Moreover, SARDH methylation was found to be a significant prognostic factor for recurrence‑free survival in RCC patients showing statistical independence from the clinical prognosticators, grade, stage and state of metastasis.
Additionally, attenuated SDH activity following SDHC knockdown promoted HCC-cell growth and metastasis both in vitro and in vivo via elevated reactive oxygen species levels and subsequent activation of nuclear factor-κB signaling.
SDH-deficient GISTs show distinctive clinical and pathologic features including absence of KIT and PDGFRA mutations, exclusive gastric location, common lymph node metastasis, a prognosis not predicted by size and mitotic rate, and indolent behavior of metastases.