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According to the generally accepted principles , it is believed that the gene and its protein product may be involved in tumorigenesis , tumor tissue if is detectable chromosomal abnormalities and / or mutation of this gene , and the expression and function of the gene encoded proteins are significantly disorder . It appears that the receptors triiodothyronine (TR) is one of these proteins. This hypothesis is supported by four facts . Firstly, the physiological effects of triiodothyronine (T3) , exerted via TR , to regulate cell proliferation, differentiation and apoptosis , or processes that are profoundly impaired in the tumor tissue . Secondly , the action of TR activity is associated with certain proto-oncogenes (c- Jun, Mdm2 ), and tumor suppressors (p53 ) . Thirdly, in tumor tissues are often observed loss of heterozygosity ( LOH ) of chromosome fragments containing , inter alia, TR allele . Practically all examined types of tumors observed aberrant TR on mRNA and protein level . Fourth, TR is a cellular equivalent of v - erbA , a viral oncogene that has the characteristics of a dominant negative mutant . Furthermore, very often in the presence of tumors were TR gene point mutations changing the amino acid sequence as a consequence of impaired receptor function as a transcriptional activator . For example, liver cancer has also been shown that the mutant TR behave as dominant-negative mutants . It seems that in liver cancer and papillary thyroid malfunction TR may be jointly responsible for tumorigenesis .

The Editorial Board
Andrzej Łukaszyk - przewodniczący, Zofia Bielańska-Osuchowska, Szczepan Biliński, Mieczysław Chorąży, Aleksander Koj, Włodzimierz Korochoda, Leszek Kuźnicki, Aleksandra Stojałowska, Lech Wojtczak

Editorial address:
Katedra i Zakład Histologii i Embriologii Uniwersytetu Medycznego w Poznaniu, ul. Święcickiego 6, 60-781 Poznań, tel. +48 61 8546453, fax. +48 61 8546440, email:

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