What mechanism could explain why midgut carcinoid tumors are observed when single nucleotide changes in the gene for succinate

Question

What mechanism could explain why midgut carcinoid tumors are observed when single nucleotide changes in the gene for succinate dehydrogenase (Complex II) are detected?
 Defects in succinate dehydrogenase result in increased production of ROS, damage to DNA, and mutations that lead to
unregulated cell division.
 Defects in succinate dehydrogenase completely block oxidative phosphorylation, and the lack of intracellular ATP
triggers apoptosis.
Defects in succinate dehydrogenase inhibit binding to ubiquinone resulting in the flow of protons through the
uncoupling protein UPC1 and cell hyperthermogenisis.
Defects in succinate dehydrogenase completely block the citric acid cycle, causing carcinogenic intermediates
to accumulate.
Defects in succinate dehydrogenase lead to a buildup of NADH, which stimulates cells to divide more rapidly than
usual, leading to tumor growth.

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