What drives tumor growth? Is it a few rogue cells imposing their will upon healthy tissue, or diseased tissue bringing out the worst in otherwise peaceable cells? Or is it a back-and-forth, a dialogue between the two?
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Many cancer stem cells possess an RAS gene that, when mutated, allows tissue stem cells to ignore normal environmental signals and control tissue growth. To better understand the intricacies of this interaction, researchers turned their attention to squamous cell carcinoma. The team began by inducing mutant HRAS (the most common RAS family member in skin cancers) in individual skin stem cells and monitoring the interaction of the cancer stem cells with the surrounding tissue. This observation raised the possibility that many cancer mutations do not fix the course of a disease but lock it in place, affirming a malignant progression already determined by aberrant crosstalk between a cancer stem cell and its microenvironment. By further studying how the cancer stem cell changed in the face of this new self-imposed malignant tumor microenvironment, the team realized that invasive cancer stem cells unexpectedly began expressing the leptin receptor, Lepr. The researchers used CRISPR technology to show that Lepr and leptin receptor signaling were critical for progression from benign to malignant. The team is now investigating ways to block leptin receptors in tumors because doing so could throw a molecular monkey wrench into the vicious loop and derail the cancer.