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Keywords = Cancer

  • Open Access Research Article
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    Trends Journal of Sciences Research 2018, 3(2), 60-68. http://doi.org/10.31586/Cancer.0302.01
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    Abstract
    Objective: To evaluate the efficacy and safety of nimotuzumab in combination with radiochemotherapy as the primary treatment in patients with locoregionally advanced nasopharyngeal carcinoma (NPC). Methods: We retrospectively reviewed patients with locoregionally advanced nasopharyngeal carcinoma from September 2012 to December 2016. 188 newly diagnosed patients with stage III?IVB nasopharyngeal carcinoma
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    Objective: To evaluate the efficacy and safety of nimotuzumab in combination with radiochemotherapy as the primary treatment in patients with locoregionally advanced nasopharyngeal carcinoma (NPC). Methods: We retrospectively reviewed patients with locoregionally advanced nasopharyngeal carcinoma from September 2012 to December 2016. 188 newly diagnosed patients with stage III?IVB nasopharyngeal carcinoma were treated with at least 1-2 cycles of chemotherapy concurrently with planned IMRT. 88 patients received nimotuzumab 200 mg/week. Acute and late radiation-related toxicities were graded according to the Acute and Late Radiation Morbidity Scoring Criteria of Radiation Therapy Oncology Group. Results: After 3 months of treatment, the complete response rates of nasopharyngeal tumors in the study group and the control group were 78.4% and 65.5%, respectively (?2=4.070, P=0.044). The total complete response rates of cervical lymph nodes in the study group and the control group were 80.7% and 67.6% respectively (?2=4.022, P=0.045).The median cycle for nimotuzumab addition was 6.3 weeks. With a median follow-up of 36.3 months (range, 12?72 months), the estimated 3-year progression failure-free survival and overall survival rates for the study group and the control group were 85.24% vs 81.97% and 96.67% vs 90.0%, respectively. The 3-year local recurrence-free survival rates for the study group and the control group were 96.67% vs 83.60%, respectively (P=0.047). Grade 3 radiation-induced mucositis accounted for 36.4% of treated patients. No skin rash and infusion reaction were observed, distinctly from what is reported in control patients. Conclusion: Nimotuzumab plus chemoradiotherapy in the treatment of locoregionally advanced nasopharyngeal carcinoma showed promising outcomes in terms of locoregional control, without increasing the incidence of radiation-related toxicities for patients.  Full article
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    References
    [1]
    Tang LL, Chen WQ, Xue WQ, He YQ, Zheng RS, ZengYX, Jia WH. Global trends in incidence and mortality of nasopharyngeal carcinoma. Cancer Lett. 2016; 374:22?30.
    [2]
    Lee N, Xia P, Quivey JM, et al. Intensity-modulated radiotherapy in the treatment of nasopharyngeal carcinoma: an update of the UCSF experience. Int J Radiat Oncol Biol Phys. 2002;53:12?22.
    [3]
    Chen L, Mao YP, Xie FY, Liu LZ, Sun Y, Tian L, TangLL, Lin AH, Li L, Ma J. The seventh edition of UICC/AJCC staging system for nasopharyngeal carcinoma is prognostically useful for patients treated with intensity modulated radiotherapy from an endemic area in China. Radiother Oncol. 2012;104:331-337.
    [4]
    Lee AW, Tung SY, Chua DT, Ngan RK, Chappell R, Tung R, Siu L, Ng WT, Sze WK, Au GK, Law SC, O?Sullivan B, Yau TK, et al. Randomized trial of radiotherapy plus concurrent-adjuvant chemotherapy vs radiotherapy alone for regionally advanced nasopharyngeal carcinoma. J Natl Cancer Inst. 2010; 102:1188?98.
    [5]
    Fountzilas G, Ciuleanu E, Bobos M, Kalogera-Fountzila A, Eleftheraki AG, Karayannopoulou G, et al. Induction chemotherapy followed by concomitant radiotherapy and weekly cisplatin versus the same concomitant chemoradiotherapy in patients with nasopharyngeal carcinoma: a randomized phase II study conducted by the Hellenic Cooperative Oncology Group (HeCOG) with biomarker evaluation. Ann Oncol. 2012; 23:427?35.
    [6]
    Huang PY, Cao KJ, Guo X, Mo HY, Guo L, Xiang YQ, et al. A randomized trial of induction chemotherapy plus concurrent chemoradiotherapy versus induction chemotherapy plus radiotherapy for locoregionally advanced nasopharyngeal carcinoma. Oral Oncol. 2012; 48:1038?44.
