Pub Date : 2018-01-01DOI: 10.4172/2329-6917.1000251
H. Ahmed, S. Aziz, Abeera Hassan
Angiopoietins and TIE2 are necessary for blood and lymphatic vessel remodeling during embryonic, postnatal development and homeostasis of the mature vasculature and expected to be a valuable marker in acute leukemia. The present study aimed to assess the expression of TIE2 and angiopoietin-2 in acute leukemia and its correlation with disease behaviour. The study included 62 patients and 19 sex- and age-matched healthy controls, divided into 2 groups, 21 Acute Lymphoblastic Leukaemia (ALL) patients, and 41 Acute Myeloid Leukaemia (AML) patients and 19 sex- and age-matched healthy controls. Bone marrow (BM) aspirate examination, Immunophenotyping and assessment of TIE2 expression for peripheral or BM samples by Flow cytometer and serum angiopoietin-2 by using enzyme-linked immunosorbent assay. The study results showed that TIE2 & Angiopoietin2 were expressed in AML patients more than ALL patients. In ALL patients CD45 and CD5 showed statistically significant correlation with TIE2 but CD45, CD14 showed statistical significance correlation with Angiopoietin2 in AML patients. CD33 was correlated with TIE2 and Angiopoietin2 in AML patients. ROC curve for TIE2 in ALL Cut off >3.8 AUC 0.977 with Sensitivity 90.5% & Specificity 94.7% P-value941 AUC 0.753 with Sensitivity 71.4% & Specificity 78.9% P-value0.002 While in AML TIE2 Cut off>4.8 AUC 0.997 with Sensitivity 95.1% & Specificity 100% P-value1838 AUC 0.871 with Sensitivity 60.9% & Specificity100% P-value <0.001. Univariate logistic regression Analysis of leukemic patients showed that Angiopoietin2, TIE2, WBCs count, Platelets count were Statistically Significant. The present study concluded that TIE2 and angiopoietin-2 positive expression are independent prognostic factor in adult acute leukemia and its expression could characterize a group of acute leukemic patients with monocytic lineage.
{"title":"Correlation of Tie2 in Acute Leukemia with Disease Behaviour and Lineage Selection","authors":"H. Ahmed, S. Aziz, Abeera Hassan","doi":"10.4172/2329-6917.1000251","DOIUrl":"https://doi.org/10.4172/2329-6917.1000251","url":null,"abstract":"Angiopoietins and TIE2 are necessary for blood and lymphatic vessel remodeling during embryonic, postnatal development and homeostasis of the mature vasculature and expected to be a valuable marker in acute leukemia. The present study aimed to assess the expression of TIE2 and angiopoietin-2 in acute leukemia and its correlation with disease behaviour. The study included 62 patients and 19 sex- and age-matched healthy controls, divided into 2 groups, 21 Acute Lymphoblastic Leukaemia (ALL) patients, and 41 Acute Myeloid Leukaemia (AML) patients and 19 sex- and age-matched healthy controls. Bone marrow (BM) aspirate examination, Immunophenotyping and assessment of TIE2 expression for peripheral or BM samples by Flow cytometer and serum angiopoietin-2 by using enzyme-linked immunosorbent assay. The study results showed that TIE2 & Angiopoietin2 were expressed in AML patients more than ALL patients. In ALL patients CD45 and CD5 showed statistically significant correlation with TIE2 but CD45, CD14 showed statistical significance correlation with Angiopoietin2 in AML patients. CD33 was correlated with TIE2 and Angiopoietin2 in AML patients. ROC curve for TIE2 in ALL Cut off >3.8 AUC 0.977 with Sensitivity 90.5% & Specificity 94.7% P-value941 AUC 0.753 with Sensitivity 71.4% & Specificity 78.9% P-value0.002 While in AML TIE2 Cut off>4.8 AUC 0.997 with Sensitivity 95.1% & Specificity 100% P-value1838 AUC 0.871 with Sensitivity 60.9% & Specificity100% P-value <0.001. Univariate logistic regression Analysis of leukemic patients showed that Angiopoietin2, TIE2, WBCs count, Platelets count were Statistically Significant. The present study concluded that TIE2 and angiopoietin-2 positive expression are independent prognostic factor in adult acute leukemia and its expression could characterize a group of acute leukemic patients with monocytic lineage.","PeriodicalId":90223,"journal":{"name":"Journal of leukemia (Los Angeles, Calif.)","volume":"06 1","pages":"1-6"},"PeriodicalIF":0.0,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70269710","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2018-01-01DOI: 10.4172/2329-6917.1000249
N. El-Attar, Azaa mohyiAssal, Mohamed E. Amin, Rowida M.S. Sleem
