, dysplastic lesions in the colon | Fre et al.85 |
| 2009 | Apc 1322T | Nonsense mutation at codon 1322, transcript retain the first 20- armadillo repeats | High number of adenomas of the proximal small intestine, small number in the colon and stomach | Pollard et al.86 |
| 2010 | APC Δ242 | Gene trap cassette placed between exons 7 and 8 of Apc gives truncated fusion transcript without armadillo repeats | Adenomas found higher in numbers, smaller in size, histology same as for ApcMin/+ mice | Crist et al.87 |
| 2010 | Apc 15lox/+ | Exon 15 flanked by loxP sites, induction by Fabpl (Fatty acid binding protein) Cre | Increased survival due to small number of tumors, larger tumors found in the colon. Ninety-one percent of mice have low-grade adenoma, 50% adenocarcinoma | Robanus-Maandag et al.88 |
| 2010 | Apc 580S/+ | Nonsense mutation in codon 580 of the Apc gene40 (armadillo repeats present), induction by Cre transgene under control of Carbonic anhydrase 1 promoter (limited to large intestine) | Transgene expression limited to the large intestine, adenoma formation without malignancy. | Xue et al.89 |
| 2010 | Apc fle 1-15 | Complete deletion of the entire APC gene (exons 1–15) by Villin-Cre | More severe polyposis compared to Apc Min/+ mice | Cheung et al.90 |
| 2010 | APC CKO/FRT/Kras | Removal of exon 14 of APC68 by orthotopic application of Adenoviral-Cre, mated to mice with K-ras G12D activation mutation | Adenocarcinomas of the colon, 20% liver metastasis | Hung et al.,14 Roper et al.91 |
| 2010 | Apc Min/+ Fbw7ΔG | APC Min/+ mutation21 simultaneous with E3 ubiquitination ligase F box and WD repeat containing 7 (Fbw7) exon 5 deleted | APC Min+/− Fbw7 −/− mice had enhanced tumor numbers and tumor size, APC Min+/− Fbw7 +/− mice increased tumor number but not tumor size. | Sancho et al.92 |
| 2010 | Apc Min/+ IL17A −/− |
Apc Min/+21 IL17A (exons 1 and 2 deleted)93 |
Intestinal tumorigenesis reduced, recovery of thymic and splenic cellularity. | Chae et al.94 |
| 2010 | Apc Min/+ MYD88 −/− |
Apc Min/+21 mutation simultaneous with MYD8895 (innate immune signal transduction adaptor) removal. | Lower phospho-ERK levels, fewer and smaller intestinal epithelial cell tumors than Apc Min/+ mice. | Lee et al.96 |
| 2011 | Apc Min/+ IL-17F −/− |
Apc Min/+21 IL-17F (exons two deleted)97 |
Inhibition of spontaneous intestinal tumorigenesis, partially restores thymic atrophy, does not affect splenomegaly. | Chae et al.98 |
| 2012 | Apc Min/+ MCP1 −/− |
Apc Min/+21 MCP1/CCL2 −/− (Monocyte chemoattractant protein, purchased from Jackson Labs) |
MCP1 knockout decreased polyps 20–45%. | McClellan et al.99 |
| 2012 | Apc Min/+ IKKβ(transgene/overexpression) |
Apc Min/+21 IKKβ (inhibitor of NF-kB). |
More early lesions and visible small intestinal and colonic tumors than Apc Min/+. | Shaked et al.100 |
| 2013 | Apc 580S/+ CDX2P-CreERT2 | APC 580S40 conditional knockout by CDX2P-CreERT2-Cre regulation through tamoxifen added to chow. | Apc knockout led to changes in proliferation, apoptosis, morphology, mitotic spindle axis misorientation, b-catenin nuclear localization, induction of stem cell marker and Sox9, ectopic Paneth-like cell so observed. | Feng et al.101 |
| 2013 | APC CKO/FRT/BrafVE | Removal of exon fourteen of APC68 and exons 15–17 of Braf (BrafV600E) by orthotopic application of Adenoviral-Cre leads to focal inactivation of Apc and activation of Braf. | Sessile serrated adenoma with dysplasia, adenocarcinoma, and invasive carcinoma. | Coffee et al.102 |
| 2013 | Apc Min/+ IL-8 human transgene/overexpression |
Apc Min/+21 IL-8 (interleukin 8/initiator of inflammation) transgene not found naturally in mice. | Increased tumorigenesis with transgene. | Asfaha et al.103 |