    [7]
    Baujat B, Audry H, Bourhis J, Chan AT, Onat H, ChuaDT, Kwong DL, Al-Sarraf M, Chi KH, HareyamaM,Leung SF, Thephamongkhol K, Pignon JP, and MAC-NPC Collaborative Group. Chemotherapy in locally advanced nasopharyngeal carcinoma: an individual patient data meta analysisof eight randomized trials and 1753 patients. Int J Radiat Oncol Biol Phys. 2006; 64:47?56.
    [8]
    Zhang MX, Li J, Shen GP, Zou X, Xu JJ, Jiang R, et al. Intensity-modulated radiotherapy prolongs the survival of patients with nasopharyngeal carcinoma compared with conventional two-dimensional radiotherapy: A10-year experience with a large cohort and long follow-up. Eur J Cancer. 2015;51: 2587-95.
    [9]
    Lee AW, Sze WM, Au JS, Leung SF, Leung TW, Chua DT, et al. Treatment results for nasopharyngeal carcinoma in the modern era: the Hong Kongexperience. Int J Radiat Oncol Biol Phys. 2005; 61: 1107-16.
    [10]
    Wu F, Wang R, Lu H, Wei B, Feng G, Li G, et al. Concurrent chemoradiotherapy in locoregionally advanced nasopharyngeal carcinoma: treatment outcomes of a prospective, multi centric clinical study. Radiother Oncol. 2014; 112:106?11.
    [11]
    Vallath S, Hynds RE, Succony L, Janes SM, Giangreco A. Targeting EGFR signalling in chronic lung disease: therapeutic challenges and opportunities. Eur Respir J. 2014,44:513?522.
    [12]
    Reddy BK, Lokesh V, Vidyasagar MS, Shenoy K, Babu KG, Shenoy A, et al. Nimotuzumab provides survival benefit to patients with inoperable advanced squamous cell carcinoma of the head and neck: a randomized, open-label, phase IIb, 5-year study in Indian patients. Oral Oncol. 2014; 50:498?505.
    [13]
    Wang SS, Guan ZZ, Xiang YQ, Wang B, Lin TY, Jiang WQ, et al. Significance of EGFR and p-ERK expression in nasopharyngeal carcinoma. Chin J Oncol?2006,28?1??28-31.
    [14]
    Chua DT, Nicholls JM, Sham JS, Au GK. Prognostic value of epidermal growth factor receptor expression in patients with advanced stage nasopharyngeal carcinoma treated with induction chemotherapy and radiotherapy. Int J Radiat Oncol Biol Phys. 2004;59(1):11?20.
    [15]
    Modjtahedi H, Essapen S. Epidermal growth factor receptor inhibitors incancer treatment: advances, challenges and opportunities. Anti-Cancer Drugs. 2009;20(10):851?5.
    [16]
    Crombet T, Osorio M, Cruz T, Roca C, del Castillo R, Mon R, et al. Use of the humanized anti-epidermal growth factor receptor monoclonal antibody h-R3 in combination with radiotherapy in the treatment of locally advanced head and neck cancer patients. J Clin Oncol. 2004; 22:1646-54.
    [17]
    Lo HW, Hsu SC, Ali-Seyed M, Gunduz M, Xia W, Wei Y, et al. Nuclear interaction of EGFR and STAT3 in the activation of the iNOS/NO pathway. Cancer Cell 2005,7:575?589.
    [18]
    Cuneo KC, Nyati MK, Ray D, Lawrence TS. EGFR targeted therapies andradiation: optimizing efficacy by appropriate drug scheduling and patients election. Pharmacol Ther. 2015;154:67-77.
    [19]
    Talavera A, Friemann R, Gomez-Puerta S, Martinez-Fleites C, GarridoG,Rabasa A, Lopez-Requena A, Pupo A, Johansen RF, Sanchez O, et al. Nimotuzumab, an antitumor antibody that targets the epidermal growth factor receptor, blocks ligand binding while permitting the active receptor conformation. Cancer Res. 2009;69(14):5851?9.
