Pub Date : 2017-05-28DOI: 10.4172/2329-6917.1000234
Ya Gao, Ying Xu, Jie Song, Jia-Qiong Hong, W. Zhuo, Chunguang Yang, Yu Zhang, Z. Fan, Yan Guo, C. Yue, Hai-Tao Sun, B. Ping
Objectives: Human bone marrow mesenchymal stem cells (hBMSCs) have been used for the prevention and treatment of acute graft-versus-host disease (aGVHD) in post-hematopoietic stem cell transplant patients. In this study, we compared the biological characteristics and immunosuppressive activity of human amniotic mesenchymal stem cells (hAMSCs) and hBMSCs to provide experimental evidence for the potential use of hAMSCs for treating aGVHD, thus solving the problem of insufficient hBMSCs sources. Methods: HAMSCs were isolated by enzymatic digestion. hBMSCs were isolated using Ficoll-Hypaque density gradients. The biological characteristics of both stem cell types were compared by morphological analysis, analysis of cell growth, cell cycle profiling, immunophenotyping, and immunofluorescence assays. An in vitro co-culture of MSCs and peripheral blood mononuclear cells (PBMCs) was performed and lymphocyte proliferation measured using the Cell Counting Kit-8(CCK-8) assay. IFN-γ production was determined in the co-culture supernatant using enzyme linked immunosorbent assay (ELISA). Results: Both hAMSCs and hBMSCs had fibroblast-like morphology. hAMSCs could be maintained for at least 15 culture passages, but hBMSCs started to show signs of aging and remarkably reduced proliferation at 6-7 passages. There was no significant difference in the proportion of cells in G2/M phase between hAMSCs and hBMSCs (P>0.05). Immunophenotyping revealed positive expression of CD105, CD90, and CD73 and negative expression of CD34, CD45, CD11b, CD19, and HLA-DR on the surface of both hAMSCs and hBMSCs. hAMSCs were positive for Oct-3/4, but hBMSCs were not. Both hAMSCs and hBMSCs expressed vimentin. PHA-stimulated PBMCs proliferation was inhibited by hAMSCs and hBMSCs. This inhibition was stronger, as the proportion of MSCs increased. There were not significant differences between the inhibitory effects of the two MSCs types on PBMCs proliferation (P>0.05). Interferon-γ (IFN-γ) production was lower when PBMCs were co-cultured with either hAMSCs or hBMSCs than when they were cultured alone (P 0.05). Conclusion: The results of this study demonstrated that hAMSCs have higher proliferation activity and clearer stem cell properties than hBMSCs. Both hAMSCs and hBMSCs were able to suppress the proliferation of allogeneic peripheral blood lymphocytes and reduce IFN-γ secretion stimulated by PHA in vitro.
{"title":"Human Amniotic Mesenchymal Stem Cells Exhibit Similar Immunosuppressive Ability with Bone Marrow Mesenchymal Stem Cells and Possess a Higher Proliferation Activity and Clearer Stem Cell Properties in vitro","authors":"Ya Gao, Ying Xu, Jie Song, Jia-Qiong Hong, W. Zhuo, Chunguang Yang, Yu Zhang, Z. Fan, Yan Guo, C. Yue, Hai-Tao Sun, B. Ping","doi":"10.4172/2329-6917.1000234","DOIUrl":"https://doi.org/10.4172/2329-6917.1000234","url":null,"abstract":"Objectives: Human bone marrow mesenchymal stem cells (hBMSCs) have been used for the prevention and treatment of acute graft-versus-host disease (aGVHD) in post-hematopoietic stem cell transplant patients. In this study, we compared the biological characteristics and immunosuppressive activity of human amniotic mesenchymal stem cells (hAMSCs) and hBMSCs to provide experimental evidence for the potential use of hAMSCs for treating aGVHD, thus solving the problem of insufficient hBMSCs sources. Methods: HAMSCs were isolated by enzymatic digestion. hBMSCs were isolated using Ficoll-Hypaque density gradients. The