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Hdac Inhibitor
However, subsequent repair might be suppressed for some unknown reason.The premature mitotic entry of defective cells before proper chromosome segregation leads to mitotic catastrophe and cell death upon entering mitosis. Our IF results showed that DCZ treatment led to a mitotic catastrophe and confirmed these speculations.Mitotic catastrophe shares several biochemical hallmarks of apoptosis. We observed caspasedependent apoptosis induced by DCZ in vitro and necrosis in xenotransplanted tumors in vivo.Significantly, unlike normal cells, most cancer cells have aberrant cell cycle checkpoints, especially G phase checkpoint, and are prone to mitotic catastrophe. However, BTZ resistance can arise through the therapyinduced selection of a minor resistant cell subpopulation present in MM. Detailed concentrations of DCZ and BTZ used in the synergistic experiments.DCZ was synergistic with the histone deacetylase inhibitor panobinostat in NCIHR and RPMIR cells.The myeloma stem cell concept, revisited: from phenomenology to operational terms.Multiple myeloma cancer stem cells.Glioma stem cells promote radioresistance by preferential activation of the DNA damage response.Preclinical activity of DCZ, a novel arylguanidino compound in the therapy of multiple myeloma.Flow cytometric quantification of all phases of the cell cycle and apoptosis in a twocolor fluorescence plot.R loops are linked to histone H S phosphorylation and chromatin condensation.G checkpoint abrogation and checkpoint kinase targeting in the treatment of cancer.The when and wheres of CDC phosphatases.WSTF regulates the HA.X DNA damage response via a novel tyrosine kinase activity.Role of RADAP in homologous recombination DNA repair and carcinogenesis.Determinants of mitotic catastrophe on abrogation of the G DNA damage checkpoint by UCN.Oncotarget. Publishers Note Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. An estimated to of all patients with cancer have hypercalcemia at some point in their disease trajectory, particularly in advanced disease.Aggressive Targetmol‘s Povidone-iodine saline hydration and varying doses of furosemide continue to be the standard of care for emergency management.However, a review of the evidence for the use of furosemide in the medical management of hypercalcemia yields only case reports published before the introduction of bisphosphonates, in contrast to multiple randomized, controlled trials supporting the use of bisphosphonates.The use of furosemide in the management of hypercalcemia should no longer be recommended.Because patients with hypercalcemia cannot concentrate urine and therefore become significantly dehydrated, saline hydration is important but rarely sufcient in moderate to severe cases.Common treatments included tumor excision when possible, steroids, plicamycin, intravenous phosphate, sulfate, or ethylenediamine tetraacetate.These treatments were not benign, which made furosemide seem to be an attractive alternative.Beginning in, reports on the use of furosemide to increase calciuresis were published. Forced saline diuresis subsequently became the standard of care; however, physicians did not use the methods described in these articles.In, a randomized, controlled trial of gallium nitrate and etidronate found gallium to be superior. Pamidronate and zoledronic acid followed; both were demonstrated to have improved efcacy. Nonetheless, most current textbooks continue to recommend rstline management with saline and furosemide.Although many comment that adequate hydration is needed before the use of furosemide, our anecdotal experience is that this recommendation is not routinely followed.We therefore sought evidence to support the use of furosemide as primary therapy for hypercalcemia.
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