    [20]
    Huang XD, Yi JL, Gao L, Xu GZ, Jin J, Yang WZ, Lu TX, Wu SX, Wu RH, Hu WH, Xie WC, Han F, Gao YH, Gao JM, Pan JJ, Chen CB, Lang JY, Li T, Dong Y, Fu, YB, Fan L, Li BS, Li J, Wang XH, Chen BX, Gao XS, Zhang P, Wu XW, Hu BQ. Multi-center phase 2 clinical trial of humanized anti-epidernal fator receptor monoclonal antibody h-R3 combined with radiotherapy for locoregionally advanced nasopharyngeal carcinoma . Chin J Oncol?2007, 29?3??197-200.
    [21]
    HM Li, P Li, YJ Qian, et al. A retrospective paired study: efficacy andtoxicity of nimotuzumab versus cisplatinconcurrent with radiotherapy innasopharyngeal carcinoma. BMC Cancer (2016) 16:946.
    [22]
    F Wang, C Jiang, Z Ye, Q Sun, T Liu, M Xu, et al. Efficacy and safety of nimotuzumab with neoadjuvant chemotherapy followed by concurrent chemoradiotherapy for locoregionally advanced nasopharyngeal carcinoma. Oncotarget, 2017, 8: 75544-75556.
    [23]
    R You, YJ Hua, YP Liu, et al. Concurrent Chemoradiotherapy with or without Anti-EGFR-Targeted Treatment for Stage II-IVb Nasopharyngeal Carcinoma: Retrospective Analysis with a Large Cohort and Long Follow-up. Theranostics 2017, 7:2314-2324.
    [24]
    R Zhai, H Ying, F Kong, et al. Experience with combination of nimotuzumab and intensity-modulated radiotherapy in patients with locoregionally advanced nasopharyngeal carcinoma. Onco Targets and Therapy 2015:8 3383?3390.
    [25]
    F Wang, C Jiang, Z Ye, T Liu, F Yan, L Wang, et al. Long-Term Use of Nimotuzumab in Combination with Intensity-Modulated Radiotherapy and Chemotherapy in the Treatment of Locoregionally Advanced Nasopharyngeal Carcinoma: Experience of a Single Institution. Onco Res, 2017, 26:277-287.
    [26]
    Z Li, Y Li,S Yan, J Fu, Q Zhou, X Huang, et al. Nimotuzumab combined with concurrent chemoradiotherapy benefits patients with advanced nasopharyngeal carcinoma. OncoTargets and Therapy 2017:10 5445?5458.
    [27]
    WMA, World Medical Association. Declaration of Helsinki. J Am Med Assoc. 2013;227:925?26.
  • Open Access Mini Review
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    Trends Journal of Sciences Research 2018, 3(2), 75-81. http://doi.org/10.31586/Nursing.0302.03
    47 Views 28 Downloads PDF Full-text (2.583 MB)  HTML Full-text
    Abstract
    Genotype and lifestyle factors have been implicated as the causes of non-communicable diseases including diabetes, cardiovascular diseases, cancer and chronic respiratory disease. Lifestyle factors constitute physical activity, smoking, alcohol intake and dietary habits. These factors alongside genetic factors have been studied over the past years on their relationships with non-communicable
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    Genotype and lifestyle factors have been implicated as the causes of non-communicable diseases including diabetes, cardiovascular diseases, cancer and chronic respiratory disease. Lifestyle factors constitute physical activity, smoking, alcohol intake and dietary habits. These factors alongside genetic factors have been studied over the past years on their relationships with non-communicable diseases. This review examined and compared the strengths of the two factors, lifestyle and genotype, in causing non-communicable diseases. A search was done online, predominantly with PubMed, to identify articles that contained the keywords, lifestyle, diet, exercise, genotype, gene, non-communicable diseases, cardiovascular diseases, cancer, chronic respiratory disease, diabetes. For diabetes, the results of this review showed that management of lifestyle factors can be used to prevent type 2 diabetes among genetically predisposed persons. Cancers studies have suggested that a Mediterranean diet is associated with lower cancer risk for both genetically susceptible people and non-susceptible individuals. Similar findings were gotten for cardiovascular diseases and chronic respiratory diseases. The results suggest a strong impact of lifestyle-related factors as a cause of non-communicable diseases though genetic factors cannot be underestimated. With good management of lifestyle factors, non-communicable diseases can be prevented and the risks reduced even among genetically high-risk individuals.  Full article
    References
    [1]
    World Health Organisation, Global action plan for the prevention and control of non-communicable diseases 2013-2020. Available at: who.int/iris/bitstream/10665/94384/1/9789241506236_eng.pdf. 2013. Accessed March 22, 2017.