Objective: To evaluate role of P-selectin as a marker of platelets activation in coronary slow flow patients Patients: A case control study, where seventy two patients underwent cardiac catheterization for suspected coronary artery disease. There were divided into patients group (primary coronary slow flow patients) and control group (normal coronary angiography). Methods: All patients were subjected to history, physical examination and laboratory investigation included CBC serum glucose, lipid profile and immune phenotyping of platelets activation (p selectin CD 62p by flow cytometery). Results: We have two groups: Group1 (patients group): Patients with primary coronary slow flow phenomenon=36 patients. Mean age of cases 49.33 ± 4.99 years with range of (34-55) years. In patients group there was 24 male and 12 female. Group II (control group): Patients with normal coronary angiography=36 patients. Mean age in control group 51.44 ± 3.36 years with range of (43-55) years. Conclusion: The results of the present study revealed that there is very high statistically significant difference in P-selectin level between group 1 (primary coronary slow flow patients) and group 2 (normal coronary angio patients) and there is statistically significant association between P-selectin and TIMI frame count in coronary slow flow.
{"title":"Role of P-Selectin In Patients with Slow Coronary Flow.","authors":"N. El-Attar, Azaa mohyiAssal, Mohamed E. Amin, Rowida M.S. Sleem","doi":"10.4172/2329-6917.1000249","DOIUrl":"https://doi.org/10.4172/2329-6917.1000249","url":null,"abstract":"Objective: To evaluate role of P-selectin as a marker of platelets activation in coronary slow flow patients Patients: A case control study, where seventy two patients underwent cardiac catheterization for suspected coronary artery disease. There were divided into patients group (primary coronary slow flow patients) and control group (normal coronary angiography). Methods: All patients were subjected to history, physical examination and laboratory investigation included CBC serum glucose, lipid profile and immune phenotyping of platelets activation (p selectin CD 62p by flow cytometery). Results: We have two groups: Group1 (patients group): Patients with primary coronary slow flow phenomenon=36 patients. Mean age of cases 49.33 ± 4.99 years with range of (34-55) years. In patients group there was 24 male and 12 female. Group II (control group): Patients with normal coronary angiography=36 patients. Mean age in control group 51.44 ± 3.36 years with range of (43-55) years. Conclusion: The results of the present study revealed that there is very high statistically significant difference in P-selectin level between group 1 (primary coronary slow flow patients) and group 2 (normal coronary angio patients) and there is statistically significant association between P-selectin and TIMI frame count in coronary slow flow.","PeriodicalId":90223,"journal":{"name":"Journal of leukemia (Los Angeles, Calif.)","volume":"06 1","pages":"1-6"},"PeriodicalIF":0.0,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70269640","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2018-01-01DOI: 10.4172/2329-6917.1000250
M. Yilmaz, S. S. Durusoy, Alperen Kizikli, M. Yeral, I. Kozanoglu, Salih Subari, A. Ablyev, S. Cangi
{"title":"Association of Chronic Lymphocytic leukemia and Acute Myeloid leukemai in three patients","authors":"M. Yilmaz, S. S. Durusoy, Alperen Kizikli, M. Yeral, I. Kozanoglu, Salih Subari, A. Ablyev, S. Cangi","doi":"10.4172/2329-6917.1000250","DOIUrl":"https://doi.org/10.4172/2329-6917.1000250","url":null,"abstract":"","PeriodicalId":90223,"journal":{"name":"Journal of leukemia (Los Angeles, Calif.)","volume":"36 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70269659","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2018-01-01DOI: 10.4172/2329-6917.1000245
Maha Saad Almenshawy, I. Ibrahim, N. Khalifa, Gamal Zakaria Al-Mursy
Objectives: Assessment of angiogenic activity through evaluation of Vascular endothelial growth factor concentration and determination of endothelial cells percentage in the peripheral blood of patients with Chronic myeloid leukemia compared to healthy subjects in order to investigate their role in the pathogenesis and for early detection of the disease progression.Subjects and Methods: Twenty patients with Chronic myeloid leukemia and 15 healthy controls were studied. Evaluation of Vascular endothelial growth factor level in serum was measured by enzyme-linked immunosorbent assay. Determination of circulating endothelial cells percentage expressing CD133 and/or CD34 by flow cytometry in the peripheral blood was also done.Results: The level of Vascular endothelial growth factor was significantly elevated in all groups when compared to controls (p=<0.001). A significant increase of endothelial cells was observed in Chronic myeloid leukemia patients with blast crisis phase compared to other phases (p=<0.001). In patients with chronic phase and accelerated phase the number of endothelial cells was slightly increased compared to the control group but the differences were not statistically significant.Conclusion: The level of Vascular endothelial growth factor was highly elevated in all phases of Chronic myeloid leukemia. While the flow cytometric evaluation of endothelial cell surface markers in the blood of Chronic myeloid leukemia patients can identify a subset of patients with a more aggressive disease course.
