Key result
Eosinophilic vacuolated tumors of the kidney are characterized by mTORC1 activation, and loss of chromosome 1 in EVT with MTOR mutation may provide a selective advantage.
Why the study?
Recent molecular genetic advances have identified novel biological subtypes among renal tumors with predominantly eosinophilic/oncocytic cytoplasm beyond traditionally recognized entities, warranting better classification.
Provides an integrated view of eosinophilic vacuolated tumor of the kidney, highlighting mTORC1 activation and morphological features to assist in differential diagnosis.
EVT warrants inclusion in eosinophilic renal tumor classification; extends molecular taxonomy but leaves open clinical behavior and management.
Recent advances in molecular genetics have expanded our knowledge of renal tumors and enabled a better classification. These studies have revealed that renal tumors with predominantly "eosinophilic/oncocytic" cytoplasm include several novel biological subtypes beyond the traditionally well-recognized renal oncocytoma and an eosinophilic variant of chromophobe renal cell carcinoma. Herein, we present a comprehensive review of the eosinophilic vacuolated tumor (EVT) building upon a case report including radiology, histopathology, electron microscopy, and next-generation sequencing. EVTs are characterized by mTORC1 activation. We speculate that loss of chromosome 1 in EVT with MTOR mutation may be driven in part by an advantage conferred by loss of the remaining MTOR wild-type allele. mTORC1 is best known for its role in promoting protein translation and it is interesting that dilated cisterns of rough endoplasmic reticulum (ER) likely account for the cytoplasmic vacuoles seen by light microscopy. We present an integrated view of EVT as well as cues that can assist in the differential diagnosis.
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Kapur et al. (2021) conducted a review in Eosinophilic vacuolated tumor of the kidney (n=1). MTOR mutation and chromosome 1 loss was evaluated. Eosinophilic vacuolated tumors of the kidney are characterized by mTORC1 activation, and loss of chromosome 1 in EVT with MTOR mutation may provide a selective advantage.
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