MAX Mutant Small-Cell Lung Cancers Exhibit Impaired Activities of MGA-Dependent Noncanonical Polycomb Repressive Complex

The MYC axis is disrupted in cancer, predominantly through activation of the MYC family oncogenes but also through inactivation of the MYC partner MAX or of the MAX partner MGA. Researchers demonstrated that MAX-deficient small-cell lung cancer cells have either ASCL1 or NEUROD1 or combined characteristics.