{"title":"Angiogenic Activity in Chronic Myeloid Leukemia","authors":"Maha Saad Almenshawy, I. Ibrahim, N. Khalifa, Gamal Zakaria Al-Mursy","doi":"10.4172/2329-6917.1000245","DOIUrl":"https://doi.org/10.4172/2329-6917.1000245","url":null,"abstract":"Objectives: Assessment of angiogenic activity through evaluation of Vascular endothelial growth factor concentration and determination of endothelial cells percentage in the peripheral blood of patients with Chronic myeloid leukemia compared to healthy subjects in order to investigate their role in the pathogenesis and for early detection of the disease progression.Subjects and Methods: Twenty patients with Chronic myeloid leukemia and 15 healthy controls were studied. Evaluation of Vascular endothelial growth factor level in serum was measured by enzyme-linked immunosorbent assay. Determination of circulating endothelial cells percentage expressing CD133 and/or CD34 by flow cytometry in the peripheral blood was also done.Results: The level of Vascular endothelial growth factor was significantly elevated in all groups when compared to controls (p=<0.001). A significant increase of endothelial cells was observed in Chronic myeloid leukemia patients with blast crisis phase compared to other phases (p=<0.001). In patients with chronic phase and accelerated phase the number of endothelial cells was slightly increased compared to the control group but the differences were not statistically significant.Conclusion: The level of Vascular endothelial growth factor was highly elevated in all phases of Chronic myeloid leukemia. While the flow cytometric evaluation of endothelial cell surface markers in the blood of Chronic myeloid leukemia patients can identify a subset of patients with a more aggressive disease course.","PeriodicalId":90223,"journal":{"name":"Journal of leukemia (Los Angeles, Calif.)","volume":"6 1","pages":"1-5"},"PeriodicalIF":0.0,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4172/2329-6917.1000245","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70270096","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2017-10-27DOI: 10.4172/2329-6917-C1-001
E. Glatstein
{"title":"Personal primer on radiation oncology for the non-radiation oncologists","authors":"E. Glatstein","doi":"10.4172/2329-6917-C1-001","DOIUrl":"https://doi.org/10.4172/2329-6917-C1-001","url":null,"abstract":"","PeriodicalId":90223,"journal":{"name":"Journal of leukemia (Los Angeles, Calif.)","volume":"05 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2017-10-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70270497","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2017-10-27DOI: 10.4172/2329-6917-C1-003
J. Maness, Ryan Campbell
{"title":"Awareness of legal needs and rights of patients 18+ in a pediatric setting","authors":"J. Maness, Ryan Campbell","doi":"10.4172/2329-6917-C1-003","DOIUrl":"https://doi.org/10.4172/2329-6917-C1-003","url":null,"abstract":"","PeriodicalId":90223,"journal":{"name":"Journal of leukemia (Los Angeles, Calif.)","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2017-10-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70270584","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2017-09-21DOI: 10.4172/2329-6917.1000240
M. AlvaradoIbarra, M. Zepeda, J. AlvarezVera, M. OrtizZepeda, R. JimenezAlvarado, M. LopezHernandez
Introduction: Chronic myeloid leukemia Ph+ (CML) is a myeloproliferative neoplasm that originates in a pluripotent and abnormal bone marrow cell, consistently associated with the BCR-ABL fusion gene, 1 located on the Ph chromosome, represents 15% of all leukemias. Treatment has evolved along with the disease using alkylators, antimetabolites, immunomodulators, and tyrosine kinase inhibitors (TKI), that have significantly improved patient survival, including ponatinib, effective for the T315I mutation. Objective: To know the overall survival and progression-free survival of TKIs (imatinib, nilotinib and dasatinib) in patients with Ph+ CML treated at the CMN Hematology Service "20 de Noviembre" ISSSTE, in a long-term followup. Patients and Methods: Over 15 years with Ph+ CML from 1999 to 2016 not treated with ITQ and without contraindication to receive them. Those who rejected this treatment were not included. Those who died due to some comorbidity not related