Table 1.
Host/Strain | Genetic Manipulation | Carcinogen | Irritant or Manipulation | Incidence and Duration | Inflammatory Reaction | Reference |
---|---|---|---|---|---|---|
Swiss H mouse | No | No | Mainstream cigarette smoke | Lung adenosquamous carcinomas (52%), bronchioloalveolar carcinoma (20%), squamous cell carcinoma (18%), and squamous cell carcinoma in situ (5%) at 30 weeks | Mainstream cigarette smokes evoke chronic inflammation in the lungs | [20] |
C57BL/6 mouse | No | B[a]p | LPS | Lung tumors (97%) at 30 weeks | ↑ IL-1β, cleaved IL-1β, IL-18, NLRP3, NLRP6, and caspase-1 | [23] |
A/J mouse | No | NNK | LPS | Lung tumors (100%) at 27 weeks | LPS induces recruitment of macrophages and located at the periphery of the tumors ↑ NF-kB |
[16] |
C57BL/6 mouse | No | B[a]p | LPS | Non-small cell lung cancers (almost 100%) at 30 weeks | Acceleration of tumor malignancy by LPS-induced inflammation | [24] |
BALB mouse | No | MCA | Butylated hydroxytoluene | Lung tumor (100%) at 20 weeks | Butylated hydroxytoluene-induced inflammation | [25] |
WBN/Kob rat | No | No | Alloxan | Forestomach well-differentiated squamous cell carcinoma (20%) at 50 weeks | Accumulation of neutrophils and stimulation of superoxide production ↑ iNOS and COX-2 |
[35] |
CD-1 mouse neonatal | No | No | Monosodium glutamate | HCC (43%) at 54 weeks | Infiltration of neutrophils, lymphocytes, and fibrosis | [57] |
CD-1 mouse neonatal | No | DEN | Monosodium glutamate | Foci of cellular alteration (100%), adenoma (80%), and HCC (50%) at 21 weeks | Infiltration of macrophages and ROS ↑ TNF-α, IL-1ß, IL-6, F4/80 and CCL2 |
[56] |
F344 rat | No | DEN | Thioacetamine | Pre-neoplastic hepatocellular lesions and glutathione S-transferase placental (GST-P) form at 8 weeks | Induction of hepatic macrophages and CD3+ T cells ↑ IL-1ß, COX-2, HO-1, and MMP-12 |
[66] |
C57BL/6 mouse | Gankyrinhep TG | No | CCl4 | Hepatic tumors at 16 weeks | Chronic inflammation and fibrosis ↑ TGF-β, Collagen-1, and TIMP1 |
[72] |
F344 rat | No | No | CCl4 | HCC (6%) and hepatic altered cell foci at 104 weeks | Cirrhosis, fibrosis, and fatty changes | [68] |
FVB mouse | K-rasG12D | No | Caerulein | Pancreatic cancer develop in K-rasG12D mice at 48 weeks. Caerulein shortened to 11 weeks. Caerulein formed high-grade pre-malignant PanIN at 4 weeks, and low-grade PanIN at 8 weeks and developed PDAC | There were foci of cancer cells that were surrounded by a reactive stroma characterized by smooth muscle actin expression | [76] |
C57BL/6 mouse | K-rasG12V | No | Caerulein | Pancreatic cancer never developed in K-rasG12V mice at least until 80 weeks. Caerulein developed PDAC (100%) at 32 weeks | Caerulein induces chronic pancreatitis and fibrosis. Inflammatory infiltrates consisting of neutrophils and eosinophils, CD3+ T cells and B cells, and macrophages | [144] |
Sprague-Dawley rat | No | No | Carrageenan | Colorectal squamous cell carcinoma (20%), adenocarcinoma (13%), adenoma (5%), and metaplasia (98%) at 96 weeks | Induction of colitis | [145] |
Wister Furth rat | No | DMBA | No | Mammary carcinoma resistant strain | ↑CX3CL1, IL11RA, IL-4, C3, CCL11, ITGB2, CXCL12, and CXCR7 ↓ CCL20 |
[146] |
Sprague-Dawley rat | No | No | Carrageenan | Rectal squamous metaplasia and colonic adenomatous polyps at 24 weeks | Acute and chronic inflammatory, in which aggregation of macrophages in the lamina propria and submucosa | [147] |
Wister rat | No | No | Carrageenin | Sarcomas (15%) at 93 weeks and 28% at 118 weeks | Neutrophils and macrophages with phagocytosed carrageenin, fibroblasts and mature collagen fibers were formed | [148] |
Syrian hamster | No | No | DSS | Colorectal adenocarcinoma (50%), adenoma (13%), and dysplasia (50%) at 26 weeks | Infiltration of neutrophils | [81] |
CBA mouse | No | No | DSS | Colorectal adenocarcinoma (8%) and dysplasia (52%) at 27 weeks | Focal inflammatory cell infiltration including neutrophils and gland loss or crypt abscess formation; mucosal ulceration was observed by DSS treatment | [149] |
ACI rat | No | No | DSS | Colorectal papilloma (53%), adenoma (3%), squamous cell carcinoma (13%), adenocarcinoma (17%), cecum adenocarcinoma (3%), and intestinal tumor (73%) formed until 94 weeks | [150] | |
