http___medlib.mef.hr_567__2.xml
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Malčić, Ana and Jukić, Silvana and Anić, Ivica and Pavelić, Božidar and Kapitanović, Sanja and Krušlin, Božo and Pavelić, Krešimir (2008) Alterations of FHIT and P53 genes in keratocystic odontogenic tumor, dentigerous and radicular cyst. Journal of Oral Pathology & Medicine, 37 (5). Abstract BACKGROUND: The purpose of this study was to determine fragile histidine triad (FHIT) and p53 protein expression, and to analyze FHIT and p53 gene status in keratocystic odontogenic tumor (KOT), dentigerous cysts (DC) and radicular cysts (RC). ----- METHODS: The methods used were immunohistochemistry and molecular genetic methods including loss of heterozygosity (LOH) and gene sequencing. ----- RESULTS: FHIT protein expression was different among groups. Aberrant expression was the highest in KOT, then in RC and DC. p53 protein expression was different among groups. LOH in paraffin-embedded specimens was detected in 22.6% and 12.9% for FHIT and p53 respectively. Mutation of p53 gene at codon 237 was observed in only two specimens (one KOT and one DC). Of the six frozen specimens, three exhibited FHIT gene LOH (two RC and one KOT). KOT showed loss of exons 6-7 at FHIT locus and mutation at codon 237 at p53 locus, but this could be a chance result. ----- CONCLUSION: Aberrations of FHIT and p53 genes/proteins could be considered markers responsible for the development of odontogenic lesions. Actions (login required) Downloads Downloads per month over past year
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Lončar, Božo (2008) Poremećaj funkcije gena FHIT u karcinomima debelog i završnog crijeva. PhD thesis, Sveučilište u Zagrebu. Abstract Colorectal adenocarcinoma is one of the most common cancers and the second leading cause of death in the Western world. This disease arises from the accumulation of mutations in oncogenes and tumor-suppressor genes during progression from normal epithelium to adenoma and malignant invasive carcinoma. Fragile histidine triad (FHIT) gene, a candidate tumor suppressor gene located at 3p14.2, has been shown to be involved in carcinogenesis of many human tumors, including digestive tract tumors. The main goal of this study was to investigate genetic changes in FHIT gene in order to elucidate the mechanisms of its role in development and progression of sporadic colon cancer. Loss of heterozygosity (LOH) of FHIT gene was positive in 19,2% of sporadic colon cancers. FHIT gene mRNA expression in tumor cells was statistically significant decreased in comparison to adjacent normal mucous tissue (p 0.00002). The most of sporadic colon tumor specimens were negative for FHIT protein expression (51,7%). We showed that positive LOH, decreased mRNA and protein expression of FHIT gene significantly correlate with the progression of sporadic colon cancer, with tumor size, differentiation and Dukes’ stage. The results of this study could be used in the future for more efficient surveillance of the patients with sporadic colon cancer. Abstract in Croatian Karcinom debelog crijeva jedan je od najčešćih zloćudnih tumora i drugi po redu uzrok smrti od raka u razvijenim zemljama. Većina karcinoma debelog crijeva posljedica je stupnjevitog procesa tijekom kojeg iz dobroćudnog adenoma kao posljedica naslijeđenih i/ili stečenih mutacija nastaje zloćudni invazivni tumor. Gen FHIT (od engl. Fragile Histidine Triad), tumor supresorski gen smješten je na kromosomu 3 u čovjeka (3p14.2) i promijenjen je u različitim tumorima čovjeka uključujući i tumore probavnog sustava. Cilj našeg istraživanja bio je ispitati gubitak heterozigotnosti te ekspresiju gena FHIT na razini specifične mRNA i proteina u sporadičnim karcinomima kolona. Rezultati naših istraživanja su pokazali su da je gubitak heterozigotnosti gena FHIT prisutan u 19,2% sporadičnih karcinoma kolona. Razina ekspresije gena FHIT u tumorima bila je statistički značajno niža u odnosu na ekspresiju u pripadajućoj normalnoj sluznici (p 0,00002). U našem je istraživanju najveći broj uzoraka sporadičnih karcinoma kolona bio negativan na prisustvo proteina FHIT (51,7%). Naši rezultati pokazuju jasnu korelaciju između gubitka heterozigotnosti te smanjene ekspresije gena FHIT na razini specifične mRNA kao i proteina s napredovanjem i metastaziranjem sporadičnih karcinoma kolona. Smanjena ili potpuno ugašena ekspresija proteina FHIT mogla bi biti prognostički biljeg za sporadične karcinome kolona s tim da bi postojeće rezultate trebalo proširiti na veći broj uzoraka te analizu preživljenja. Actions (login required) Downloads Downloads per month over past year