    [2]
    Melaku YA, Temesgen AM, Deribew A, Tessema GA, Deribe K, Sahle BW, et al. The impact of dietary risk factors on the burden of non-communicable diseases in Ethiopia: findings from the Global Burden of Disease study 2013. International Journal of Behavioral Nutrition and Physical Activity 13 (2016) 122-134.
    [3]
    Hosseini-Esfahani F, Mirmiran P, Daneshpour MS, Mottaghi A, Aziz F. The effect of interactions of Single Nucleotide Polymorphisms of APOA1/APOC3 with food group intakes on the risk of metabolic syndrome. Avicenna J Med Biotech 9 (2017) 94-103.
    [4]
    Chikwere P, Annan RA. Dietary habit and other lifestyles and serum lipid profile of type 2 diabetes patients: a systematic review. Nutrition & Food Science 46 (2016) 161-170.
    [5]
    Chikwere P, Nsiah K, Tandoh MA. Relation of unsupported and unsupervised exercise with anthropometric and biochemical indices among type 2 diabetic patients. Turk J Med Sci 47 (2017) 85-90.
    [6]
    Naicker A, Venter CS, MacIntyre, UE, Ellis S. Dietary quality and patterns and non-communicable disease risk of an Indian community in KwaZulu-Natal. South Africa Journal of Health, Population and Nutrition 33 (2015) 12-20.
    [7]
    Chikwere P, Nsiah K, Tandoh MA, Agyenim-Boateng K. The relation of dietary pattern to serum lipid profile and uric acid among type 2 diabetes patients. J. Nutr. Ecol. Food Res 2 (2014) 207-213.
    [8]
    Neel JV. Diabetes mellitus: a ??thrifty?? genotype rendered detrimental by ??progress??? Am J Hum Genet 14 (1962) 353-362.
    [9]
    Langenberg C, Sharp S, Forouhi NG, Franks P, Schulze MB, Kerrison N, et al. The InterAct Project: An Examination of the Interaction of Genetic and Lifestyle Factors on the Incidence of Type 2 Diabetes in the EPIC Study. Diabetologia 54 (2011) 2272-2282.
    [10]
    Langenberg C, Sharp SJ, Franks PW, Scott RA, Deloukas P, Forouhi NG, et al. Gene-lifestyle interaction and type 2 diabetes: The EPIC InterAct case-cohort study. PLoS Med 11 (2014) e1001647.
    [11]
    Walker CG, Solis-Trapala I, Holzapfe C, Ambrosini GL, Fuller NR, Loos RJF, et al. Modelling the interplay between lifestyle factors and genetic predisposition on markers of type2 diabetes mellitus risk. PLoS ONE 10 (2015) e0131681.
    [12]
    Phillips CM. Nutrigenetics and metabolic disease: current status and implications for personalised nutrition. Nutrients 5 (2013) 32-57.
    [13]
    Hivert M, Jablonski KA, Perreault, L. Updated genetic score based on 34 con?rmed type 2 diabetes loci is associated with diabetes incidence and regression to normoglycemia in the diabetes prevention program. Diabetes 60 (2011) 1340-1348.
    [14]
    Chikwere P. Functional foods and nutraceuticals, wonders in cancer risks - a review. World Scientific News 64 (2017) 18-33.
    [15]
    Buckland G, Agudo A, Luj?n L, Jakszyn P, Bueno-de-Mesquita H, Palli D, et al. Adherence to a Mediterranean diet and risk of gastric adenocarcinoma within the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort study. Am J Clin Nutr 91 (2010) 381-390.
    [16]
    Ib??ez-Sanz G, D?ez-Villanueva A, Henar Alonso M, Rodr?guez-Moranta F, P?rez-G?mez B, Bustamante M, et al. Risk Model for Colorectal Cancer in Spanish Population Using Environmental and Genetic Factors: Results from the MCC-Spain study. Scientific Reports 7 (2017) 43263.
    [17]
    Stein B, Anderson JC, Rajapakse R, Alpern ZA, Messina CR, Walker G. Body mass index as a predictor of colorectal neoplasia in ethnically diverse screening population. Dig Dis Sci 55 (2010) 2945-2952.
    [18]
    Abul? A, Fern?ndez-Rozadilla C, Alonso-Espinaco V, Mu?oz J, Gonzalo V, Bessa X, et al. Case-control study for colorectal cancer genetic susceptibility in EPICOLON: previously identified variants and mucins. BMC Cancer 11 (2011) 339-346.
