Tumor Models for Efficacy Determination

Abstract

Th e fi rst in vivo tumor models were developed in the mid-1960s. Th ese models were mouse leukemia models grown as ascites. Th e growth pattern was like that of bacteria in vivo and therefore it was possible to apply similar mathematics of growth and response to these tumors as had been worked out for bacteria. Since the development of the murine leukemia models, investigators have devoted a large eff ort to modeling solid tumors in mice. Th ere are now a variety of models including syngeneic mouse tumors and human tumor xenografts grown as s.c. nodules, syngeneic mouse tumors and human tumor xenografts grown in orthotopic sites, models of disseminated disease, "labeled" tumor models that can be visualized using varied technologies, and transgenic tumor models. Each of these types of models has advantages and disadvantages to the "drug hunter" searching for improved treatments. [Mol Cancer Th er 2006;5(10):2435-43]

Resveratrol Exerts Differential Effects in Vitro and in Vivo against Ovarian Cancer Cells

“…injections beginning on the 7 th day post-implantation, significantly inhibited the growth of xenografted SKOV3 carcinoma in nu/nu mice via apoptosis regulated through the mitochondrial apoptotic pathway (Guo et al, 2010). Although a tumor xenograft model may not be readily interpreted as the true physiologic or clinical condition (Gescher & Steward, 2003;Becher & Holland, 2006;Teicher, 2006), our results may indicate differential response of resveratrol on orthotopic ovarian cancer as compared to xenograft models.…”

In vivo evaluation of cetuximab-conjugated poly(γ-glutamic acid)-docetaxel nanomedicines in EGFR-overexpressing gastric cancer xenografts

“…23,30,31 The four groups tested were: group 1: control saline (n=4); group 2: free DOCT (n=4); group 3: nontargeted DOCT-γ-PGA Nps (n=4) and group 4: targeted CET MAb-DOCT-γ-PGA Nps (n=4). Three doses (10 mg/kg of DOCT and Nps with equivalent DOCT) were administered intravenously for 3 weeks (1 dose/week) to mice bearing tumors of an average volume of 150 mm 3 .…”

Lobe-Specific Carcinogenesis in the Transgenic Adenocarcinoma of Mouse Prostate (TRAMP) Mouse Model

“…Considering the facts that PCA is a complex disease of uncertain etiology and multifocal phenotypic heterogeneity, a desirable model should recapitulate some critical features of human PCA: initiation of PCA with PIN (prostatic intraepithelial neoplasia), followed by progression to invasive adenocarcinoma, and subsequent metastasis with defined kinetics. Although no single model is perfect, transgenic models are widely used to delineate the mechanisms of prostate carcinogenesis and evaluate the chemopreventive efficacy of candidate agents because the lesions/cancers develop ''naturally'' in situ in the genetically engineered hosts and can be followed over a long time course [4].…”