| Abstract: |
Chromophobe renal cell carcinoma (ChRCC) is the second most common variant histology RCC. ChRCC is distinct from clear cell RCC (ccRCC) in terms of genetics, genomics, metabolism, cell of origin, and response to targeted and immune therapies. The pathogenesis of ChRCC remains unclear, but current data suggest two potential mechanisms: mTORC1 hyperactivation through PTEN pathway mutations and mitochondrial dysfunction leading to oxidative stress. There are no specific approved treatments for ChRCC, although some responses to tyrosine kinase and mTOR inhibitors have been observed. Response to immunotherapy is generally limited. Targetable pathways involving innate lymphoid cells/IL-15 and cysteine homeostasis/ferroptosis have recently been identified. © 2023 Elsevier Inc. |
| Keywords: |
cancer survival; treatment response; gene mutation; genetics; clinical feature; pathogenesis; note; drug targeting; metabolism; cancer immunotherapy; tumor marker; cancer therapy; histology; renal cell carcinoma; kidney neoplasms; protein tyrosine kinase inhibitor; tumor suppressor gene; kidney tumor; carcinoma, renal cell; phosphatidylinositol 3,4,5 trisphosphate 3 phosphatase; genomics; innate immunity; immunity, innate; hypoxia inducible factor; upregulation; oxidative stress; cancer classification; birt hogg dube syndrome; mammalian target of rapamycin inhibitor; homeostasis; lymphocyte; lymphocytes; everolimus; interleukin 15; von hippel lindau protein; tuberous sclerosis; cysteine; gene structure; mitochondrial dna; clear cell renal cell carcinoma; molecularly targeted therapy; tumor immunology; disorders of mitochondrial functions; mammalian target of rapamycin complex 1; chromophobe renal cell carcinoma; innate lymphoid cell; immune checkpoint inhibitor; cancer prognosis; ferroptosis; humans; human; hereditary tumor syndrome; biomarkers, tumor
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