Somatic mutations of MMR gene are not often present in HNPCC and in sporadic RER+ colorectal cancers. Complete studies were made according to Bethesda and Amsterdam Criteria, and 35 patients belonged to the group with sporadic colorectal cancer, and 9 patients belonged to HNPCC group. The results of our studies showed that there is no significant difference between RER phenotype of HNPCC and sporadic cancer (p>0,05) in regard to microsatellite status. It can be a good indicator that there are so called 'susspected' on HNPCC among sporadic cancers which were not detected yet. The reason for this was an incomplete familial history of illness of patients and as such it was selected as sporadic cancer. Microsatellite analysis together with medical and familial history of illness can be a successful instrument for efficient HNPCC identification. However, successful solving of this problem lies in making an accurate diagnosis in comparative findings, which can be provided by genetic and clinical tests.

Colorectal cancer with its frequency, high mortality rate as well as many etiological unknowns is a challenge to contemporary science. Finally, genetic information could be used in near future for prevention of colorectal cancer, its early diagnosis and selection for the most suitable hospital treatment. In this study, we analysed genetic alterations of tumor suppressor genes and the possibility of quick and efficient screening method for identification of colorectal cancer. The study consisted of 54 samples of tumor and surrounding healthy tissue of patients with colorectal cancer, which is clasificated according to Bethesda and Amsterdams criterias. The investigation showed that genetic alterations of tumor suppressor gene NM 23 were present in 19/35 (54,29%) samples, and tumor suppressor gene p53 in 18/35 (51,43%), APC in 18/35 (51,43%), DCC2 tumor suppressor gene in 12/35 (34,29%), tumor suppressor gene RB1 in 8 /35 (22, 86%) and DCC 1 in 10/35 ( 28,57%) tumor tissue.

The objectives of this research were to establish the recessive phenotype frequency of the(in)ability of tongue rolling (fr) and frequency of the(in)ability of tongue folding. The data were collected by means of direct analysis and interviews with pupils from 5th to 8th grade. The research was conducted in rural and urban areas of Zivinice Municipality (OS Zivinice and OS Basigovci). The sample comprised 438 persons of both sexes (202 boys and 236 girls) 11-16 years of age. 197 respondents were from urban and 241 from rural area. The analysis of the obtained results showed that the phenotype frequency of the (in)ability of tongue rolling in Zivinice Municipality is 20,30% with relative frequency of recessive allele qr=0,45, while in the Basigovci area the phenotype frequency of the(in)ability of tongue rolling is 41,90%, with relative frequency of recessive allele qr=0,64. The phenotype frequency of the(in)ability of tongue folding in Zivinice is 32,48%, relative frequency of recessive allele qu=0,56, while the incidence of same phenotipe in Basigovci is 44,81%, and relative frequency of recessive allele is qu=0,66. The analysis of the results in Živinice Municipality show that the frequency of recessive allele is not different from the one found in the previous researeches in the regions of B&H and has approximate value of the frequency of reccesive allele from Gradacac qr=0,55.

HNPCC (Hereditary non-polyposis colorectal cancers) development is caused by mutation of genes included in system of mismatch repair genes. The mutation exists at 60% of patients in hMSH2 gene, 30% in hMLH1 and 10% both in hPMS1and hPMS2 genes. RER+ exists in about 90% in hereditary non-polyposis colorectal cancer and about 15-28% in sporadic cancers. The purpose of the study was to determine highly sensitive microsatellite markers which can be fast and efficient way of microsatellite screening for detection of HNPCC patients. Moreover, we have analysed the loss of heterozygosity of tumour suppressor genes which could have the diagnostic value in detection of HPNCC patients.

Familial adenomatous polyposis (FAP) is an autosomal dominant illness with the highest risk for appearance of colorectal cancer's disease. In our study, we have used Bethesda criteria that define colorectal cancers which can be tested on microsatellite instability. The aim of our study is make an analysis of microsatellite instability (MSI), appearance of RER+ phenotype, genetic alteration of tumor suppressor genes as like as one of responsible factor for genesis of adenomatous polyposis. The base for this study were shown families with clinical diagnosed FAP. In this study two families with clinical diagnosed adenomatous polyposis were involved. Our study of both families showed that three tumor tissues belonged to RER negative phenotype, but only one belonged to RER positive phenotype. Microsatellite analysis showed instability of mononucleotide marker Bat 40 at 4 samples and Bat 26 at 2 samples, but Bat 25 and in 1 sample. Dinucleotide marker TP 53 did no show any microsatellite alterations. Genetic alteration of tumor suppressor gene APC appeared at 4 samples, p53 at 3 samples, RB1 at 2 samples and NM23 only at 1 sample, but tumor suppressor genes DCC1 and DCC2 were homozygote. Our results are agree with results of earlier studies and also the got results confirm the fact that loss of heterozygosity of tumor suppressor gene APC and p53 are responsible for genesis of adenomatous polypose and it also represents the characteristic of genetic changes FAP's patients in our region.