CITE-seq from tumors generated via subcutaneous injection of VBPN, VBPNA, VBPNC organoids into C57BL/6 mice
BRAF mutant colorectal cancer displays a unmet clinical need with poor overall survival. Here we modeled this cancer in the murine system and created organoids with Braf activation mutation, Trp53 deletion and Nicd1 expression. Additionally, we created cell lines that have a Apc deletion (VBPNA) or Ctnnb1 activation mutation (VBPNC). These mutations activate the WNT pathway which plays a critical role in the tumor progression but is under-explored in BRAF mutated colorectal cancer. To investigate the effect of the WNT pathway genes mutations on the cancer cell state and the tumor microenvironment, we performed CITE-seq.
BRAF mutant colorectal cancer displays a unmet clinical need with poor overall survival. Here we modeled this cancer in the murine system and created organoids with Braf activation mutation, Trp53 deletion and Nicd1 expression. Additionally, we created cell lines that have a Apc deletion (VBPNA) or Ctnnb1 activation mutation (VBPNC). These mutations activate the WNT pathway which plays a critical role in the tumor progression but is under-explored in BRAF mutated colorectal cancer. To investigate the effect of the WNT pathway genes mutations on the cancer cell state and the tumor microenvironment, we performed CITE-seq.
European Bioinformatics Institute