Patients with mutations in the β-subunit of the succinate dehydrogenase () have the highest risk to develop incurable malignant phaeochromocytomas and paragangliomas (PPGLs). Therapy development is hindered by limited possibilities to test new therapeutic strategies in vivo. One possible molecular mechanism of -associated tumorigenesis originates in an overproduction of reactive oxygen species (ROS) due to mitochondrial dysfunction.
View Article and Find Full Text PDF