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.