biological characteristics of both stem cell types were compared by morphological analysis, analysis of cell growth, cell cycle profiling, immunophenotyping, and immunofluorescence assays. An in vitro co-culture of MSCs and peripheral blood mononuclear cells (PBMCs) was performed and lymphocyte proliferation measured using the Cell Counting Kit-8(CCK-8) assay. IFN-γ production was determined in the co-culture supernatant using enzyme linked immunosorbent assay (ELISA). Results: Both hAMSCs and hBMSCs had fibroblast-like morphology. hAMSCs could be maintained for at least 15 culture passages, but hBMSCs started to show signs of aging and remarkably reduced proliferation at 6-7 passages. There was no significant difference in the proportion of cells in G2/M phase between hAMSCs and hBMSCs (P>0.05). Immunophenotyping revealed positive expression of CD105, CD90, and CD73 and negative expression of CD34, CD45, CD11b, CD19, and HLA-DR on the surface of both hAMSCs and hBMSCs. hAMSCs were positive for Oct-3/4, but hBMSCs were not. Both hAMSCs and hBMSCs expressed vimentin. PHA-stimulated PBMCs proliferation was inhibited by hAMSCs and hBMSCs. This inhibition was stronger, as the proportion of MSCs increased. There were not significant differences between the inhibitory effects of the two MSCs types on PBMCs proliferation (P>0.05). Interferon-γ (IFN-γ) production was lower when PBMCs were co-cultured with either hAMSCs or hBMSCs than when they were cultured alone (P 0.05). Conclusion: The results of this study demonstrated that hAMSCs have higher proliferation activity and clearer stem cell properties than hBMSCs. Both hAMSCs and hBMSCs were able to suppress the proliferation of allogeneic peripheral blood lymphocytes and reduce IFN-γ secretion stimulated by PHA in vitro.","PeriodicalId":90223,"journal":{"name":"Journal of leukemia (Los Angeles, Calif.)","volume":"5 1","pages":"1-6"},"PeriodicalIF":0.0,"publicationDate":"2017-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4172/2329-6917.1000234","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43130119","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 : 2017-05-22DOI: 10.4172/2329-6917.1000233
V. Malone, J. Chenbhanich, F. Liu, D. Guarderas-Paredes, Lee Yh, S. Aufranc, K. Seetharaman
Introduction: Less than 1% of patients with CML or acute leukemia transformations of other chronic disorders such as myeloproliferative neoplasms, particularly myelofibrosis, will present with and extramedullary presentation. Sites of isolated myeloid sarcoma include bone, periosteum, soft tissues, and lymph nodes, and less commonly the orbit, intestine, mediastinum, epidural region, uterus, and ovary. Methods: We conducted a systematic review of cases reported in the literature since 2005 to 2013. We identified similar cases to the actual ones that presented to our practice. The patients were diagnosed with myeloid sarcoma with an atypical presentation as a hematoma. We described 2 case reports, both have an atypical presentation of myeloid sarcoma mimicking a hematoma in different parts of the body. Results: We found in the literature a total of 4 cases with myeloid sarcoma with an atypical presentation as a hematoma. About, 3 of them (n=3, 75%) reported subdural hematomas. Only 1 case (n=1, 25%) reported an ocular involvement/retro-orbital hematoma. We present 2 cases that presented to our practice with a diagnosis of myeloid sarcoma and later on complicated as a subcutaneous hematoma. Discussion: We analyzed the fact that myeloid sarcoma has a very unusual presentation as a hematoma. The review of the literature supports this fact. However this should make as aware that even though this is an unusual and unique presentation we should think about it and always test the biopsy sample for IHC and flow cytometry in order to later on diagnose and treat
