Cancer cells that disseminate from a tumor can enter a period of dormancy that may persist from months to decades before metastasis. Efforts to improve adjuvant therapy to remove residual cancer cells are hindered by an insufficient understanding of the long-term viability of cancer dormancy. Identifying these mechanisms can greatly improve treatments and prevent relapse. In a study published in Nature Cancer titled, “TGFβ induces an atypical EMT to evade immune mechanosurveillance in lung adenocarcinoma dormant metastasis,” researchers from Memorial Sloan Kettering Cancer Center (MSK) have uncovered how cancer cells evade the immune system by changing their shape in a mouse model. “When cancer cells are round, they have much lower surface tension, and it’s harder for the immune cells to attack them and pop them like a balloon,” said Joan Massagué, PhD, director of MSK’s Sloan Kettering Institute and corresponding author of the study. “Our research suggests that if we can stop cancer cells from entering this soft state, or re-stiffen them, we might help the immune system find and clear dormant metastases before they can seed a new tumor,” said Zhenghan Wang, PhD, a senior research scientist in the Massagué Lab and first author on the paper. Different forms of epithelial-to-mesenchymal transition (EMT) occur during tumor progression. Transforming Growth Factor (TGF) is a family of proteins crucial for cell growth, differentiation, and tissue repair. The phenotypic plasticity of EMTs has important roles in development, injury repair, cancer invasion, and metastasis. During EMT, epithelial cells remodel cell adhesion contacts, assemble contractile actin stress fibers, adopt a spindly morphology, gain anteroposterior polarity,…