ACI rat | No | No | DSS | Colon adenoma (19%), adenocarcinoma (19%), papilloma (12%), cecum adenoma (23%), adenocarcinoma (8%), and intestinal tumor (58%) until 31 weeks | Infiltration of inflammatory cells and hemorrhage | [151] |
C57BL/6 mouse | TSP-1−/− | No | DSS | Colonic dysplasia (66%) at 12 weeks | No significant changes in inflammation were observed between the genotypes; myeloperoxidase (MPO) activity was higher in the colon of TSP-1−/− mice ↑ VEGF and bFGF |
[82] |
CD-1 mouse | No | DMH | Chrysazin | Colonic adenocarcinoma (48%) and adenoma (57%) at 54 weeks | Mucosal gland was hypertrophic and infiltration of inflammatory cells with fibrosis in submucosal areas | [152] |
C57BL/6 mouse | KK-Ay | AOM | No | Aberrant crypt foci (ACF) (100%) and colorectal tumor including well- and moderate-differentiated adenocarcinoma, and mucinous carcinoma (87%) at 25 weeks | Macrophage infiltration ↑ CSF1, IL-1ß, MCP1, and OPN |
[103] |
CBA mouse | No | AOM | DSS | Colorectal tumors at 11 weeks | Infiltration of inflammatory cells on the left side of the large intestine followed by the transverse colon | [83] |
CD-1 mouse | No | AOM | DSS | Colonic adenocarcinoma (100%) and adenoma (38%) at 20 weeks | β-catenin-, COX2- and iNOS-positive inflammatory cells were infiltrated into mucosal ulceration | [80] |
F344 rat | No | AOM | DSS | Aberrant crypts foci at 6 weeks | - | [153] |
C57BL/6 mouse | No | AOM | DSS Chronic subordinate colony housing |
Colonic dysplasia (100%) at 27 weeks | Increase regulatory CD3+FoxP3+ cells within mesenteric lymph node ↑ TNF, FoxP3, COX-2, and ß-catenin ↓ IFN-γ |
[90] |
C57BL/6 mouse | Lf−/− | AOM | DSS | Colonic dysplasia (31%) at 18 weeks | Acceleration of colitis ↑ IL-1ß, IL-6, CXCL1, MCP1, TNF-α, IFN-γ, NF-κB, and COX-2 |
[104] |
C57BL/6 mouse | Nrf2−/− | AOM | DSS | Colonic tumors (93%) at 20 weeks and tumors consisted of adenomas (20%) and adenocarcinomas (80%) | Increased stromal nitrotyrosine-positive cells ↑ COX-2 (PGE2) and 5-LOX (LTB4) |
[154] |
C57BL/6 mouse | Syndecan-1−/− | AOM | DSS | Colonic adenomas (100%) with high-grade dysplasia at 9 weeks | Severe inflammation especially macrophage infiltration ↑ IL-6 and CCL2 |
[106] |
C57BL/6 mouse | TLR2−/− | AOM | DSS | Large colorectal tumors, higher grade dysplasia (carcinoma in situ), and ACF at 9 weeks | Increased inflammatory cell infiltration ↑ IL-6, IL-17A, and phospho-STAT3 |
[155] |
C57BL/6 mouse | No | AOM | TNBS | Aberrant crypts foci at 6 weeks | Severe colonic inflammation, mainly neutrophils and edema of submucosal and muscle layers | [87] |
Wister rat | No | No | Ferric nitrilotriacetate | Renal adenoma or adenomatous hyperplasia (58%) and adenocarcinoma (54%) at 36 weeks | Acute nephrotoxicity in the proximal tubular epithelium and ROS generation by Fe2+ through Fenton reaction | [127] |
F344 rat | No | No | Nickel subsulfide plus magnesium carbonate or iron |
Renal mesenchymal tumors formed nickel alone (63%), nickel + magnesium (20%), and nickel + iron (60%) until 104 weeks | Nickel induced necrosis, inflammation (macrophages), fibrosis in the proximal tubular epithelium at the injection site | [128] |
SKH-1 hairless mouse | Ptch1+/− | No | UVB | Basal cell carcinoma (100%) at 30 weeks | Recruitment of macrophages, neutrophils, mast cells, myeloid-derived suppressor cells (MDSCs), dendritic cells, NK cells, T cells, and B cells | [133] |
Balb/c nude mouse | Xpa−/− | No | UVB | Skin tumor formation at 25 weeks | Neutrophil infiltration and ROS generation ↑ CXCL1, PGE2, TNF-α, and 8-OHdG |
[134] |
Abbreviations used are AOM, Azoxymethane; B[a]p, Benzo[a]pyrene; CCl4, carbon tetrachloride; DEN, N-diethylnitrosamine; DMBA, 7,12-Dimethylbenz[a]anthracene; DMH, 1,2-Dimethylhydrazine; DSS, Dextran sulfate sodium; HCC, hepatocellular carcinoma; iNOS; inducible nitric oxide synthase; LPS, lipopolysaccharide; MCA, 3-methylcholanthrene; NNK, nicotine-derived nitrosamine ketone [4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone]; PDAC, pancreatic ductal adenocarcinoma; TNBS, 2,4,6-Trinitrobenzenesulfonic acid; and UVB, ultraviolet B.