    [19]
    Huo D, Zheng Y, Ogundiran TO, Adebamowo C, Nathanson KL, Domchek SM, et al. Evaluation of 19 susceptibility loci of breast cancer in women of African ancestry. Carcinogenesis 33 (2012) 835?840.
    [20]
    Ko K-P, Kim S-W, Ma SH, Park B, Ahn Y, Lee JW, et al. Dietary intake and breast cancer among carriers and noncarriers of BRCA mutations in the Korean Hereditary Breast Cancer Study. Am J Clin Nutr 98 (2013) 1493-1501.
    [21]
    Toledo E, Salas-Salvad? J, Donat-Vargas C, Buil-Cosiales P, Estruch R, Ros E, et al. Mediterranean Diet and Invasive Breast Cancer Risk Among Women at High Cardiovascular Risk in the PREDIMED Trial: A Randomized Clinical Trial. JAMA Intern Med 175 (2015) 1752-1760.
    [22]
    Sanchez NF, Stierman B, Saab S, Mahajan D, Yeung H, Francois F. Physical activity reduces risk for polyps in a multiethnic colorectal cancer screening population. BMC Research Notes 5 (2012) 312-319.
    [23]
    Folkersen L, van?t Hooft F, Chernogubova E, Agardh HE, Hansson GK, Hedin U. Association of genetic risk variants with expression of proximal genes identifies novel susceptibility genes for cardiovascular disease. Circ Cardiovasc Genet 3 (2010) 365-373.
    [24]
    Sotos-Prieto M, Baylin A, Campos H, Qi L, Mattei J. Lifestyle Cardiovascular Risk Score, Genetic Risk Score, and Myocardial Infarction in Hispanic/Latino Adults Living in Costa Rica. J Am Heart Assoc 5 (2016) e004067.
    [25]
    Corella D, Asensio EM, Coltell O, Sorl?, J. V., Estruch, R., Martinez-Gonz?lez, M.A, et al. CLOCK gene variation is associated with incidence of type 2 diabetes and cardiovascular diseases in type 2 diabetic subjects: dietary modulation in the PREDIMED randomized trial. Cardiovascular Diabetology 15 (2016) 4-15.
    [26]
    Garg V, Muth AN, Ransom JF, Schluterman MK, Barnes R, King IN, et al. Mutation in NOTCH1 cause aortic valve disease. Nature 437 (2005) 270-274.
    [27]
    Khera AV, Emdin CA, Drake I. Genetic risk, adherence to a healthy lifestyle, and coronary disease. N Engl J Med 375 (2016) 2349-2358.
    [28]
    Micha R, Pe?alvo JL, Cudhea F, Imamura F, Rehm CD, Mozaffarian D. Association between dietary factors and mortality from heart disease, stroke, and type 2 diabetes in the United States. JAMA 317 (2017) 912-924.
    [29]
    Estruch R, Ros E, Salas-Salvad? J. Primary Prevention of Cardiovascular Disease with a Mediterranean Diet. N Engl J Med 368 (2013) 1279-1290.
    [30]
    McKeever TM, Lewis SA, Cassano PA, Ock? M, Burney P, Britton J, Smit HA, et al. Patterns of dietary intake and relation to respiratory disease, forced expiratory volume in 1 s, and decline in 5-y forced expiratory volume. Am J Clin Nutr 92 (2010) 408-415.
    [31]
    Powell R, Davidson D, Divers J, Manichaikul A, Jeffrey Carr J, Detrano R, et al. Genetic ancestry and the relationship of cigarette smoking to lung function and per cent emphysema in four race/ethnic groups: a cross-sectional study. Thorax 68 (2013) 634-642.
    [32]
    Sorli-Aguilar M, Martin-Lujan F, Flores-Mateo G, Arija-Val V, Basora-Gallisa J, Sola-Alberich R. Dietary patterns are associated with lung function among Spanish smokers without respiratory disease. BMC Pulmonary Medicine 16 (2016) 162-173.
    [33]
    Sabater-Lleal M, M?larstig A, Folkersen L, Artigas MS, Baldassarre D, Kavousi M, Almgren P, et al. Common Genetic Determinants of Lung Function, Subclinical Atherosclerosis and Risk of Coronary Artery Disease. PLoS ONE 9 (2014) e104082.