| 2014 | Apc Min/+ on hybrid background | Apc Min/+21 model described earlier82 on different backgrounds, treated with DSS | Histology reassessed, tumors develop in the distill colon, with occasional progression to adenocarcinoma. | Paul Olson et al.104 |
| 2014 | Apc 580S/+ Kras LSL-G12D/+ CAC+ | CAC-Cre under the control of Carbonic anhydrase promoter inactivates APC40 and Kras | Adenomas formed. | Byun et al.105 |
| 2014 | Apc 580S Pten fl/fl Kras LSL/+ Villin-Cre (ERT) |
APC 580S: conditional knockout40 PTEN: Exons 4–5 flanked by LoxP106 Kras (LoxP/Stop/LoxP)107 gives G12V inducible oncogenic mutation. Villin-Cre ERT78 is under the control of the Estrogen receptor promoter. |
Survival reduction, adenomas, occasional adenocarcinomas of the small intestine, no metastasis. | Davies et al.108 |
| 2015 | Sh Apc Kras G12D P53 fl/fl Lgr5 +/+ |
Short hairpin RNA regulated by doxycycline responsive promoter/Cre suppresses Apc expression in colonic epithelium. The effects of compound mutations to Kras (activation) and p53 (deactivation) and reversible Apc loss are examined. | The histological and molecular features of colon cancer are recapitulated and are reversed upon Apc re-expression. Apc loss increases MYC-dependent proliferation. | Dow et al.109 |
| 2015 | Apc Δ 716 TGFBR2 fl/fl Villin-Cre (ERT) |
Apc36 and TGFBR2 are conditionally knocked down using Villin-Cre (ERT) | Only invasive adenocarcinomas found to have inflammatory microenvironment; treatment with DSS caused invasive colon cancer. TGFΒ signaling disruption in the presence of inflammation is sufficient to produce colon cancer | Oshima et al.110 |
| 2015 | Apc fl/fl KrasG12D/+ PIK3CA+ |
Apc fl/fl68 Kras G12D PIK3CA Cre-Adenovirus (orthotopic injection) |
Additional mutations to Apc cause progression to adenocarcinoma and metastasis. | Hadac et al.111 |
| 2016 | A/J Apc Min/+ | Apc Min/+21 on A/J background | Increased tumor initiation in intestine, increased progression (50% adenocarcinoma). Carcinoma of the colon (21%). | Sødring et al.112 |
| 2016 | Apc CKO/FRT LSL Kras G12D CDX2P9.5-G22Cre |
Apc68 inactivation, Kras activation by CDX2P9.5-G22Cre (“CDX2” is caudal type homeobox protein, normally expressed in the proximal colon). | Moderately differentiated adenocarcinomas of the proximal colon, Kras mutation did not increase malignancy. | Kawaguchi et al.113 |
| 2016 | Apc CKO/FRT Kras LSL G12D/+ P53KO Smad4 fl/fl Car1CreER |
Apc68 inactivation, Kras activation, p53 knockout, Smad4 inactivation using Car1CreERT2 (Carbonic anhydrase promoter enhancer under the control of Estrogen receptor 2 controls Cre recombinase upon tamoxifen induction). | No adenomas of the small intestine. Apc and Kras led to colonic adenomas. Compound mutations Apc, Kras, p53, Smad4 led to aggressive colonic carcinomas with occasional lymph-node invasion. | Tetteh et al.114 |
| 2017 | Apc Δ716 TP53 +/LSL-R270H Apc Δ716 TP53 LSL-R270H/LSL-R270H Villin-Cre ER |
Apc36 inactivation by Villin-Cre, TP53 mutant allele TP53R270H/R270H generated after removal of floxed TP53 by Villin-Cre ER. | Apc Δ716 with homozygous mutation to p53 die of lymphoma, heterozygotes have invasive adenocarcinomas with evidence of epithelial to mesenchyme transition (EMT). | Nakayama et al.115 |
| 2017 | Apc CKO/FRT | Orthotopic injection of PGK::Cre lentivirus, Ad5CMV::Cre, Villin-Cre ER, or U6::sgApc-EFS::Cas9-P2A-GFP into “mucosa bubble” of Apc CKO/FRT68 mice inactivates Apc. | Rapid tumor formation with histological features of adenomatous change and CTNNB1 nuclear localization using PGK::Cre lentivirus, Villin-Cre ER. U6::sgAPC-efs::Cas9-P2A-GFP delivered the Crispr-Cas9 system and inactivated Apc produced tumors in 34% of the mice. (The study also looked at tumor-associated genes TP52 and Kras in combination with Apc). |
