Pathogenesis
Different molecular mechanisms are involved in PRCC development, which further result in distinct histologic features and clinical outcomes.Type 1 PRCC 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 PRCC 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 papillary renal cell carcinoma tumors exhibited somatic FH gene mutation, which is closely associated with HLRCC syndrome. Diagnosis
Currently, cross-sectional imaging with computed tomography (CT) and magnetic resonance imaging (MRI) is known as the best option for diagnosing papillary renal tumors. Computed tomography (CT)
Contrast-enhanced computed tomography (CT) is most commonly used to identify the subtypes of RCC. PRCC can be differentiated from other types of RCC due to its distinguishing features, displaying a small hypovascular renal tumor on T2 weighted images.
According to the National Cancer Database, PRCC was more common in the Non-Hispanic Black population (38.9%) when compared to other races – Asian American (18.0%), Non-Hispanic White (13.2%), and Hispanic White populations (6.1%). References


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