3.Thalidomide in combination with interferon and interleukin 2 in the induction therapy for relapsed refractory acute myeloid leukemia: two case report and literature review.
Hao AI ; Yanli ZHANG ; Xudong WEI ; Qingsong YIN ; Ping WANG ; Ruihua MI ; Yongping SONG
Chinese Journal of Hematology 2014;35(10):954-956
4.Inhibition of Corneal Angiogenesis by Orally Administered Thalidomide.
Ju Yeoun LEE ; Jung Min KIM ; Tea Hoon CHOI ; Jung Woo KIM
Journal of the Korean Ophthalmological Society 1997;38(12):2098-2107
Thalidomide, a potent teratogen, is Known as an angiogenic inhibitor. This study was performed to examine the effect of thalidomide on corneal angiogenesis in rabbit cornea induced by chemical cauterization. We applied Whatman filter paper disc soaked in 30% silver nitrate (AgNO3) application on corneas of 12 white rabbits. After 5days, we administered oral dose of 100mm2 thalidomide to the 6 animals everyday and examined the length and extent of neovascularization to evaluate the area of neovascularization. After 2 days of oral administration, the increase of neovascularization is 14.3+/-11.7mm2in thalidomide-treated group and 27.9+/-14.6mm2 in cotrol grop. The area of neovascularization reached to its maximum at day 9 in thalidomide-treated group compared to day 11 in control group and decreased thereafter in both groups. The increase of the area of vascularized cornea revealed 28.0+/-13.5mm2 in thalidomide-treated group and 44.4+/-12.7mm2 in control group at the day 9 (p=0.04, Wilkoxon Matched-pairs signed-rank test). This fact means that treatment with thalidomide resulted in an inhibition of the area of vascularized cornea with the median inhibition of 37.3%. On light micrographs, there were infiltration of inflammatory cell and capillary lumens in corneal stroma in both animals. Electron micrographs of thalidomide-treated animals showed loss of vascular endothelial cell junction, mitochondrial swelling and loss of cristae which were not found in control animals. This results suggest that orally-administered thalidomide has a direct effect on the growing vasculature and an inhibitory effect on corneal angiogenesis.
Administration, Oral
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Animals
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Capillaries
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Cautery
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Cornea
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Corneal Neovascularization*
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Corneal Stroma
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Endothelial Cells
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Mitochondrial Swelling
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Rabbits
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Silver Nitrate
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Thalidomide*
5.Curative Efficacy of Lenalidomide plus Low Dose Dexamethasone for Multiple Myeloma.
Journal of Experimental Hematology 2016;24(2):498-501
OBJECTIVETo explore the clinical efficacy and safety of lenalidomide plus low dose dexamethasone for treating patients with multiple myeloma (MM).
METHODSA total of 19 MM patients were enrolled to receive the therapeutic schedule of lenalidomide plus dexamethasone in our hospital from May 2013 to June 2015. Lenalidomide 25 mg was taken orally daily for 21 days and resting for 7 days, and dexamethasone 10 mg was taken orally daily on the day 1-4, 7-10 and 13-16. The regimens were Rd (lenalidomide and dexamethasone, n = 12), and RCd (lenalidomide, ifosfamide and dexamethasone, n = 7).
RESULTSAmong 19 patients received 1 cycle of treatment 3 patients achieved complete remission (CR), 3 patients achieved very good partial remission (VGPR), 10 patients achieved partial remission (PR) and 3 patients in stable disease (SD) with an overall response rate (ORR = CR + VGPR + PR) of 84%; their ORR rate was 89% after 2 cycles of treatment. In the early stage of treatment, the renal function was improved in 4 out of 5 patients with renal dysfunction. And the common adverse reactions were hematologic toxicity in 4 patients, 1 degree rash in 5 patients, and gastrointestinal side effects in 4 patients.
CONCLUSIONThe lenalidomide plus dexamethasone regimen has a good anti-multiple myeloma effect, which can control the disease rapidly and overcome the multidrug resistance in MM, improving the poor prognosis with renal dysfunction, and showing high remission rate in the patients exposed to bortezomib with low toxicity.
Antineoplastic Combined Chemotherapy Protocols ; Dexamethasone ; administration & dosage ; therapeutic use ; Humans ; Ifosfamide ; therapeutic use ; Multiple Myeloma ; drug therapy ; Remission Induction ; Thalidomide ; administration & dosage ; analogs & derivatives ; therapeutic use
6.Efficacy of different thalidomide regimens for patients with multiple myeloma and its relationship with TNF-alpha level.