  • Open Access Mini Review
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    Trends Journal of Sciences Research 2014, 1(1), 26-27. http://doi.org/10.31586/Radiotherapy.0101.04
    1 Views 173 Downloads PDF Full-text (280.622 KB)  HTML Full-text
    Abstract
    Dose calculations based on Monte Carlo (MC) often require sophisticated treatment planning stations with long processing time, and this could be issue for many cancer centers. Hence, most of the commercial treatment planning system include faster dose calculation engines for the daily clinical routine. Due to advancement in technology and
    [...] Read more.
    Dose calculations based on Monte Carlo (MC) often require sophisticated treatment planning stations with long processing time, and this could be issue for many cancer centers. Hence, most of the commercial treatment planning system include faster dose calculation engines for the daily clinical routine. Due to advancement in technology and computing power, it is now possible to implement MC based dose calculation algorithms in the clinical environment. This report summarizes the major findings of various researchers who have investigated Acuros XB algorithm, which is the MC based dose calculation algorithm commercially available for dose calculations in radiotherapy.  Full article
    References
    [1]
    Lu L. Dose calculation algorithms in external beam photon radiation therapy. Int J Cancer Ther Oncol 2013; 1(2):01025.
    [2]
    Han T, Followill D, Mikell J, Repchak R, Molineu A, Howell R, Salehpour M, Mourtada F. Dosimetric impact of Acuros XB deterministic radiation transport algorithm for heterogeneous dose calculation in lung cancer. Med Phys. 2013; 40(5):051710.
    [3]
    Kan MW, Leung LH, So RW, Yu PK. Experimental verification of the Acuros XB and AAA dose calculation adjacent to heterogeneous media for IMRT and RapidArc of nasopharygeal carcinoma. Med Phys. 2013 Mar; 40 (3): 031714.
    [4]
    Stathakis S, Esquivel C, Quino L, Myers P, Calvo O, Mavroidis P, Guti?rrez A and Papanikolaou P. Accuracy of the Small Field Dosimetry Using the Acuros XB Dose Calculation Algorithm within and beyond Heterogeneous Media for 6 MV Photon Beams. Int Jour of Med Phys Clin Eng Radiat Onc 2012; 1 (3): 78-87.
    [5]
    Ojala JJ, Kapanen MK, Hy?dynmaa SJ, Wigren TK, Pitk?nen MA. Performance of dose calculation algorithms from three generations in lung SBRT: comparison with full Monte Carlo-based dose distributions. J Appl Clin Med Phys. 2014; 15(2):4662.
    [6]
    Kroon PS, Hol S, Essers M. Dosimetric accuracy and clinical quality of Acuros XB and AAA dose calculation algorithm for stereotactic and conventional lung volumetric modulated arc therapy plans. Radiat Oncol. 2013; 8(1):149.
    [7]
    Kathirvel M, Subramanian S, Clivio A, et al. Critical appraisal of the accuracy of Acuros-XB and Anisotropic Analytical Algorithm compared to measurement and calculations with the compass system in the delivery of RapidArc clinical plans. Radiat Oncol 2013; 8:140.
    [8]
    Liu HW, Nugent Z, Clayton R, Dunscombe P, Lau H, Khan R. Clinical impact of using the deterministic patient dose calculation algorithm Acuros XB for lung stereotactic body radiation therapy. Acta Oncol. 2013 Aug 19. [Epub ahead of print]
    [9]
    Fogliata A, Nicolini G, Clivio A, Vanetti E, Cozzi L. Critical appraisal of Acuros XB and Anisotropic Analytic Algorithm dose calculation in advanced non-small-cell lung cancer treatments. Int J Radiat Oncol Biol Phys. 2012; 83(5):1587-95.
    [10]
    Rana S. Clinical dosimetric impact of Acuros XB and analytical anisotropic algorithm (AAA) on real lung cancer treatment plans: review. Int J Cancer Ther Oncol 2014; 2(1):02019.
    [11]
    Ojala J. The accuracy of the Acuros XB algorithm in external beam radiotherapy ? a comprehensive review. Int J Cancer Ther Oncol 2014; 2(4):020417.
    [12]
    Chetty IJ, Curran B, Cygler JE, et al. Report of the AAPM Task Group 105: Issues associated with clinical implementation of Monte Carlo-based photon and electron external beam treatment planning. Med Phys. 2007; 34(12):4818?53.