{"title":"Atypical Presentation of Myeloid Sarcoma Mimicking a Subcutaneous Hematoma as Complication of MDS and AML","authors":"V. Malone, J. Chenbhanich, F. Liu, D. Guarderas-Paredes, Lee Yh, S. Aufranc, K. Seetharaman","doi":"10.4172/2329-6917.1000233","DOIUrl":"https://doi.org/10.4172/2329-6917.1000233","url":null,"abstract":"Introduction: Less than 1% of patients with CML or acute leukemia transformations of other chronic disorders such as myeloproliferative neoplasms, particularly myelofibrosis, will present with and extramedullary presentation. Sites of isolated myeloid sarcoma include bone, periosteum, soft tissues, and lymph nodes, and less commonly the orbit, intestine, mediastinum, epidural region, uterus, and ovary. Methods: We conducted a systematic review of cases reported in the literature since 2005 to 2013. We identified similar cases to the actual ones that presented to our practice. The patients were diagnosed with myeloid sarcoma with an atypical presentation as a hematoma. We described 2 case reports, both have an atypical presentation of myeloid sarcoma mimicking a hematoma in different parts of the body. Results: We found in the literature a total of 4 cases with myeloid sarcoma with an atypical presentation as a hematoma. About, 3 of them (n=3, 75%) reported subdural hematomas. Only 1 case (n=1, 25%) reported an ocular involvement/retro-orbital hematoma. We present 2 cases that presented to our practice with a diagnosis of myeloid sarcoma and later on complicated as a subcutaneous hematoma. Discussion: We analyzed the fact that myeloid sarcoma has a very unusual presentation as a hematoma. The review of the literature supports this fact. However this should make as aware that even though this is an unusual and unique presentation we should think about it and always test the biopsy sample for IHC and flow cytometry in order to later on diagnose and treat","PeriodicalId":90223,"journal":{"name":"Journal of leukemia (Los Angeles, Calif.)","volume":" ","pages":"1-3"},"PeriodicalIF":0.0,"publicationDate":"2017-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48241270","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 : 2017-05-17DOI: 10.4172/2329-6917.1000232
K. Zhao, Shushu Yuan, Lingling Yin, Jieyun Xia, K. Xu
The purpose of this report was to evaluate the effect of IL1RAP sepecifc CAR-T cell on inducing IL1RAP positive chronic myeloid leukemia cell apoptosis. Leukemic stem cells (LSCs) as the main initiating factor of leukemia relapse still cannot be eradicated thoroughly. Even though Tyrosine kinase inhibitors (TKI) revolutionized the therapy of chronic myeloid leukemia (CML), it alone does not cure this disease for the no response to quiescent LSCs. Human IL1RAP identified by Landberg N and we can be used as a specific surface marker and tumor burden indicator of LSC in CML. Therefore, IL1RAP chimeric antibody receptor (CAR) T cell specific targeting LSCs might be a novel strategy to CML therapy. Here, we demonstrated that IL1RAP CAR T cell showed more powerful cytotoxicity to kill IL1RAP positive CML cell lines than that to directly block IL1RAP expression by shRNA. Furthermore, compared with shRAN group and blank vector treated group, higher rate of apoptosis and lower proliferation of leukemia cells were showed in IL1RAP CAR T cell co-cultured group. In conclusion, in the present study a potential creative therapeutic target to eliminate LSCs and assistant strategy to cure CML was proved.