to CML, those who switched to progenitor hematopoietic stem cell transplantation, those who refused to continue receiving TKIs or when treatment was suspended for administrative reasons (loss of right to institutional insurance). Results: A total of 82 patients were analyzed. In 37% of the patients, the initial treatment was chemotherapy. Patients who achieved molecular remission had a mean of 5 months before starting TKIs. Imatinib was only used in the first line (n=65), nilotinib was the majority in the second line (n=18) and dasatinib was the only one indicated in the third line (n=8). Molecular remission was profound in 26 patients and greater in 24%. No remission was achieved in four patients. The PFS, recorded from the start of any TKIs, was likely 0.83 to 156 months of follow-up. The OS was 0.92 to 191 months. Conclusions: Imatinib was used in our hospital in 2001. Until then, it was treated with hydroxyurea, busulfan, or cytarabine + IFN. The patients who started receiving TKIs during the first two months, after diagnosis, had OS as well as those who were delayed more than this time. The depth of remission was related to the time at which TKIs administration was started and only reached remission in those who started it within the first six months. We found no significant difference between the three TKIs. Failure to respond was the most frequent condition. The months elapsed waiting for a response was greater than 6 months, which is prolonged, particularly in the case of the passage from first to second line. This delay, in our cases, is related to the lack of second-generation TKIs. More than half had molecular remission, major or profound, with one or more of the inhibitors employed. However, the SG is not affected by the existence of cytogenetic or molecular remission.
{"title":"Long-Term Outcomes of Tyrosine Kinase Inhibitors Treatment for Chronic Myeloid Leukemia","authors":"M. AlvaradoIbarra, M. Zepeda, J. AlvarezVera, M. OrtizZepeda, R. JimenezAlvarado, M. LopezHernandez","doi":"10.4172/2329-6917.1000240","DOIUrl":"https://doi.org/10.4172/2329-6917.1000240","url":null,"abstract":"Introduction: Chronic myeloid leukemia Ph+ (CML) is a myeloproliferative neoplasm that originates in a pluripotent and abnormal bone marrow cell, consistently associated with the BCR-ABL fusion gene, 1 located on the Ph chromosome, represents 15% of all leukemias. Treatment has evolved along with the disease using alkylators, antimetabolites, immunomodulators, and tyrosine kinase inhibitors (TKI), that have significantly improved patient survival, including ponatinib, effective for the T315I mutation. \u0000Objective: To know the overall survival and progression-free survival of TKIs (imatinib, nilotinib and dasatinib) in patients with Ph+ CML treated at the CMN Hematology Service \"20 de Noviembre\" ISSSTE, in a long-term followup. \u0000Patients and Methods: Over 15 years with Ph+ CML from 1999 to 2016 not treated with ITQ and without contraindication to receive them. Those who rejected this treatment were not included. Those who died due to some comorbidity not related to CML, those who switched to progenitor hematopoietic stem cell transplantation, those who refused to continue receiving TKIs or when treatment was suspended for administrative reasons (loss of right to institutional insurance). \u0000Results: A total of 82 patients were analyzed. In 37% of the patients, the initial treatment was chemotherapy. Patients who achieved molecular remission had a mean of 5 months before starting TKIs. Imatinib was only used in the first line (n=65), nilotinib was the majority in the second line (n=18) and dasatinib was the only one indicated in the third line (n=8). Molecular remission was profound in 26 patients and greater in 24%. No remission was achieved in four patients. The PFS, recorded from the start of any TKIs, was likely 0.83 to 156 months of follow-up. The OS was 0.92 to 191 months. \u0000Conclusions: Imatinib was used in our hospital in 2001. Until then, it was treated with hydroxyurea, busulfan, or cytarabine + IFN. The patients who started receiving TKIs during the first two months, after diagnosis, had OS as well as those who were delayed more than this time. The depth of remission was related to the time at which TKIs administration was started