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carnosol/tumori dojke

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ČlanciKliničkim ispitivanjimaPatenti
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Carnosol has been proved to have anti-breast cancer effect in previous research. But its ER subtype's specific regulation and mediation mechanisms remain unclear. The aim of this study is to observe the effect of carnosol on cell proliferation and its estrogen receptor α and β's specific regulation

Carnosol induces ROS-mediated beclin1-independent autophagy and apoptosis in triple negative breast cancer.

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BACKGROUND In this study we investigated the in vitro and in vivo anticancer effect of carnosol, a naturally occurring polyphenol, in triple negative breast cancer. RESULTS We found that carnosol significantly inhibited the viability and colony growth induced G2 arrest in the triple negative
We have previously demonstrated that carnosol, a naturally occurring diterpene, inhibited in vitro cell viability and colony growth, as well as induced cell cycle arrest, autophagy and apoptosis in human triple negative breast cancer (TNBC) cells. In the present study, we evaluated the

(+)-Dehydroabietylamine derivatives target triple-negative breast cancer.

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Breast cancer remains the leading cause of cancer-related death among women. The invasive triple-negative subtype is unresponsive to estrogen therapy, and few effective treatments are available. In search of new chemical scaffolds to target this disease, we conducted a phenotypic screen against the
Extracts of the spice Rosemary officinalis L. have been reported to inhibit experimental carcinogenesis. Two rosemary components, carnosol and ursolic acid, appear to be partly responsible for the antitumorigenic activity of rosemary. The present studies were conducted in order to evaluate the

CYP1A1 regulates breast cancer proliferation and survival.

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Cytochrome P450-1A1 (CYP1A1) is an extrahepatic phase I metabolizing enzyme whose expression is suppressed under physiologic conditions but can be induced by substrates via the aryl hydrocarbon receptor (AhR). Recent studies have shown that the majority of breast cancer tumors constitutively express
Neoadjuvant treatment options for human epidermal growth factor receptor-2 (HER-2)-enriched and luminal B molecular subtypes of clinical breast cancer include HER-2-targeted therapy with chemotherapy or anti-hormonal therapy. These treatment options result in systemic toxicity and acquired tumor
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