  • Open Access Research Article
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    Trends Journal of Sciences Research 2015, 2(4), 134-140. http://doi.org/10.31586/Biology.0204.04
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    Abstract
    Methionine, a sulfur amino acid, is the first amino acid that is required for many proteins, during synthesis. Our preliminary studies showed that this compound was produced during the late (post-stationary) secondary phase of growth. Therefore, restriction of methionine may be a useful strategy in limiting cancer growth. The bacterial
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    Methionine, a sulfur amino acid, is the first amino acid that is required for many proteins, during synthesis. Our preliminary studies showed that this compound was produced during the late (post-stationary) secondary phase of growth. Therefore, restriction of methionine may be a useful strategy in limiting cancer growth. The bacterial strain used in this study was Citrobacter freundii (NRRL B-2643) and their vgb+ recombinant strain. A 1/100 inoculum of overnight cultures grown in LB was made in 50 ml LB in 150 ml Erlenmeyer flasks. Inocula in flasks were grown for 24 h at 30 ?C in a 200 rpm water-bath. For MGL production, 250 ?L of this O/N culture was then inoculated into 150 mL conical flask containing 50 mL of sterile mineral salts medium supplemented with 1 % or 0.1 % (w/v) glucose, respectively. This was incubated for 96 h at 30 ?C, 200 rpm on an orbital shaker. The highest MGL concentration (2,02) was reached by the recombinant strain of Cf[pUC8:15] 72 h after the start of incubation MM+0,1% glucose source. In comparison, the wild type strain produced 3,14 of MGL concentration 72 h was reached MM+0,1% glucose source. The poor media and secondary phase (72 h and up) was used to for MGL production. This is more appropriate. Plasmid is disadvantages in the secondary stage.  Full article
    Figures

    Figure 1 of 5

    References
    [1]
    Cavuoto P, Fenech M.F. (2012). A review of methionine dependency and the role of methionine restriction in cancer growth control and life-span extension. Cancer Treatment Rev. 38, 726-736.
    [2]
    Sato D, Nozaki T. (2009). Methionine Gamma-Lyase: The unique reaction mechanism, physiological roles, and therapeutic applications against infectious diseases and cancers. IUBMB Life. 61(11), 1019-1028.
    [3]
    Kudou D, Misaki S, Yamashita M, Tamura T, Esaki N, Inagaki K. (2008). The role of cysteine 116 in the active site of the antitumor enzyme L-methionine ?-lyase from Pseudomonas putida. Biosci Biotechnol Biochem. 72(7), 1722- 1730.
    [4]
    Morozova E.A., Kulikova V.V., Yashin D.V., Anufrieva N.V., Anisimova N.Y., Revtovich S.V., Kotlov M.I., Belyi Y.F., Pokrovsky V.S., Demidkina T.V. (2013). Kinetic Parameters and cytotoxic activity of recombinant methionine ?-lyase from Clostridium tetani, Clostridium sporogenes, Porphyromonas gingivalis and Citrobacter freundii. Acta Naturae. 5(3), 92-98.
    [5]
    Lua S, Chena G.L., Rena C, Kwabi-Addob B, Epner D.E. (2003). Methionine restriction selectively targets thymidylate synthase in prostate cancer cells. Biochem Pharm. 66, 791-800.
    [6]
    Saa L, Mato J.M., Pavlov V. (2012). Assays for methionine ?- lyase and S-adenosyl-L-homocysteine hydrolase based on enzymatic formation of CdS quantum dots in situ. Anal Chem, 84, 8961-8965.
    [7]
    Revtovich S.V., Morozova E.A., Khurs E.N., Zakomirdina L.N., Nikulin A.D., Demidkina T.V., Khomutov R.M. (2011). Three dimensional structures of noncovalent complexes of Citrobacter freundii methionine ?-lyase with substrates. Biochemistry, 76(5), 564-570.
    [8]
    Benavide M.A., Oelschlager D.K., Zhang H.G., Stockard C.R., Vital-Reyes V.S., Katkoori V.R., Manne U, Wang W, Bland K.I., Grizzle W.E. (2007). Methionine inhibits cellular growth dependent on the p53 status of cells. Am J Surgery. 193, 274- 283.
    [9]
    Li H, Huang Y, Zhang J, Du J, Tan H, Lu Y., Zhou, S. (2011). Identification and characterization of a novel methionine ?-lyase gene from deep-sea sediment metagenomic library. World J Microbiol Biotechnol. 27, 2729-2736.
