For adrenocortical carcinoma, MCT2 is listed as “High (good prognosis)”, yet the mechanism described states “lactate uptake…leading to inhibition of cancer cell growth”. This contradicts the established role of lactate uptake promoting tumor progression in most cancers. How do the authors reconcile this apparent paradox? Are there mechanistic studies supporting this unique protective role?
The paper mentions retinal abnormalities and neurotoxicity only briefly. Given that MCT1 is essential for retinal function and brain metabolism, how do the authors propose to overcome these dose-limiting toxicities that have already emerged in clinical trials (NCT01791595)?