Naslov (srp)

Uloga ćelijske senescencije indukovane onkogenima u malignoj transformaciji i progresiji tumora dojke

Autor

Jovanović, Dalibor, 1984-

Doprinosi

Mitrović, Slobodanka, 1967-
Stanković, Vesna, 1964-
Mijović, Milica, 1971-
Spasić, Marko, 1980-

Opis (srp)

Uprkos značaju pojedinih prognostičkih faktora, njihova tačnost u proceniishoda i određivanju strategija lečenja obolelih od karcinoma dojke je ograničena.Stoga bi definisanje novih molekularnih biomarkera moglo pružiti pouzdanijipristup u predviđanju prognoze ove bolesti.Cilj ove studije je ispitivanje ekspresije markera p16, p53, p21, pRb i GLB1 ubenignim i malignim promenama dojke, kao i njihovog učešća u malignojtransformaciji.Istraživanje je obuhvatilo analizu tkivnog materijala benignih i malignihpromena pacijentkinja operisanih u UKC Kragujevac. Na H&E obojenim preparatimadefinisani su svi makro i mikromorfološki prognostički faktori (histološki tipi gradus tumora, veličina, nodalni status, dezmoplazija, nekroza, mononuklearnareakcija i td.) Imunohistohemijski, primenom antitela (p16,p53,p21,pRb,GLB1),određivana je tkivna ekspresija markera semikvantitativnim očitavanjem pozitivnereakcije. Definisanjem cut off vrednosti, karcinomi su svrstavani u pozitivnu inegativnu grupu za svaki analizirani marker.Ekspresija svih markera raste sa progresijom citoloških promena u epitelu.Njihova ekspresija je u pozitivnoj korelaciji sa različitim promenama u dojci, saproliferativnim indeksom i HER2+ tumorima. Ekspresija p16, pRb, p21, GLB1 jenajveća u HER2+ karcinomima dojke, dok je ekspresija p53 najveća u TNBC. Značajnakorelacija je utvrđena između ekspresije p16 i p53, p21 i pRb, p21 i GLB1, kao iizmeđu pRb i GLB1 u invazivnom karcinomu.Analizirani markeri igraju važnu ulogu u proliferaciji, malignojtransformaciji, kao i u progresiji karcinoma dojke, što ih preproručuje za daljaistraživanja i moguće korišćenje u dijagnostičke, prognostičke i prediktivne svrhe.

Opis (srp)

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Opis (eng)

Despite the importance of certain prognostic factors, their accuracy in assessingoutcomes and determining treatment strategies for breast cancer patients is limited. Therefore,the definition of new molecular biomarkers could provide a more reliable approach forprediction of the prognosis of this disease.The aim of this study was to examine the expression of markers p16, p53, p21, pRband GLB1 in benign and malignant breast changes, as well as their participation in malignanttransformation.The research included the analysis of tissue material of benign and malignant changesin patients operated at the University Clinical Center Kragujevac. All macro andmicromorphological prognostic factors (histological type and grade of tumor, size, nodalstatus, desmoplasia, necrosis, mononuclear reaction, etc.) were defined on H&E stainedpreparations. Immunohistochemically, using antibodies (p16, p53, p21, pRb, GLB1) tissueexpression of markers were determined by a semiquantitative reading of a positive reaction.By defining cut-off values, cancers were classified into positive and negative groups for eachanalyzed marker.The expression of all markers increased with the progression of cytological changes inthe epithelium. Their expression positively correlated with various changes in the breast, withthe proliferative index and HER2+ tumors. The expression of p16, pRb, p21, GLB1 is thehighest in HER2+ breast cancers, while the expression of p53 is the highest in TNBC. Asignificant correlation was found between the expression of p16 and p53, p21 and pRb, p21and GLB1, as well as between pRb and GLB1 in invasive cancer.The analyzed markers play an important role in proliferation, malignanttransformation, as well as in the progression of breast cancer, which recommends them forfurther research and possible use for diagnostic, prognostic and predictive purposes.

Jezik

srpski

Datum

2022

Licenca

Creative Commons licenca
Ovo delo je licencirano pod uslovima licence
Creative Commons CC BY-ND 3.0 AT - Creative Commons Autorstvo - Bez prerada Austria License.

http://creativecommons.org/licenses/by-nd/3.0/at/legalcode

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