The experimental renal cell carcinoma model in the chick embryo

Abstract

The clear cell subtype of renal carcinoma (CCRCC) is highly vascularized and despite a slow progression rate, it is potentially a highly aggressive tumor. Although a doubling of median progression-free survival in CCRCC patients treated by targeted therapies has been observed, the fact that tumors escape after anti-VEGF treatment suggests alternative pathways. The chick chorioallantoic membrane (CAM) is a well-established model, which allows in vivo studies of tumor angiogenesis and the testing of anti-angiogenic molecules. However, only a few data exist on CCRCC grafted onto CAM. We aimed to validate herein the CAM as a suitable model for studying the development of CCRCC and the interactions with the surrounding stroma. Our study uses both CCRCC cell lines and fresh tumor samples after surgical resection. We demonstrate that in both cases CCRCC can be grafted onto the CAM, to survive and to induce an angiogenic process. We further provide insights into the transcriptional regulation of the model by performing a differential analysis of tumor-derived and stroma-derived transcripts.

Use of the Chick Embryo Model in Uveal Melanoma

“…The chick embryo as a model to study tumour metastasis has been reported in a variety of cancer types including glioma [11], prostate [12], colorectal [13], renal [14], ovarian [15] and small-cell lung cancer [16]. In uveal melanoma, a small number of groups including our own have begun to examine the suitability of this model to monitor the growth and metastatic properties of uveal melanoma cells either grafted onto the CAM, injected intravenously or transplanted into the optic cup.…”

New ex-ovo colorectal-cancer models from different SdFFF-sorted tumor-initiating cells

“…Advantages are that the CAM model lacks immunological and inflammatory cells, making it an attractive system to avoid effects of the tumor microenvironment interfering with tumor development [6]. This has been used to provide highly reproducible models for glioblastoma [7,8], bone and osteosarcoma [5,9], pancreatic adenocarcinoma [10], ovarian cancer [11], head and neck squamous carcinoma [12], and more recently renal carcinoma [13], as well as CRC [14]. In the last case, the development of CRC and therapeutic escape may be caused by the presence of tumor-initiating cells (TICs) [3,15], which are responsible for driving growth and treatment resistance [16,17].…”

Inhibition of endogenous hydrogen sulfide production in clear-cell renal cell carcinoma cell lines and xenografts restricts their growth, survival and angiogenic potential

“…We evaluated the effects of inhibiting/stimulating endogenous H 2 S production on ccRCC cell lines in vitro by quantifying cell growth, metabolism and viability in the VHL-deficient ccRCC cell lines 786-O and 769-P, as well as the VHL wild-type ccRCC cell lines Caki-1 and the 786-O VHL knock-in (786-O VHL+). We further evaluated the effects of H 2 S inhibition on xenograft neovascularization in vivo using an avian xenograft model previously developed for RCC [34]. …”