and only reached remission in those who started it within the first six months. We found no significant difference between the three TKIs. Failure to respond was the most frequent condition. The months elapsed waiting for a response was greater than 6 months, which is prolonged, particularly in the case of the passage from first to second line. This delay, in our cases, is related to the lack of second-generation TKIs. More than half had molecular remission, major or profound, with one or more of the inhibitors employed. However, the SG is not affected by the existence of cytogenetic or molecular remission.","PeriodicalId":90223,"journal":{"name":"Journal of leukemia (Los Angeles, Calif.)","volume":"2017 1","pages":"1-7"},"PeriodicalIF":0.0,"publicationDate":"2017-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4172/2329-6917.1000240","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43654060","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2017-09-11DOI: 10.4172/2329-6917.1000239
Ayad A, Kababri M, Kili A, Hsissen L, Khattab M
Children with Down syndrome (DS) are at higher risk of developing acute leukemia and has been recognized to have unique clinical features and significant differences in treatment response and toxicity profiles compared to patients without Down syndrome. One of the challenges faced in treating children with Down syndrome and leukemia is balancing curative therapy against potential toxicities. A retrospective review of the clinical features, treatment outcomes of DS children with acute leukemia was conducted in the Center for Pediatric Hematology and Oncology in rabat child hospital.(CHOP) from 2006 to 2016. This review included a total of 30 patients with DS. Ten were diagnosed with acute lymphoblastic leukemia and 20 had acute myeloid leukemia (AML). This study points out that investigators will have to carefully assess the balance between the antileukemic efficacy and treatment-related mortality of current chemotherapy regimens. Several studies are currently in progress that will answer some of the many questions raised in this field.
{"title":"Acute Leukemia in Down Syndrome Children, A Morroccan Retrospective Review","authors":"Ayad A, Kababri M, Kili A, Hsissen L, Khattab M","doi":"10.4172/2329-6917.1000239","DOIUrl":"https://doi.org/10.4172/2329-6917.1000239","url":null,"abstract":"Children with Down syndrome (DS) are at higher risk of developing acute leukemia and has been recognized to have unique clinical features and significant differences in treatment response and toxicity profiles compared to patients without Down syndrome. One of the challenges faced in treating children with Down syndrome and leukemia is balancing curative therapy against potential toxicities. \u0000 \u0000A retrospective review of the clinical features, treatment outcomes of DS children with acute leukemia was conducted in the Center for Pediatric Hematology and Oncology in rabat child hospital.(CHOP) from 2006 to 2016. This review included a total of 30 patients with DS. Ten were diagnosed with acute lymphoblastic leukemia and 20 had acute myeloid leukemia (AML). This study points out that investigators will have to carefully assess the balance between the antileukemic efficacy and treatment-related mortality of current chemotherapy regimens. Several studies are currently in progress that will answer some of the many questions raised in this field.","PeriodicalId":90223,"journal":{"name":"Journal of leukemia (Los Angeles, Calif.)","volume":"2017 1","pages":"1-6"},"PeriodicalIF":0.0,"publicationDate":"2017-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4172/2329-6917.1000239","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41529860","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2017-08-05DOI: 10.4172/2329-6917.1000238
Uzma Nisar, Maria Khan, Shahana Nisar, Shamrez Khan
Primary breast lymphoma (PBL) is a unique clinical finding accounting for 0.4–0.5% of all neoplasms in breast with a painless palpable mass being a most common presentation. On histopathological findings and radiological imaging, Diffuse large B-cell lymphoma (DLBCL) is the most widespread identifiable type of PBL. We report a case who presented with Primary breast lymphoma having multiple metastatic lesions in lymph nodes, muscles and bones.
