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lactate dehydrogenase/rinnavähk
Link salvestatakse lõikelauale
Leht 1 alates 430 tulemused
In-cell determination of Lactate Dehydrogenase Activity in a Luminal Breast Cancer Model ⁻ ex vivo Investigation of Excised Xenograft Tumor Slices Using dDNP Hyperpolarized [1-13C]pyruvate.
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[1-13C]pyruvate, the most widely used compound in dissolution-dynamic nuclear polarization (dDNP) magnetic resonance (MR), enables the visualization of lactate dehydrogenase (LDH) activity. This activity had been demonstrated in a wide variety of cancer models, ranging from cultured
p53/Lactate dehydrogenase A axis negatively regulates aerobic glycolysis and tumor progression in breast cancer expressing wild-type p53.
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Tumor suppressor p53 is a master regulator of apoptosis and plays key roles in cell cycle checkpoints. p53 responds to metabolic changes and alters metabolism through several mechanisms in cancer. Lactate dehydrogenase A (LDHA), a key enzyme in glycolysis, is highly expressed in a variety of tumors
Lactate dehydrogenase downregulation mediates the inhibitory effect of diallyl trisulfide on proliferation, metastasis, and invasion in triple-negative breast cancer.
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The Warburg effect plays a critical role in tumorigenesis, suggesting that specific agents targeting Warburg effect key proteins may be a promising strategy for cancer therapy. Previous studies have shown that diallyl trisulfide (DATS) inhibits proliferation of breast cancer cells by inducing
Removal of lactate dehydrogenase-elevating virus from human-in-mouse breast tumor xenografts by cell-sorting.
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Lactate dehydrogenase-elevating virus (LDV) can infect transplantable mouse tumors or xenograft tumors in mice through LDV-contaminated mouse biological materials, such as Matrigel, or through mice infected with LDV. LDV infects specifically mouse macrophages and alters immune system and tumor
Comparative effects of 17 beta-estradiol, progestin R5020, tamoxifen and RU38486 on lactate dehydrogenase activity in MCF-7 human breast cancer cells.
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The effects of 17 beta-estradiol (estradiol), synthetic progestin R5020 and their antagonists, tamoxifen (Tam) and synthetic RU38486 on lactate dehydrogenase (LDH) activity in MCF-7 human breast cancer cells during the growth period were studied. A specially developed quantitative cytochemical assay
Effects of progestins, estrogens, and antihormones on growth and lactate dehydrogenase in the human breast cancer cell line T47D.
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We have previously reported progestin stimulation of growth and lactate dehydrogenase (LDH) in the human breast cancer cell line T47D. Our further findings now show that growth stimulation by progestins occurs in a dose-responsive manner at physiological concentrations and is inhibited by the
[Lactate dehydrogenase, adenosine deaminase and thymidine phosphorylase activity of blood and tissues in breast cancer].
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Lactate dehydrogenase (LDH), adenosine deaminase and thymidine phosphorylase activity was analyzed in the blood serum, primary tumor and adjacent uninvolved breast tissues from 49 women with adenocarcinoma and from 10 ones with benign adenofibroma. The LDH activity was increased in both cancerous
Effect of filgrastim on serum lactate dehydrogenase and alkaline phosphatase values in early breast cancer patients.
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To improve chemotherapy dose intensity and to optimize the use of granulocyte-colony stimulating factor, 506 patients with early breast cancer were randomly assigned to high dose epirubicin and cyclophospamide (EC) with or without prophylactic subcutaneously filgrastim, according to 5 different
An explorative analysis of the prognostic value of lactate dehydrogenase for survival and the chemotherapeutic response in patients with advanced triple-negative breast cancer.
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Serum lactate dehydrogenase (LDH) level is predictive of prognosis in various malignancies. Nevertheless, the association between the prognosis of patients with advanced triple-negative breast cancer (TNBC) and LDH is not well understood. This explorative and retrospective study was conducted to
Diagnostic and prognostic significance of serum cholinesterase and lactate dehydrogenase in breast cancer.
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Serum cholinesterase (ChE) and Lactate dehydrogenase (LDH) activities were estimated in 40 cases of carcinoma breast, 25 cases of benign tumours and compared with healthy controls (30 cases). Significant difference in enzyme activities were obtained between benign and malignant neoplasms of the
Breast cancer diagnosis by lactate dehydrogenase isozymes in nipple discharge.
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BACKGROUND
The diagnosis of breast cancer based on nipple discharge, often the only clinical manifestation of early breast cancer, is currently unsatisfactory. Because M subunits of lactate dehydrogenase (LDH) have been noted to increase in cancer tissue, the author assessed the value of using LDH
No relationship between lactate dehydrogenase and estrogen receptor levels in clinical human breast cancer.
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The level of lactate dehydrogenase has been reported to increase in a human breast cancer cell line as a result of estrogen action [4]. This finding suggests that lactate dehydrogenase may be useful in clinical human breast cancer as a marker for intactness of the estrogen receptor pathway and for
Oestrogen receptors, lactate dehydrogenase and cellularity in human breast cancer.
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Oestrogen receptor (ER) concentrations in breast tissues are almost universally expressed in relation to total soluble protein, though the latter does not fully correct for gross variations in receptor concentration due to variations in tissue cellularity. It was considered possible that the
A progestin effect on lactate dehydrogenase in the human breast cancer cell line T-47D.
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The human breast cancer cell line T-47D has high levels of progesterone receptor even in the absence of exogenously added estrogen. Because of this it is a good line in which to study aspects of progestin action. It has been shown by others that lactate dehydrogenase in MCF-7 cells is responsive to
Progestin stimulation of lactate dehydrogenase in the human breast cancer cell line T-47D.
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We have previously reported that physiological levels of progestins alone stimulate lactate dehydrogenase in a dose-responsive manner in the progesterone-receptor-rich human breast cancer cell line T-47D. Using isozyme electrophoresis, we have not found that lactate dehydrogenase isozyme 5 is the
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