Prognostic markers in quadruple negative breast cancer

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dc.contributor.authorYaneva, Galina
dc.contributor.authorDimitrova, Tsonka
dc.contributor.authorStoyanov, Stoyan
dc.contributor.authorIvanova, Nikoleta
dc.contributor.authorNenkova, Galina
dc.contributor.authorCherneva, Djeni
dc.contributor.authorBoycheva, Petya
dc.contributor.authorIvanov, Dobri
dc.date.accessioned2024-11-19T05:46:25Z
dc.date.available2024-11-19T05:46:25Z
dc.date.issued2023-01-10
dc.description.abstractQuadruple-negative breast cancer (QNBC) presents with negative expression of estrogen, progesterone, and androgen receptors and of human epidermal growth factor receptor 2. This BC subtype has the worst prognosis. In QNBC, there is a greater paucity of prognostic biomarkers than in androgen receptors-positive triple negative BC (TNBC). Absent androgen receptor expression confers a more aggressive QNBC course and correlates with the expression of cancer stem cell phenotype, COX-2, and basal markers such as CK5 and nestin. Basal-like phenotype is significantly associated with adverse prognostic markers including high KI-67, COX-2 expression, and cancer stem cell phenotype. Engrailed-1 expression is associated with unfavorable overall survival in QNBC patients. Non-coding ribonucleic acids play a significant role in BC tumourigenesis by virtue of their oncogenic and tumour-suppressive properties. The identification of QNBC-specific circulating microribonucleic acids may improve tumour detection and prognosis. There is an obvious necessity to intensify the problem-oriented interdisciplinary research on the hot topic of prognostic biomarkers of QNBC.
dc.identifier.issn1314-6246
dc.identifier.urihttps://doi.uni-plovdiv.bg/handle/store/316
dc.language.isoen
dc.publisherPlovdiv University Press “Paisii Hilendarski”
dc.subjectquadruple negative breast cancer
dc.subjecttriple negative breast cancer
dc.subjectandrogen receptor expression
dc.subjectbiomarkers
dc.subjectprognosis
dc.titlePrognostic markers in quadruple negative breast cancer
dc.typeArticle
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