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Cyclophosphamide and Etoposide as a Salvage Treatment in Metastatic Osteosarcoma Patients

Journal of Cancer Therapy 2018年第7期9卷 529-537页

作者： fatma mf akl Mohamed Farouk akl Clinical Oncology and Nuclear Medicine Department Mansoura University Mansoura Egypt

Background and Objective: Osteosarcoma is a rare bone cancer with approximately 30% - 35% of patients who will relapse either systemically or locally, with the lung being the commonest site of relapse. The objective of this trial was to evaluate the efficacy of cyclophosphamide and etoposide, in treatment of metastatic osteosarcoma patients progressed after one or more chemotherapy lines, with the progression free survival and treatment response as the primary endpoints, while the secondary endpoints were overall survival and treatment toxicity. Patients and Methods: Twenty seven metastatic osteosarcoma patients were enrolled into this trial and received cyclophosphamide and etoposide chemotherapy. Cyclophosphamide was given at a dose of 500 mg/m2 per day, I.V for 5 days and etoposide (100 mg/m2 per day I.V for 5 days). Response was assessed after 3 cycles according to Response Evaluation Criteria in Solid Tumors (RECIST) version 1.1. Chemotherapy Toxicity was graded according to the Common Terminology Criteria for Adverse Events (CTCAE). Results: The median overall survival time and progression-free survival were 12 months and 8 months, respectively. Four patients (14.8%) achieved partial response;14 patients (51.9%) had stationary disease (SD);and 9 (33.3%) expressed tumor progression. Hematologic toxicity was the main toxicity. None of the patients had G4 or life threatening toxicities. Conclusion: The combination of cyclophosphamide and etoposide represents an efficient and tolerable treatment option for patients with metastatic osteosarcoma.

关键词： Cyclophosphamide Etoposide Metastatic Osteosarcoma Salvage Chemotherapy

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Hypofractionated versus Conventionally Fractionated Radiotherapy in Post-Mastectomy Breast Cancer Patients

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Journal of Cancer Therapy 2018年第11期9卷 941-954页

作者： fatma M. F. akl Ashraf Khater Clinical Oncology & Nuclear Medicine Department Mansoura University Egypt Surgical Oncology Department Oncology Center Mansoura University Egypt

Background & Objective: Hypofractionation has been used in curative setting in breast conservative surgery, but still no adequate information about its application in the adjuvant setting after mastectomy in breast cancer patients. The aim of this trial was to assess the efficacy and toxicity of hypofractionation radiotherapy (40 Gy in 15 fractions) in post mastectomy breast cancer patients and to compare these results with those of post mastectomy patients treated retrospectively by conventional radiotherapy (50 Gy in 25 fractions) as regard overall survival (OS), disease free survival (DFS), locoregional disease free survival (LDFS), and toxicities. Patients & Methods: One hundred post mastectomy breast cancer patients were included into this study, they were divided into 2 groups, the 1st included 50 patients treated prospectively with hypofractionated radiotherapy regimen (40 Gy in 15 fractions), and the 2nd (control group) included 50 patients treated retrospectively with conventionally fractionated radiotherapy regimen (50 Gy in 25 fractions). Results: The 2 year overall survival were 96% & 94% respectively (p = 0.7), while the disease free survival were 91% & 89.8%, respectively (p = 0.9), and the LDFS were 95.8% & 93.3%, respectively (p = 0.9), G1 acute dermatitis was observed in 22 (44%) & 25 (50%) patients in group I & II respectively, G2 in 8 (16%) & 10 (20%) patients respectively, no G4 skin toxicity was detected. Radiation pneumonitis was observed in 2 patients (4%) only in group II. Conclusion: post-mastectomy hypofractionated radiation therapy achieved comparable survival and toxicity to the conventionally fractionated radiotherapy with the advantage of reducing overall treatment time, treatment burden & cost.

关键词： Breast Cancer Adjuvant Radiotherapy Hypofractionation Conventional Fractionation

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Central role of myeloid MCPIP1 in protecting against LPSinduced inflammation and lung injury

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Signal Transduction and Targeted Therapy 2017年第1期2卷 18-32页

作者： Yong Li Xuan Huang Shengping Huang Hui He Tianhua Lei fatma Saaoud Xiao-Qiang Yu Ari Melnick Anil Kumar Christopher J Papasian Daping Fan Mingui Fu Department of Biomedical Science and Shock/Trauma Research Center School of MedicineUniversity of Missouri-Kansas CityKansas CityMissouriMOUSA Institute of Translational Medicine Nanchang UniversityNanchangJiangxiP.R.China Department of Cell Biology and Anatomy University of South Carolina School of MedicineColumbiaSCUSA Division of Molecular Biology and Biochemistry School of Biological SciencesUniversity of Missouri-Kansas CityKansas CityMissouriMOUSA Division of Hematology and Medical Oncology Weill Cornell Medical CollegeNew YorkNYUSA Division of Pharmacology and Toxicology School of PharmacyUniversity of Missouri-Kansas CityKansas CityMissouriMOUSA

Although systemic inflammatory responses attributable to infection may lead to significant lung injury,the precise molecular mechanisms leading to lung damage are poorly understood and therapeutic options remain ***,we show that myeloid monocyte chemotactic protein-inducible protein 1(MCPIP1)plays a central role in protecting against LPS-induced inflammation and lung ***-specific MCPIP1 knockout mice developed spontaneous inflammatory syndromes,but at a late age compared to global MCPIP1 knockout ***,mice with a myeloid-specific deletion of MCPIP1 were extremely sensitive to LPS-induced lung injury due to overproduction of proinflammatory cytokines and *** identified C/EBPβand C/EBPδ,two critical transcriptional factors that drive cytokine production and lung injury,as targets of MCPIP1 *** administration caused MCPIP1 protein degradation in the *** inhibition of MALT1,a paracaspase that cleaves MCPIP1,by MI-2 selectively increased the MCPIP1 protein levels in macrophages and in the ***,administration of MI-2 protected mice from LPS-induced inflammation,lung injury and ***,these results indicate that myeloid MCPIP1 is central in controlling LPS-induced inflammation and lung *** inhibition of MALT1 protease activity may be a good strategy to treat inflammatory diseases by enhancing MCPIP1 expression in myeloid cells.

关键词： inflammation myeloid lung

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