301x301px Different molecular mechanisms are involved in<unk>  development, which further result in distinct histologic features and clinical outcomes. Type 1<unk>  is caused by a genetic mutation or a gain in chromosome 7 where the MET gene is positioned, resulting in the promotion of oncogenic pathways in renal epithelial cells. Typically, the MET gene is upregulated for renal tissue repair and regeneration by encoding the receptor tyrosine kinase c-MET of hepatocyte growth factor. However, activation of the oncogenic pathway in the MET gene will manifest invasion, anti-apoptosis, angiogenesis, and metastasis. Type 2<unk>  is associated with irregularity of several signaling pathways, which includes CDKN2A silencing, mutation in chromatin-modifying genes, and a GpG island methylator phenotype (CIMP). CDKN2A is a tumor suppressor gene, while loss of its expression results in enhanced tumorigenesis and metastasis. Moreover, mutation of gene involved in chromatin remodeling (SETD2, BAP1, or PBRM) may lead to higher rate of TFE3/TFEB fusion. Additionally, CIMP<unk>  tumors exhibited somatic FH gene mutation, which is closely associated with HLRCC syndrome.
Papillary renal cell carcinoma
Renal medullary carcinoma
Renal anaplastic sarcoma
Renal medullary fibroma
Renal oncocytoma
Clear cell renal cell carcinoma
Clear cell papillary renal cell carcinoma
Renal cell carcinoma