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aclarubicin/نخر

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مقالاتالتجارب السريريةبراءات الاختراع
10 النتائج

Aclarubicin-induced apoptosis and necrosis in cells derived from human solid tumours.

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الدخول التسجيل فى الموقع
In the present study, we investigated the response of A549 (non-small cell lung-cancer), HepG2 (human hepatoma) and MCF-7 (human breast adenocarcinoma) cell lines to treatment with aclarubicin (ACL). The aim of this research was to compare the ability of ACL to induce apoptosis or necrosis in solid

Aclarubicin enhances tumor necrosis factor-related apoptosis-inducing ligand-induced apoptosis through death receptor 5 upregulation.

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الدخول التسجيل فى الموقع
Anthracycline drugs are potent anti-tumor agents. Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a death ligand with promising anti-cancer effects. However, some tumor types develop resistance to TRAIL. We examined the effect of aclarubicin (ACR), an anthracycline, in combination

Involvement of reactive oxygen species in aclarubicin-induced death of human trisomic and diabetic fibroblasts.

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We investigated the mode of cell death induced by aclarubicin in human trisomic and diabetic fibroblasts. The cells were incubated with aclarubicin for 2 h and then were cultured in drug-free medium for up to 96 h. Aclarubicin in trisomic and diabetic fibroblasts, compared with normal cells, induced

Analysis of aclarubicin-induced cell death in human fibroblasts.

يمكن للمستخدمين المسجلين فقط ترجمة المقالات
الدخول التسجيل فى الموقع
In the present study we investigated the mode of cell death induced by aclarubicin (ACL) in trisomic (BB) and normal (S-2) human fibroblasts. Cells were incubated with ACL for 2h and then cultured in drug-free medium for up to 96h. Using fluorescence microscopy, agarose gel electrophoresis and comet

Comparison of anthracycline-induced death of human leukemia cells: programmed cell death versus necrosis.

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We investigated the mode of cell death induced by the anthracyclines, aclarubicin, doxorubicin and daunorubicin in the human leukemia cell lines, HL60 and Jurkat. The cells were incubated with drug concentrations up to 500 nM for periods between 3 and 24 hours, followed by morphological and

Low-dose doxorubicin-induced necrosis in Jurkat cells and its acceleration and conversion to apoptosis by antioxidants.

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We treated rapidly growing Jurkat cells with 40 nmol/l of doxorubicin for 72 h. After 36 h, the G2-arrested cells became larger and some of them started endoreplication. Nuclear staining with Hoechst 33342 combined with propidium iodide (PI) exclusion revealed that about 90% of the cells were

Aclarubicin-induced ROS generation and collapse of mitochondrial membrane potential in human cancer cell lines.

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الدخول التسجيل فى الموقع
The cytotoxicity of aclarubicin (ACL) in A549 (human non-small lung), HepG2 (human hepatoma) and MCF-7 (human breast adenocarcinoma) cancer cell lines was evaluated and compared with that of doxorubicin (DOX). Changes in mitochondrial transmembrane potential (DeltaPsim), and production of reactive

Mechanisms of induction of apoptosis by anthraquinone anticancer drugs aclarubicin and mitoxantrone in comparison with doxorubicin: relation to drug cytotoxicity and caspase-3 activation.

يمكن للمستخدمين المسجلين فقط ترجمة المقالات
الدخول التسجيل فى الموقع
We examined molecular events and morphological features associated with apoptosis induced by anthraquinone anticancer drugs aclarubicin, mitoxantrone and doxorubicin in two spontaneously immortalized cell lines (NIH 3T3 and B14) in relation to cytotoxicity of these drugs. The investigated cells

[Effects of aclarubicin on growth, differentiation and apoptosis of tumor cells in vitro].

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Aclarubicine induces various effects after several days of incubation with human leukemic cells HL60: cell growth inhibition, inductions of differentiation, necrosis and apoptosis. Several methods of detection of differentiated and apoptotic cells were studied. The methods utilizing optical

[Targeting cancer chemotherapy using lipiodol as a carrier of anticancer drugs for hepatocellular carcinoma].

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We have found that the lipid lymphographic agent, Lipiodol ultrafluid, remains selectively in hepatocellular carcinoma and other malignant solid tumors. Lipiodol administered arterially flows into the normal blood vessels of normal tissues and into the neovasculature of the tumor. Selective
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