Tumor specifikus DNS/gén dózis szerepe a papilláris vesetumor kialakulásában

Abstract

The classification of renal cell carcinoma (RCC) is traditionally based of the microscopis evalutation of HE stained slides. After classification systems based on cytological and architectural alterations, a change in the paradigm happened in the late 80’ and early 90’s: the new classification was based on specific chromosomal changes in tumors (Kovacs, 1993 a,b). The Heidelberg classification notices tumor-specific genetical alterations that identify the type of the tumor, even in cases, when histological analysis is controversial (Kovacs et al., 1997). Papaillary renal cell carcinoma can show high histological variability, but it shows well defined choromosomal and genetical changes. During tumor development, first the trisomy of tetrasomy of choromosomes 7 and 17 develop. This is may be followed by the loss of chromosome Y. The later chromosomal trisomies of 3q, 8, 12, 16, 20 might also develop, which merks the progression into a more aggressive tumor (Kovacs 1993a, Szponar et al., 2009). These data have high significance knowing the currently used WHO classification, where the difference between the papillary adenoma and carcinoma is made only by the size of the tumor. Thus a tumor under 15mm-s is benign, and above 15mms is malignant (Moch et al., 2016). This might lead to a false prediction of the prognosis. There are two theories about the development of papillary renal cell carcinoma. According to the opinion of the WHO and ISUP (International Society of Urological Pathologists) the papillary renal cell tumors originate from the differentiated mature cells of the renal tubules, similarly to conventional renal cell carcinoma. A different theory states, that the development of papillary renal cell carcinoma follows a sequence of developmental disorder – precursor lesion – adenoma – carcinoma (Kovacs, 1993 a,b). The most important tool in the differentiation between adenoma and carcinoma is genetic analysis.