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colchicine/rinnavähk

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ArtiklidKliinilistes uuringutesPatendid
Leht 1 alates 172 tulemused

Proliferation inhibition and apoptosis of breast cancer MCF-7 cells under the influence of colchicine.

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This study was designed to explore the effect of colchicine on the proliferation and apoptosis of Breast Cancer Michigan Cancer Foundation - 7 (MCF-7) cells. The experiment was conducted at the University Laboratory of East Provincial Hospital in April, 2015. The first inhibitory effect of
The subunit protein of microtubules is tubulin, which has been the target for some of the most successful and widely used anti-tumor drugs. Most of the drugs that target tubulin bind to the β subunit. There are many isotypes of β-tubulin and their distributions differ among different tissues. The
BACKGROUND One of the main reasons for disease recurrence in the curative breast cancer treatment setting is the development of drug resistance. Microtubule targeted agents (MTAs) are among the most commonly used drugs for the treatment of breaset cancer and therefore overcoming taxane resistance is
Colchicine (COL) shows strong anticancer activity but due to its toxicity towards normal cells its wider application is limited. To address this issue, a library of 17 novel COL derivatives, namely N-carbamates of N-deacetyl-4-(bromo/chloro/iodo)thiocolchicine, has been tested against two types of
G-protein-coupled estrogen receptor 1 (GPER1) has been reported to play a significant role in mediating the rapid estrogen actions in a wide range of normal and cancer cells. G-1 was initially developed as a selective agonist for GPER. However, the molecular mechanisms underlying the actions of G-1
A series of naphthalene-chalcone derivatives (3a-3t) were prepared and evaluated as tubulin polymerisation inhibitor for the treatment of breast cancer. All compounds were evaluated for their antiproliferative activity against MCF-7 cell line. The most of compounds displayed potent
Originally purified as a major lipid component of a strain of the cyanobacterium Lyngbya majuscula isolated in Curaçao, curacin A is a potent inhibitor of cell growth and mitosis, binding rapidly and tightly at the colchicine site of tubulin. Because its molecular structure differs so greatly from

[Adjuvant colchicine pharmaceuticals in the combined surgical treatment of breast cancer (author's transl)].

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Histologic effects of colchicine on breast cancer tissue.

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Delocalization of gamma-tubulin due to increased solubility in human breast cancer cell lines.

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The centrosome is the major organelle responsible for the nucleation and organization of microtubules into arrays. Recent studies demonstrate that microtubules can nucleate outside the centrosome. The molecular mechanisms controlling acentrosomal microtubule nucleation are currently poorly defined,

Design and pharmacophore modeling of biaryl methyl eugenol analogs as breast cancer invasion inhibitors.

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Cell invasion and migration are required for the parent solid tumor cells to metastasize to distant organs. Microtubules form a polarized network, enabling organelle and protein movement throughout the cell. Cytoskeletal elements coordinately regulate cell's motility, adhesion, migration,

Perturbation by insulin of human breast cancer cell cycle kinetics.

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The growth of cultured human breast cancer cells is sensitive to physiological concentrations of insulin suggesting that it may regulate breast cancer growth in vivo. The mechanisms for the growth effects of insulin are poorly defined. In the present study, we examine the effects of insulin on the

Behçet's disease and breast cancer: A case series study.

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UNASSIGNED The relation between Behçet's disease (BD) and breast cancer (BC) is unclear. Our purpose is to investigate whether BD has an important effect on BC or vice versa. UNASSIGNED A total of 12 female BC patients with a diagnosis of BD were identified from a cohort including 5050 BC patients.

Isolation and characterization of an adriamycin-resistant breast tumor cell line.

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An adriamycin-resistant human breast tumor cell line MDA-A1R was generated by step-wise selection in increasing concentrations of drug from the parent cell line MDA-MB-231. MDA-A1R cells grow as loosely attached cell aggregates with a doubling time of 28-32 h; the MDA-MB-231 parent cell line grows
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