本报告的目的是评估IL1RAP特异性CAR-T细胞诱导IL1RAP阳性慢性髓性白血病细胞凋亡的作用。白血病干细胞(leukemia stem cells, LSCs)作为白血病复发的主要启动因子，目前仍不能彻底根除。尽管酪氨酸激酶抑制剂(TKI)彻底改变了慢性髓性白血病(CML)的治疗方法，但由于对静止LSCs没有反应，仅靠它并不能治愈这种疾病。Landberg N鉴定的人IL1RAP可作为CML中LSC的特异性表面标记物和肿瘤负荷指标。因此，IL1RAP嵌合抗体受体(CAR) T细胞特异性靶向LSCs可能是CML治疗的新策略。在这里，我们证明了IL1RAP CAR - T细胞对杀死IL1RAP阳性CML细胞系的细胞毒性比直接通过shRNA阻断IL1RAP表达的细胞毒性更强。此外，与shRAN组和空白载体处理组相比，IL1RAP CAR - T细胞共培养组白血病细胞的凋亡率更高，增殖率更低。总之，在本研究中，证明了一种潜在的创造性治疗靶点来消除LSCs和辅助治疗CML的策略。
{"title":"Potential Efficacy of Human IL-1RAP Specific CAR-T cell in Eliminating Leukemic Stem Cells of Chronic Myeloid Leukemia","authors":"K. Zhao, Shushu Yuan, Lingling Yin, Jieyun Xia, K. Xu","doi":"10.4172/2329-6917.1000232","DOIUrl":"https://doi.org/10.4172/2329-6917.1000232","url":null,"abstract":"The purpose of this report was to evaluate the effect of IL1RAP sepecifc CAR-T cell on inducing IL1RAP positive chronic myeloid leukemia cell apoptosis. Leukemic stem cells (LSCs) as the main initiating factor of leukemia relapse still cannot be eradicated thoroughly. Even though Tyrosine kinase inhibitors (TKI) revolutionized the therapy of chronic myeloid leukemia (CML), it alone does not cure this disease for the no response to quiescent LSCs. Human IL1RAP identified by Landberg N and we can be used as a specific surface marker and tumor burden indicator of LSC in CML. Therefore, IL1RAP chimeric antibody receptor (CAR) T cell specific targeting LSCs might be a novel strategy to CML therapy. Here, we demonstrated that IL1RAP CAR T cell showed more powerful cytotoxicity to kill IL1RAP positive CML cell lines than that to directly block IL1RAP expression by shRNA. Furthermore, compared with shRAN group and blank vector treated group, higher rate of apoptosis and lower proliferation of leukemia cells were showed in IL1RAP CAR T cell co-cultured group. In conclusion, in the present study a potential creative therapeutic target to eliminate LSCs and assistant strategy to cure CML was proved.","PeriodicalId":90223,"journal":{"name":"Journal of leukemia (Los Angeles, Calif.)","volume":" ","pages":"1-3"},"PeriodicalIF":0.0,"publicationDate":"2017-05-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4172/2329-6917.1000232","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47960385","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 : 2017-04-29DOI: 10.4172/2329-6917.1000231
Tomasz Chojnacki, P. Rzepecki
WHO 2016 guidelines regarding chronic myeloid leukemia (CML) do not contain groundbreaking changes [1]. Mainly criteria of acceleration phase (AP) identification were revised. Despite these changes, the guidelines are still not standardized and differ significantly, even when compared to guidelines of European Leukemia Net (ELN) [2], International Bone Marrow Transplant Registry (IBMTR) or M. D. Anderson Cancer Center, to give some examples (Table 1). Compared to previous editions of the WHO classification, new parameters appeared, the presence of which requires identification of acceleration phase. In this case, one should list e.g. chronic leukocytosis (>10 × 109/L), non-responding to treatment, chronic splenomegaly non-responding to treatment, additional clonal chromosomal aberrations (the so-called "major route") in Ph+ cells on diagnosis. New provisional criteria also appeared, related to response to therapy using tyrosine kinase inhibitors (TKI). Among the latter ones the following were distinguished: hematological TKI resistance when used as a first-line or lack of complete hematological response (CHR) during first-line treatment when using TKI; hematological, cytogenetic or molecular resistance during treatment with a subsequent second TKI; presence of two or more mutations within BCR/ABL during TKI therapy. These changes resulted in necessity to diagnose acceleration phase much more frequently, compared to e.g. ELN criteria. This presents importance, particularly for patients already treated with TKI, as it increases the percentage of patients with indications for allogenic hematopoietic stem cell transplantation (allo-HSCT). It contrasts with everyday practice and tendency to marginalize the role of transplanting hematopoietic cells in case of this disease classification unit, in the TKI era. The thesis as such is best illustrated with an example.