{"title":"Primary Breast Lymphoma with Unconventional Presentation: A Case Report","authors":"Uzma Nisar, Maria Khan, Shahana Nisar, Shamrez Khan","doi":"10.4172/2329-6917.1000238","DOIUrl":"https://doi.org/10.4172/2329-6917.1000238","url":null,"abstract":"Primary breast lymphoma (PBL) is a unique clinical finding accounting for 0.4–0.5% of all neoplasms in breast with a painless palpable mass being a most common presentation. On histopathological findings and radiological imaging, Diffuse large B-cell lymphoma (DLBCL) is the most widespread identifiable type of PBL. We report a case who presented with Primary breast lymphoma having multiple metastatic lesions in lymph nodes, muscles and bones.","PeriodicalId":90223,"journal":{"name":"Journal of leukemia (Los Angeles, Calif.)","volume":"5 1","pages":"1-3"},"PeriodicalIF":0.0,"publicationDate":"2017-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4172/2329-6917.1000238","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43933571","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2017-06-05DOI: 10.4172/2329-6917.1000235
CQ Duong, KQ Bach
Background: Chronic myeloid leukemia is a clonal myeloproliferative neoplasm, characterized by the presence of chromosomal translocation t(9; 22)(q34; q11). This is found in over 95% of the cases and results in the BCR-ABL1 fusion protein with high tyrosine kinase activity. During the last decades, imatinib and other generations of tyrosine kinase inhibitor have been used effectively for target therapy of the disease. However, many of the drug resistant cases have been reported recently, due to the mutation within kinase domain of the BCR-ABL1 fusion gene. In order to provide further information about this incidence, we performed a retrospective study of 141 imatinib-resistance chronic myeloid leukemia patients to analyze kinase domain mutation by deep sequencing. Another group of 20 untreated patients were added as control. Methods: RNA from bone marrow cells were extracted and followed by cDNA synthesis. Nested polymerase chain reaction was performed to amplify kinase domain of the BCR-ABL1 fusion gene. The amplified products were monitored size, concentration and prepared DNA sequencing library. Sequence analysis was performed using Illumina MiSeq sequencer and Sequence Pilot software. The sequencing results were randomly chose for Sanger sequencing. Results: None of the control group was positive with kinase domain mutation. There were 47 out of 141 patients (33%) detected with at least one nucleotide substitution. The sequencing results were also confirmed by Sanger sequencing. Of those 47 samples, 72 nucleotide substitutions of 28 types, altered 24 codons were identified. Among those, Y253F/H, M351T, G250E, F359V/I and M244V were the most frequent mutations, while T315I took only 4.1%. There were also a number of samples harboring multiple substitutions and new variations. Conclusion: Nextgeneration deep sequencing is a sensitive and effective method to detect kinase domain mutation and our results could provide further information about the drug-resistance mutation in chronic myeloid leukemia.
{"title":"Utilization of Next-Generation Deep Sequencing to Analyze BCR-ABL1 Kinase Domain Mutation for Imatinib-Resistant Chronic Myeloid Leukemia Patients in Vietnam","authors":"CQ Duong, KQ Bach","doi":"10.4172/2329-6917.1000235","DOIUrl":"https://doi.org/10.4172/2329-6917.1000235","url":null,"abstract":"Background: Chronic myeloid leukemia is a clonal myeloproliferative neoplasm, characterized by the presence of chromosomal translocation t(9; 22)(q34; q11). This is found in over 95% of the cases and results in the BCR-ABL1 fusion protein with high tyrosine kinase activity. During the last decades, imatinib and other generations of tyrosine kinase inhibitor have been used effectively for target therapy of the disease. However, many of the drug resistant cases have been reported recently, due to the mutation within kinase domain of the BCR-ABL1 fusion gene. In order to provide further information about this incidence, we performed a retrospective study of 141 imatinib-resistance chronic myeloid leukemia patients to analyze kinase domain mutation by deep sequencing. Another group of 20 untreated patients were added as control. Methods: RNA from bone marrow cells were extracted and followed by cDNA synthesis. Nested polymerase chain reaction was performed to amplify kinase domain of the BCR-ABL1 fusion gene. The amplified products were monitored size, concentration and prepared DNA sequencing library. Sequence analysis was performed using Illumina MiSeq sequencer and Sequence Pilot software. The sequencing results were randomly chose for Sanger sequencing. Results: None of the control group was positive with kinase domain mutation. There were 47 out of 141 patients (33%) detected with at least one nucleotide substitution. The sequencing results were also confirmed by Sanger sequencing. Of those 47 samples, 72 nucleotide substitutions of 28 types, altered 24 codons were identified. Among those, Y253F/H, M351T, G250E, F359V/I and M244V were the most frequent mutations, while T315I took only 4.1%. There were also a number of samples harboring multiple substitutions and new variations. Conclusion: Nextgeneration deep sequencing is a sensitive and effective method to detect kinase domain mutation and our results could provide further information about the drug-resistance mutation in chronic myeloid leukemia.","PeriodicalId":90223,"journal":{"name":"Journal of leukemia (Los Angeles, Calif.)","volume":"5 1","pages":"1-8"},"PeriodicalIF":0.0,"publicationDate":"2017-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4172/2329-6917.1000235","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46410461","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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