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Ultraviolet and Light Absorption Spectrometry
Published in Adorjan Aszalos, Modern Analysis of Antibiotics, 2020
Zoltan M. Dinya, Ferenc J. Sztaricskai
However, the United States Pharmacopeia [14] orders an assay for mithramycin on the basis of absorbancies at 278 and 400 nm. The visible absorption at 410 nm was established as a specific method for measuring olivomycin concentrations.
The Thyroid and the Parathyroid Glands
Published in E. George Elias, CRC Handbook of Surgical Oncology, 2020
Once primary hyperparathyroidism has been diagnosed, surgery is indicated. The use of mithramycin in the dose of 25 μg/kg body weight, not to exceed 2 mg/day, given by slow i.v. drip, once, 2 days prior to surgery will control the hypercalcemia and avoid its complications at the time of surgery and under general anesthesia.
Acquired Bleeding Disorders Associated with Disease and Medications
Published in Harold R. Schumacher, William A. Rock, Sanford A. Stass, Handbook of Hematologic Pathology, 2019
William A. Rock, Sue D. Walker
Plicamycin (mithramycin) is another antibiotic antineoplastic. Hemorrhagic tendency, severe thrombocytopenia, and even death may result from its use. Thrombocytopenia may be rapid in onset and may occur at any time during therapy. “Hemorrhagic syndrome,” the most important form of toxicity, is most likely due to abnormalities in multiple clotting factors, usually begins with epistaxis, and is dose related. The onset of an overt bleeding episode is not necessarily associated with abnormalities in clotting time or clot retraction, but abnormalities in periodically performed tests may serve as a warning of serious toxicity (134).
Recent advances in the combination delivery of drug for leukemia and other cancers
Published in Expert Opinion on Drug Delivery, 2020
Thikrayat Al-Attar, Sundararajan V. Madihally
Mithramycin (also referred to as plicamycin) an antibiotic is shown to inhibit the regulatory associated protein of mTOR/raptor, which regulates many downstream targets including kinases. Relative expression % of raptor dropped to 25% (cells were treated with 30 nM) [27]. However, mithramycin inhibition effect on K562 cells has been studied over the past two decades and maybe a feasible option for treating CML [28]. In clinical trials, mithramycin has only been shown to be effective in solid tumors [29]. K562 cells are known to be tumor necrosis factor (TNF)-related apoptosis inducing ligand (TRAIL) -resistant. The cytotoxicity effect of TRAIL is induced through SIRT1 downregulation which leads to cell death. TRAIL-resistance can be suppressed using siRNA or Amurensin G to inhibit cell growth and cause apoptosis. Apoptosis reached ~22% when treated with SIRT1 siRNA, and 25 ng/mL of TRAIL, and increased to ~27% when treated with Amurensin G and 25 ng/mL of TRAIL [30]. Vascular Endothelial Growth Factor (VEGF) is frequently targeted to inhibit the growth of solid tumors due to its established role in angiogenesis. Antisense-VEGF downregulates the expression of endogenous VEGF expressed in leukemia cells which leads to roughly 10% apoptosis [31].
Mithramycin has inhibitory effects on gliostatin and matrix metalloproteinase expression induced by gliostatin in rheumatoid fibroblast-like synoviocytes
Published in Modern Rheumatology, 2018
Naoe Tatematsu, Yuko Waguri-Nagaya, Yohei Kawaguchi, Yusuke Oguri, Kenji Ikuta, Masaaki Kobayashi, Masahiro Nozaki, Kiyofumi Asai, Mineyoshi Aoyama, Takanobu Otsuka
Clinical use of mithramycin was discontinued due to severe adverse effects, including hepatic, bone marrow, and gastrointestinal toxicity. Nevertheless, there is renewed interest in its used malignant tumors and non-cancer-related disorders. For example, some clinical trials of mithramycin against cancer and sarcoma are being conducted at National Institutes of Health in the United States. Mithramycin was also reported as a potent inducer of fetal hemoglobin production in erythroid cells from healthy human subjects and in patients with beta-thalassemia. This result might indicate potential clinical significance because an increase in fetal hemoglobin alleviates the symptoms underlying beta-thalassemia and sickle cell anemia [47]. Interestingly, several studies have also reported production of mithramycin analogs that might mitigate the toxicity of the parent drug [48,49].