Roper et al.116 |
| 2017 | Apc Min/+ TDG fl/fl Fabpl:Cre |
Apc Min/+21 mutation with Thymine DNA Glycosylase (TDG) exons 3–6 are deleted by Fabpl::Cre | TDG knockout in Apc Min/+ mice led to a two-fold increase in adenomas in female mice. | Xu et al.117 |
| 2017 | Apc Min/+ PLD1 −/− AOM/DSS |
Apc Min/+21 PLD −/− exons 13–14 deleted. |
Decreased number of adenomas. | Kang et al.118 |
| 2018 | Apc Δ716 Kras +/LSL-G12D TGFBR2 fl/fl TRP53 +/LSL-R270H FBXW7fl/fl Villin-CreER |
Various combinations examined: Apc Δ71636 Kras +/LSL-G12D119 TGFBR2 fl/fl120 TRP53 +/LSL-R270H121 FBXW7fl/fl122 Villin-CreER78 |
Apc alteration led to adenomas, addition of TRP53R270H or TGFBR2 deletion induced submucosal invasion. KrasG12D activation led to epithelial-mesenchymal transition (EMT) and lymph vessel intravasation. Apc alteration with Kras G12D and FBXW7 insufficient for submucosal invasion but not EMT histology. Apc, Kras, TGFBR2 were sufficient for metastasis. |
Sakai et al.123 |
| 2018 | Apc Min/+ | Apc Min/+21 | Computer learning-based algorithm gives quantitative analysis of immunofluorescence staining on whole colon sections, used to characterize the immune environment. Total leukocytes and T cell sub-populations are counted in colonic mucosa, lymphoid follicles, and tumors. T cells quantified in lymphoid follicles. | Cassé et al.124 |
| 2018 | Apc Min/+ Tob1 AOM/DSS treated |
Apc Min/+21 Tob1 −/− |
Reduced tumorigenesis | Li et al.125 |
| 2019 | Apc Min/+ Apc 580S Villin-Cre ERT2 Rosa |
Apc Min/+21 Apc 580S40 Villin-Cre ERT2 Rosa (reference not given) Vaccine to MYB (overexpressed transcription factor in polyps) given to both models with anti PD-1 antibody. |
The TetMYB vaccine is shown to be effective in both prophylactic and therapeutic animal models, the vaccine will be used in a future clinical trial. | Pham et al.126 |
| 2019 | Apc580S Cdx2-CreERT2 Mcl1 fl/fl LysMCre AOM/DSS |
Apc580S40 Mcl1−/− (neutrophil deficient)127 Microbiota assessed |
Neutrophils slowed colon tumor growth and progression over controls by restricting numbers of bacteria and tumor-associated inflammatory response. | Triner et al.128 |
| 2019 | Apc fle 1-15 | Apc fle 1–1590 Villin-Cre TFAMfl/fl129 |
TFAM deficiency diminishes mitochondrial formation and oxidative phosphorylation, site-specific removal prevented tumorigenesis in Apc-mutant mouse intestines. | Wen et al.130 |
| 2020 | Apc Min/+ Mucin 2 −/−(Winnie) |
Apc Min/+21 Mucin 2 −/−(Winnie)131 |
Winnie-ApcMin/+ mice combine an inflammatory background with a genetic predisposition to CRC. Aberrant crypt foci form in the colon recapitulating human CRC. | De Santis et al.132 |
| 2021 | Apc Min/+ | Apc Min/+21 pretreated with rapamycin | Rapamycin extended lifespan of Apc Min/+ mice. | Parihar et al.133 |
| 2021 | Apc Min/+ | Apc Min/+21 inoculated with Fusobacterium nucleatum, treated with aspirin. | Aspirin-supplemented chow is sufficient to inhibit F. nucleatum-potentiated colonic tumorigenesis. | Brennan et al.134 |
| 2021 | Apc fle 1-15 Cdx2P-CreERT2 |
Apc fle 1–1590 or Apc Min/+ animals treated with NSAID (sulindac) and rexinoid (bexarotene). | Significant polyp reduction. | Bowen et al.135 |
a
In Table 1, the first time an Apc mutation is mentioned the alteration is described under “Description of Genotype” and the reference for its creation given under “Reference”. When mentioned in a second study, references for all alterations are given under “Description of Genotype”, and the study examining compound gene alterations is under “Reference”.