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anacardic acid/rak dojke

Povezava se shrani v odložišče
ČlankiKliničnih preskušanjPatenti
13 rezultatov

Genome-wide miRNA response to anacardic acid in breast cancer cells.

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Prijava / prijava
MicroRNAs are biomarkers and potential therapeutic targets for breast cancer. Anacardic acid (AnAc) is a dietary phenolic lipid that inhibits both MCF-7 estrogen receptor α (ERα) positive and MDA-MB-231 triple negative breast cancer (TNBC) cell proliferation with IC50s of 13.5 and 35 μM,
OBJECTIVE To explore the effect of the Hsp90 inhibitor anacardic acid on cell proliferation, invasion and migration of breast cancer MDA-MB-231 cells. METHODS The inhibitory effect of anacardic acid on Hsp90 was assessed with in vitro ATPase inhibition assay and ATP-sepharose binding assay. MTT
Anacardic acid is a dietary and medicinal phytochemical that inhibits breast cancer cell proliferation and uncouples oxidative phosphorylation (OXPHOS) in isolated rat liver mitochondria. Since mitochondrial-targeted anticancer therapy (mitocans) may be useful in breast cancer, we examined the

Anticancer effects of plant derived Anacardic acid on human breast cancer MDA-MB-231 cells.

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Prijava / prijava
Triple negative breast cancer (TNBC) accounts for about 10-15% of all breast cancers. It is a heterogeneous disease, characterized by early relapse, aggressive behavior, and poor prognosis, when compared to other breast cancer subtypes. Interestingly, most of the heat shock protein 90 (Hsp90) client
Anacardic acid (AnAc; 2-hydroxy-6-alkylbenzoic acid) is a dietary and medicinal phytochemical with established anticancer activity in cell and animal models. The mechanisms by which AnAc inhibits cancer cell proliferation remain undefined. AnAc 24:1(omega5) was purified from geranium (Pelargonium x

Transcriptomic response of breast cancer cells to anacardic acid.

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Prijava / prijava
Anacardic acid (AnAc), a potential dietary agent for preventing and treating breast cancer, inhibited the proliferation of estrogen receptor α (ERα) positive MCF-7 and MDA-MB-231 triple negative breast cancer cells. To characterize potential regulators of AnAc action, MCF-7 and MDA-MB-231 cells were
To explore the potential of paclitaxel (PTX)-loaded anacardic acid conjugated hydrophobized gelatin nanoparticles.Nanoparticles prepared by nanoprecipitation technique were evaluated for various quality attributes (particle size, % entrapment efficiency) in
In the present study, we have modified bovine serum albumin (BSA) by covalently conjugating with anacardic acid (AA) and gemcitabine (GEM) and further used for development of docetaxel (DTX) loaded nanoparticles (AA-GEM-BSA NPs). AA is supposed to provide tumor targeting through VEGF receptors

Synthesis of benzamides related to anacardic acid and their histone acetyltransferase (HAT) inhibitory activities.

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Prijava / prijava
A group of benzamides related to anacardic acid amide CTPB with alkyl chains of defined length were prepared by a five-step sequence starting from 2,6-dihydroxybenzoic acid, and their activities were compared with those reported for the HAT inhibitor anacardic acid (AA). The subset of

A novel animal model for locally advanced breast cancer.

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Prijava / prijava
BACKGROUND Locally advanced breast cancer (LABC) poses complex management issues due to failure of response to chemotherapy and progression to local complications such as skin erosion, superinfection, and lymphedema. Most cell line and animal models are not adequate to study LABC. METHODS A
There is growing evidence that cancer-initiation could result from epigenetic changes. Y-box binding protein-1 (YB-1) is a transcription/translation factor that promotes the formation of tumors in transgenic mice; however, the underlying molecular events are not understood. To explore this in a

Lunasin-aspirin combination against NIH/3T3 cells transformation induced by chemical carcinogens.

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Prijava / prijava
Carcinogenesis is a multistage process involving a number of molecular pathways sensitive to intervention. Chemoprevention is defined as the use of natural and/or synthetic substances to block, reverse, or retard the process of carcinogenesis. To achieve greater inhibitory effects on cancer cells,
Programmed cell death ligand 1 (PD‑L1) expressed in cancer cells interacting with its receptor programmed cell death 1 (PD‑1) expressed in immune cells represents a regulatory axis linked to the suppression and evasion of host immune functions. The blockade of PD‑1/PD‑L1 interaction using monoclonal
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