Katrina Meeth

TL;DR: It is found that aged fibroblasts secrete a Wnt antagonist, sFRP2, which activates a multi-step signalling cascade in melanoma cells that results in a decrease in β-catenin and microphthalmia-associated transcription factor, and ultimately the loss of a key redox effector, APE1.

TL;DR: YUMM lines are described, a comprehensive system of mouse melanoma cell lines that are syngeneic to C57BL/6, have well‐defined human‐relevant driver mutations, and are genomically stable, which will be a useful tool for the study of tumor immunology and genotype‐specific cancer biology.

TL;DR: It is suggested that physiological serine availability restrains tumor growth and argued that tumors arising in serine-limited environments acquire a fitness advantage by upregulating serine synthesis pathway enzymes.

TL;DR: Mouse melanoma tumors generated by irradiating a parental mouse melanoma cell line carrying three driver mutations with UVB and expanding a single‐cell clone are a mutagenized model that exhibits high somatic mutation burden, establishing a new model for the evaluation of immune checkpoint inhibition and antitumor immune responses.

TL;DR: Response to PD-1 blockade therapy in tumor models requires CD4 and CD8 T cells and costimulation that is mediated by dendritic cells and macrophages, and exhibited a more inflammatory profile by RNA sequencing analysis.