Xiao-Rong MA ; Yin-Xia CHEN ; Jie LIU ; Wang-Gang ZHANG ; Xing-Mei CAO ; Ai-Li HE ; Yun YANG
Journal of Experimental Hematology 2008;16(6):1312-1315
The study was aimed to investigate the clinical efficacy and adverse reactions of different thalidomide regimens in the treatment of multiple myeloma (MM), and to explore the relationship between efficacy of thalidomide and serum level of TNF-alpha in MM patients. The 85 patients with MM were divided into 5 groups according to different combinations of thalidomide. These 5 groups were following: group with the high dose (HD-T), group with thalidomide+VAD chemotherapy (T-VAD), group with thalidomide+MP chemotherapy (T-MP), group with thalidomide plus dexamethasone (TD), and group with low dose of thalidomide (LD-T). Except 5 groups mentioned above, the group with conventional VAD chemotherapy was served as the control. Clinical effects, adverse reactions, treatment-related mortality were observed. At the same time, serum levels of TNF-alpha in 30 cases of MM treated with thalidomide (15 cases effective and 15 cases ineffective) before and after treatment were detected by double-antibody sandwich enzyme-linked immunosorbent assay (ELISA) and were compared with the clinical efficacy. The results showed that the efficient rate of HD-T, T-VAD, T-MP, TD, LD-T groups were 25.0%, 80.0%, 71.4%, 33.3%, 27.3% respectively; the efficacy of T-VAD, T-MP groups were significantly higher (p<0.05) than that of other groups and conventional VAD chemotherapy group. The incidence of significant adverse reactions (peripheral neuropathy, fatigue, abdominal distension and constipation, rash, edema, leukocyte and platelet decrease) in 5 groups were 75.0%, 30.0%, 28.6%, 14.3%, 9.1% respectively, no IV grade toxicity and deep vein thrombosis were found. The treatment-related mortality was 0%. At the same time, it was found that the serum levels of TNF-alpha in ineffective group treated with thalidomide were 44.7+/-5.7 pg/ml and 46.3+/-4.0 pg/ml before and after thalidomide treatment, and there was no significant difference (p>0.05). The serum levels of TNF-alpha (27.3+/-6.4) pg/ml in the effective group after treatment was significantly lower than that before treatment (49.2+/-7.3) pg/ml (p<0.05). It is concluded that compared with conventional chemotherapy, thalidomide is a effective drug for treating MM patients. Thalidomide in combination with chemotherapy (T-VAD, T-MP) may be one better therapeutic regimen with high efficiency and milder adverse reactions. Serum level of TNF-alpha is an indicator for finding effects of thalidomide, and plays a role in the pathogenesis of MM.
Adult
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Aged
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Antineoplastic Agents
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administration & dosage
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therapeutic use
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Female
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Humans
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Male
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Middle Aged
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Multiple Myeloma
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blood
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drug therapy
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Thalidomide
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administration & dosage
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therapeutic use
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Tumor Necrosis Factor-alpha
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blood
9.Is the Low-Thalidomide Dose MPT Regimen Beneficial?.
The Korean Journal of Internal Medicine 2011;26(4):400-402
No abstract available.
Angiogenesis Inhibitors/administration & dosage/*therapeutic use
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Antineoplastic Agents, Alkylating/administration & dosage/*therapeutic use
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Humans
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Melphalan/administration & dosage/*therapeutic use
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Multiple Myeloma/*drug therapy
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Prednisone/therapeutic use
;
Thalidomide/administration & dosage/*therapeutic use
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Treatment Outcome
10.New agents for the treatment of myelodysplastic syndromes.
Korean Journal of Medicine 2009;76(2):121-125
Myelodysplastic syndromes (MDS) are a heterogenous group of clonal stem cell disorders commonly characterized by a hypercellular and dysplastic bone marrow, cytopenias resulting from impaired peripheral blood cell production, and an increased risk of leukemic transformation. Currently, azacitidine, decitabine, and lenalidomide are approved by the US Food and Drug Administration for the treatment of MDS. The DNA methyltransferase (DNMT) inhibitors such as azacitidine and decitabine have demonstrated the ability to alter the natural history of disease and thus prolong time to leukemic transformation. In addition, azacitidine has shown the capacity to extend survival compared with the previous gold standard of conventional care regimens. Recently, decitabine has been shown to be well tolerated with a toxicity profile expected for this class of agent. Recent studies also suggest that decitabine may result in additional improvements in response. As more is learned about the mechanism of hypomethylating agents, new roles are emerging for decitabine in combination therapy for MDS. The third agent, lenalidomide, is a thalidomide analogue with significant activity in a subset of patients with low-risk MDS, anemia and chromosome 5 alterations. Several other agents are being evaluated in MDS. This review summarizes the existing clinical experience on DNMT inhibitors and other drugs for the treatment of MDS.
Anemia
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Azacitidine
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Blood Cells
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Bone Marrow
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Chromosomes, Human, Pair 5
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DNA
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Humans
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Myelodysplastic Syndromes
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Natural History
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Stem Cells
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Thalidomide
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United States Food and Drug Administration