Table 3.
Animal models used for different malignancies in studying tumor biology (other than tumor reversion)
| Model Type | Malignancy | Phenotype | References |
|---|---|---|---|
| CC10-rtTA; (tetO7)CMV-K RasG12D (Transgenic) | Lung Cancer | Bronchogenic adenocarcinomas. Phenotype is completely reversible upon Dox removal. | Fisher et al 2001 [117] |
| KPC Mouse model | Pancreatic Adenocarcinoma | It develops important key features observed in human PDA including pancreatic intraepithelial neoplasia alongside a robust inflammatory reaction including exclusion of effector T cells. KPC mouse contains a conditional point mutation in the transformation related protein 53 gene TP53R172H), and a point mutation in KRAS gene (KRASG12D) both of which generate non-functional proteins. | Hingorani et al 2005 [118] |
| NSG mice (NOD.Cg-Prkdcscid Il2rgtm1Wjl/SzJ) used for making human esophageal tumor xenograft using TE11 cell line | Esophageal squamous cell carcinoma | Subcutaneous treatment with pharmacological inhibitor entospletinib (GS-9973) for 10 days led to reduction in tumor growth by 55%. | Barbhuiya et al 2018 [119] |
| NOD-SCID mice implantation with MDA-MD-231 | Breast Cancer | hMAb173 treatment led to 60% reduction in the TNBC tumor growth compared to the control group. The microscopic study revealed that hMAb173 treatment effectively degraded AXL in tumor cells. | Wu et al 2015 [120] |
| Eμ-Tcl-1 transgenic mouse model | Chronic lymphocytic leukemia | The TCL1 gene of human origin under the control of the immunoglobulin heavy chain variable region promoter and immunoglobulin heavy chain enhancer (Eμ-Tcl-1). The model is time consuming due to disease delayed development, and TCL1 overexpression does not allow relextion of the genetic complexity of CLL. | Bichi et al 2002 [121] |
| human/mouse radiation chimera | CLL | Transplantation of CLL PBMC into peritoneal cavity of irradiated Balb/c or BNX mice, radio-protected with bone marrow from SCID mice. | Shimoni et al 1997 [122] |
| NOD/SCID | CLL | Transplantation of CLL PBMC in NOD/SCID mice and combining intravenously and in transperitoneally injection.. However, these mice still retain normal natural killer (NK), and myeloid cells, and these cells were likely responsible for interfering with the in vivo engraftment of some human leukemia’s/lymphomas. | Durig et al 2007 [123]. |
| Transgenic mice model with human MET in hepatocytes under the control of tetracycline | Hepatocellular carcinoma | In this study, early deaths prevented by feeding the mating parents and newborn pups doxycycline to repress expression of the MET transgene. Continued expression of MET is required for maintaining HCC. | Wang et al 2001 [124] |
| Transgenic mice model expressing KRas4bG12D under the control of doxycycline (a form of tetracycline) | Lung adenocarcinoma | DOX induction after two months led to development of adenoma, and adenocarcinoma of lungs, but removal of DOX in contrast caused rapid downregulation of mutant KRas RNA and auxillary apoptotic regression of an early proliferative lesions as well as tumors. | Fisher et al 2001 [117] |
| K14-rtTA/TetRE-ErbB2 ‘Tet-On’ bitransgenic mouse system | Skin carcinoma | Until ErbB2 expression induced by doxycycline (Dox), the animals were normal, but prenatal induction led to death. Skin hyperplasia observed in animals after two days, and Dox withdrawal reverted these changes to normal. | Xie et al 1999 [125] |