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Introduction Acute myeloid leukemia (AML) is an infrequent (1.3%), highly malignant neoplasm responsible for a large number of cancer-related deaths [ 1 , 2 ]. In the USA and other highly developed countries, the incidence has been near stable over the last years and is about 4 cases per 100,000 citizens per year [ 1 , 2 , 3 ]. The median age at diagnosis is 67 years [ 1 , 2 , 3 ]. AML is a heterogeneous and complex disease in which genomic and proteomic alterations and the interactions between them result in various apoptosis abnormalities [ 1 , 2 , 3

, Lu JY, Li M, Du P, Xu GL, et al. Growth of G422 glioma implanted in the mouse brain was affected by the immune ability of the host. Chin Med J (Engl). 2011;124(13):1994-8. 13. Ma YH, Yu JB, Yao HP, Zhan RY, Zheng JS. Treatment of intracerebral glioblastomas with G422 tumour cell vaccine in a mouse model. J Int Med Res. 2008;36(2):308-13. 14. Wang H, Tu HJ, Qin J, Li XJ, Huang KM, Zhou ZM, et al. [Effect of cryotherapy and 5-fluorouracil on apoptosis of G422 glioma cells]. Ai Zheng. 2004;23(4):412-5. 15. Li F, Cheng Y, Lu J, Hu R, Wan Q, Feng H. Photodynamic therapy

apoptosis via Bak/Bax if Mcl-1 is neutralized. Cancer Cell 2006;10:389-99. Vandenberg CJ Chen L Czabotar PE et al The BH3 mimetic ABT-737 targets selective Bcl-2 proteins and efficiently induces apoptosis via Bak/Bax if Mcl-1 is neutralized Cancer Cell 2006 10 389 99 [9] Scheffold A, Jebaraj BMC, Stilgenbauer S. Venetoclax: Targeting BCL2 in Hematological Cancers. Recent Results Cancer Res 2018;212:215-42. Scheffold A Jebaraj BMC Stilgenbauer S Venetoclax: Targeting BCL2 in Hematological Cancers Recent Results Cancer Res 2018 212 215 42 [10] Korycka-Wołowiec A, Wołowiec D

), interleukin 6 and 8 (IL-6, IL-8), [ 8 , 16 , 17 , 18 ,]. VEGF stimulates the formation of new blood vessels and increases vascular permeability [ 8 ]. This cytokine promotes EC survival by lowering their susceptibility to apoptosis [ 19 ]. VEGF activates phosphatidylinositol-3-kinase/ protein kinase B (PI3K/Akt) pathway and reduces the pro-apoptotic potency of chemotherapy [ 8 , 19 ]. It has been shown that VEGF significantly influences the immune system, and inhibits differentiation, and maturation of dendritic cells (DC). It results in decreased expression of major

, .: Molecular mechanisms regulating the vascular prostacyclin pathways and their adaptation during pregnancy and in the newborn. Pharmacological Reviews, 2012 8. Slomp J., et al.: Differentiation, dedifferentiation, and apoptosis of smooth muscle cells during the development of the human ductus arteriosus. Arterioscler Thromb Vasc Biol, 1997. 17(5): 1003-9 9. Hong Z., et al.: Role of dynamin-related protein 1 (Drp1)-mediated mitochondrial fission in oxygen sensing and constriction of the ductus arteriosus. Circ Res, 2013, 112 (5): 802-15 10. Obladen M.: History of the ductus

MM is caused by the infiltration of malign plasma cells in the bone marrow, which results in suppressing erythropoiesis and dysregulated apoptosis of plasma cells [ 3 , 25 ]. However, stromal and endothelial cells in bone marrow contribute to the development of anemia by producing specific cytokines, particularly interleukin 6 (IL-6) [ 8 ]. Likewise, renal insufficiency also contributes to the development of anemia in MM patients via erythropoietin deficiency [ 26 ]. Furthermore, the interaction of plasma cells with the tumor microenvironment might play a role in

blocking the cell cycle at the G1 phase [ 28 ]. Current published HDACis include valproic acid (VPA), vorinostat, entinostat, and panobinostat. VPA, a short-chained fatty acid, was demonstrated to promote growth inhibition, apoptosis induction, and reactivation of p57KIP2 and p21CIP1 in leukemic cell lines HL-60 and MOLT4 when combined with DAC [ 29 ]. However, in vivo , the combination regimen did not show antileukemia activity. A phase 1/2 and a phase 1 study revealed that the addition of VPA led to neurotoxicity, whose severity depended on the dose [ 30 , 31 ]. A

lymphocytic leukemia (CLL): dissecting the contribution of 17p deletion, TP53 mutation, p53-p21 dysfunction, and miR34a in a prospective clinical trial Blood 2009 114 13 2589 – 97 [12] Turgut B, Vural O, Pala FS, et al. 17p Deletion is associated with resistance of B-cell chronic lymphocytic leukemia cells to in vitro fludarabine-induced apoptosis. Leuk Lymphoma 2007;48(2):311–20. Turgut B Vural O Pala FS et al 17p Deletion is associated with resistance of B-cell chronic lymphocytic leukemia cells to in vitro fludarabine-induced apoptosis Leuk Lymphoma 2007 48 2 311 – 20

Fischer AM Fraenzle A Impact of radiation therapy on stem cell harvest in multiple myeloma Blood 2014 124 5822 [27] Tachikawa S, Nishimura T, Nakauchi H, Ohnuma K. Thalidomide induces apoptosis in undifferentiated human induced pluripotent stem cells. Vitr Cell Dev Biol Anim 2017;53:841–51. 10.1007/s11626-017-0192-8 Tachikawa S Nishimura T Nakauchi H Ohnuma K Thalidomide induces apoptosis in undifferentiated human induced pluripotent stem cells Vitr Cell Dev Biol Anim 2017 53 841 51 [28] Gardner R V, McKinnon E, Astle CM. Analysis of the stem cell sparing properties of

) for experiments involving humans; EU Directive 2010/63/EU for animal experiments; Uniform Requirements for manuscripts submitted to biomedical journals. References/Piśmiennictwo [1] Kipps TJ, Stevenson FK, Wu CJ, et al. Chronic lymphocytic leukaemia. Nat Rev Dis Primers 2017;3:16096. Kipps TJ Stevenson FK Wu CJ et al Chronic lymphocytic leukaemia Nat Rev Dis Primers 2017 3 16096 [2] Podhorecka M, Macheta A, Bozko M, et al. Deregulation of apoptosis – Is it still an important issue in pathogenesis of chronic lymphocytic leukemia? Curr Cancer Drug Targets 2016