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forskolin/emlőrák

A hivatkozás a vágólapra kerül
CikkekKlinikai vizsgálatokSzabadalmak
Oldal 1 tól től 97 eredmények
Triple negative breast cancer (TNBC) is an invasive, metastatic, highly aggressive tumor. Cytotoxic chemotherapy represents the current treatment for TNBC. However, relapse and chemo-resistance are very frequent. Therefore, new therapeutic approaches that are able to increase the sensitivity to
The effect of 1,25-dihydroxycholecalciferol [1,25(OH)2D3], the active form of vitamin D3, on cell growth, clonogenicity, and cyclic adenosine monophosphate (cAMP) production was examined in human breast cancer cell line T47D. 1,25(OH)2D3 markedly inhibited proliferation of T47D cells in a time- and

Synthesis of novel forskolin isoxazole derivatives with potent anti-cancer activity against breast cancer cell lines.

Csak regisztrált felhasználók fordíthatnak cikkeket
Belépés Regisztrálás
Forskolin C1-isoxazole derivatives (3,5-regioisomers) (11a-e, 14, 15a-h and 15, 16a-g) were synthesized regioselectively by adopting 1,3-dipolar cycloadditions. These derivatives were tested using estrogen receptor positive breast cancer cell lines MCF-7 and BT-474. Majority of the compounds

Forskolin increases the effect of everolimus on aromatase inhibitor-resistant breast cancer cells.

Csak regisztrált felhasználók fordíthatnak cikkeket
Belépés Regisztrálás
Aromatase inhibitor (AI) resistance is a major obstacle in the treatment of estrogen receptor-positive breast cancer. Everolimus (EVE) ameliorates AI-resistant breast cancer and is therefore used in cancer treatment. However, some patients show resistance to EVE. Here, we used 30 clones of long-term

Diazepam inhibits forskolin-stimulated adenylyl cyclase activity in human tumour cells.

Csak regisztrált felhasználók fordíthatnak cikkeket
Belépés Regisztrálás
Previous studies have shown that the benzodiazepine agonist, diazepam, suppresses adenylyl cyclase activity in rat brain, via a G protein-coupled benzodiazepine receptor. Since diazepam binding sites are also present in diverse non-neuronal tissues including tumour cells, its effects on adenylyl
Breast cancer cells secrete endothelin-1 (ET-1), which may act as a paracrine mitogen in breast tumours. The paracrine factors and signal transduction pathways responsible for regulating ET-1 production in breast cancer are unknown. In this study we have examined the involvement of the protein

Role of prostaglandin E2 receptors in migration of murine and human breast cancer cells.

Csak regisztrált felhasználók fordíthatnak cikkeket
Belépés Regisztrálás
Aberrant upregulation of COX-2 enzyme resulting in accumulation of PGE2 in a cancer cell environment is a marker for progression of many cancers, including breast cancer. Four subtypes of cell surface receptors (EP1, EP2, EP3, and EP4), which are coupled with different G-proteins, mediate PGE2

Effects of differentiation-inducing agents on maturation of human MCF-7 breast cancer cells.

Csak regisztrált felhasználók fordíthatnak cikkeket
Belépés Regisztrálás
The effects of the differentiation inducing agents (DIAS), sodium butyrate (NaBu), retinoic acid (RA), dimethylformamide (DMF), hexamethylene bisacetamide (HMBA), forskolin, and 12-O-tetradecanoylphorbol-13-acetate (TPA), on the growth, morphology, and estrogen receptor (ER) content and epithelial
We have examined the regulation of an insulin-like growth factor-binding protein-3 (IGFBP-3) protease secreted by MCF-7 human breast cancer cells using a ligand-binding assay that relies on the decrease in affinity for des(1-3)IGF-I that occurs when IGFBP-3 becomes proteolyzed. IGFBP-3 protease

Aberrant expression of aromatase in breast cancer tissues.

Csak regisztrált felhasználók fordíthatnak cikkeket
Belépés Regisztrálás
The expression of aromatase is tissue-specifically regulated through the alternative use of multiple exons 1 and promoters. We analysed expression levels of aromatase mRNA, preferential utilization of multiple exon 1 of the human aromatase gene, and transcriptional regulation of their multiple

Molecular analysis of aberrant expression of aromatase in breast cancer tissues.

Csak regisztrált felhasználók fordíthatnak cikkeket
Belépés Regisztrálás
Aromatase mRNA in non-malignant breast tissues was mainly transcribed form skin fibroblast/fetal liver-specific exon 1 (exon 1b) of the aromatase gene. However, in half the cases of breast cancers, switching of the alternative exons 1 from exon 1b to ovary-specific exon 1 (exon 1c) was observed, and

Regulation of c-fos and c-jun expression by calcitonin in human breast cancer cells.

Csak regisztrált felhasználók fordíthatnak cikkeket
Belépés Regisztrálás
Breast cancer cells (BCC) have calcitonin (CT) receptors, yet the action of the hormone on these cells is largely unknown. We found that CT produced a strong and transient time- and dose-dependent increase in c-fos mRNA in BCC lines. This event was prevented by a protein kinase A (PKA) inhibitor,

Hydrocortisone and purinergic signaling stimulate sodium/iodide symporter (NIS)-mediated iodide transport in breast cancer cells.

Csak regisztrált felhasználók fordíthatnak cikkeket
Belépés Regisztrálás
The sodium/iodide symporter (NIS) mediates a remarkably effective targeted radioiodide therapy in thyroid cancer; this approach is an emerging candidate for treating other cancers that express NIS, whether endogenously or by exogenous gene transfer. Thus far, the only extrathyroidal malignancy known
NOR-1, NGFI-B, and Nurr1 are closely related orphan nuclear receptors implicated in diverse biological processes including cell growth and differentiation. We examined the effect of retinoic acids on the expression of these putative transcription factor genes in the breast cancer cell line MCF-7 by

Membrane estrogen receptor-alpha levels in MCF-7 breast cancer cells predict cAMP and proliferation responses.

Csak regisztrált felhasználók fordíthatnak cikkeket
Belépés Regisztrálás
BACKGROUND 17beta-estradiol (E2) can rapidly induce cAMP production, but the conditions under which these cAMP levels are best measured and the signaling pathways responsible for the consequent proliferative effects on breast cancer cells are not fully understood. To help resolve these issues, we
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