    [10]
    Morozova E.A., Bazhulina N.P., Anufrieva N.V., Mamaeva D.V., Tkachev Y.V., Streltsov S.A., Timofeev V.P., Faleev N.G., Demidkina T.V. (2010). Kinetic and spectral parameters of interaction of Citrobacter freundii methionine ?-lyase with amino acids. Biochemistry. 7(10), 1272-1280.
    [11]
    Ronda L, Bazhulina N.P., Morozova E.A., Revtovich S.V., Chekhov V.O., Nikulin A.D., Demidkina T.V., Mozzarelli A. (2011). Exploring methionine ?-lyase structure-function relationship via microspectrophotometry and X-ray crystallography. Biochim Biophys Acta. 1814, 834-842.
    [12]
    Surowsky B, Fr?hling A, Gottschalk N, Schl?ter O, Knorr D. (2014). Impact of cold plasma on Citrobacter freundii in apple juice: Inactivation kinetics and mechanisms. Int J Food Microbiol. 174, 63-71.
    [13]
    Wanga Z, Xiao Y, Chen W, Tang K, Zhang L. (2009). Functional expression of Vitreoscilla hemoglobin (VHb) in Arabidopsis relieves submergence, nitrosative, photo-oxidative stress and enhances antioxidants metabolism. Plant Science. 176, 66-77.
    [14]
    Soda K. (1968). Microdetermination of D-amino acids and D- amino acid oxidase activity with 3-methyl-2-benzothiazolone hydrazone hydrochloride. Anal Biochem. 25, 228-235.
    [15]
    Tanaka H, Imahara H, Esaki N, Soda K. (1980). Selective determination of L-methionine and L-cysteine with bacterial L-methionine ?-lyase and anti-tumor activity of the enzyme. J Appl Biochem. 2, 439-444.
    [16]
    Kahraman H, Erenler S.O. (2012). Rhamnolipid production by Pseudomonas aeruginosa engineered with the Vitreoscilla hemoglobin gene. Appl Biochem Microbiol. 48(2), 188-193.
    [17]
    Pavillard V, Nicolaou A, Double J.A., Phillips R.M. (2006). Methionine dependence of tumours: A biochemical strategy for optimizing paclitaxel chemosensitivity in vitro. Biochem Pharma. 71, 772-778.
  • Open Access Case Report
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    Trends Journal of Sciences Research 2018, 3(3), 144-146. http://doi.org/10.31586/Surgery.0303.07
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    Abstract
    Central vein stenosis is a rare complication that occurs after central venous port placement. We report a case of chyle withdrawal from a central venous port in a patient receiving chemotherapy for stage IV rectal cancer. Dilated thoracic duct terminal and innominate vein stenosis both were clearly shown in the
    [...] Read more.
    Central vein stenosis is a rare complication that occurs after central venous port placement. We report a case of chyle withdrawal from a central venous port in a patient receiving chemotherapy for stage IV rectal cancer. Dilated thoracic duct terminal and innominate vein stenosis both were clearly shown in the angiography results, and innominate vein stenosis was resolved by performing percutaneous transluminal angioplasty.  Full article
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    References
    [1]
    Kao CL, Chang JP. Chyle withdrawal from an implanted port in occult innominate vein stenosis. 2001;78:138-40.
    [2]
    Yildizeli B, Laçin T, Batirel HF, Yüksel M. Complications and management of long-term central venous access catheters and ports. 2004;5:174-178.
    [3]
    Lemmers NW1, Gels ME, Sleijfer DT et al. Complications of venous access ports in 132 patients with disseminated testicular cancer treated with polychemotherapy. J Clin Oncol 1996;14:2916-2922.
    [4]
    Van Veldhuizen PJ, Taylor S. Chylothorax: a complication of a left subclavian vein thrombosis. 1996;19:99-101.
    [5]
    Kurekci E, Kaye R, Koehler M. Chylothorax and chylopericardium with a complication of a central venous catheter. 1998;132:1064-1066.
    [6]
    Wadehra D. Central Vein Stenosis. In: Yevzlin AS, Asif A, Salman L, eds. . Springer New York; 2014:131-142.
    [7]
    Song MG, Seo TS, Kang EY, Yong HS, Seo JH, Choi YY. Innominate vein stenosis in breast cancer patients after totally implantable venous access port placement. 2015;16:315-320. doi: 10.5301/jva.5000387.
    [8]
    Puel V, Caudry M, Le Métayer P et al. Superior vena cava thrombosis related to catheter malposition in cancer chemotherapy given through implanted ports. 1993;72:2248-2252.
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