{"title":"Is it really the Transplant Renaissance in CML Acceleration Phase","authors":"Tomasz Chojnacki, P. Rzepecki","doi":"10.4172/2329-6917.1000231","DOIUrl":"https://doi.org/10.4172/2329-6917.1000231","url":null,"abstract":"WHO 2016 guidelines regarding chronic myeloid leukemia (CML) do not contain groundbreaking changes [1]. Mainly criteria of acceleration phase (AP) identification were revised. Despite these changes, the guidelines are still not standardized and differ significantly, even when compared to guidelines of European Leukemia Net (ELN) [2], International Bone Marrow Transplant Registry (IBMTR) or M. D. Anderson Cancer Center, to give some examples (Table 1). Compared to previous editions of the WHO classification, new parameters appeared, the presence of which requires identification of acceleration phase. In this case, one should list e.g. chronic leukocytosis (>10 × 109/L), non-responding to treatment, chronic splenomegaly non-responding to treatment, additional clonal chromosomal aberrations (the so-called \"major route\") in Ph+ cells on diagnosis. New provisional criteria also appeared, related to response to therapy using tyrosine kinase inhibitors (TKI). Among the latter ones the following were distinguished: hematological TKI resistance when used as a first-line or lack of complete hematological response (CHR) during first-line treatment when using TKI; hematological, cytogenetic or molecular resistance during treatment with a subsequent second TKI; presence of two or more mutations within BCR/ABL during TKI therapy. These changes resulted in necessity to diagnose acceleration phase much more frequently, compared to e.g. ELN criteria. This presents importance, particularly for patients already treated with TKI, as it increases the percentage of patients with indications for allogenic hematopoietic stem cell transplantation (allo-HSCT). It contrasts with everyday practice and tendency to marginalize the role of transplanting hematopoietic cells in case of this disease classification unit, in the TKI era. The thesis as such is best illustrated with an example.","PeriodicalId":90223,"journal":{"name":"Journal of leukemia (Los Angeles, Calif.)","volume":"5 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2017-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4172/2329-6917.1000231","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46374660","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 : 2017-04-26DOI: 10.4172/2329-6917.1000230
Manar M. Ismail, Amal Zaghloul, AB AbdulateefNahla, Morsi Heba
CD66 and its isoforms modulate several physiologic processes and have a role in aggressiveness of malignancies. We aimed at investigating pan CD66, CD66 a, b, and c expression and their clinical implication in acute leukemia. This study included 85 cases, 50 AML, 33 ALL and 2 mixed lineage leukemia from King Abdullah Medical City, Saudi Arabia. Pan CD66, CD66a, CD66b and CD66c were detected by flow cytometry at diagnosis and pan CD66 was reanalyzed at day28. Pan CD66 and CD66c expression rate was 51.8% in B-ALL and significantly correlated with BCR/ABL gene, P-value 0.037. CD66a was detected in 11.1% and significantly associated with shorter overall survival (OS), P-value 0.045. In AML, the expression rates were 40%, 28% and 32% for pan CD66, CD66b and CD66c respectively. CD66b was significantly correlated with favorable cytogenetic and prolonged OS, P-value 0.001 and 0.025 respectively. CD66c was correlated with CD25 positivity, P-value 0.003. The expression of pan CD66 at diagnosis and day 28, were significantly correlated, P-value <0.0001. Accordingly, pan CD66 could be added to the panel for MRD. Our data were encouraging to our center to follow other centers that already included CD66c in their panel for MRD detection. CD66c may be tried as a target for monoclonal antibody therapy in CD66c positive acute leukemia. Large-scale studies are needed to verify the association of CD66b expression with cytogenetics and survival in AML
{"title":"Membranous Expression of pan CD66, CD66a, CD66b, and CD66c and their Clinical Impact in Acute Leukemia: Cross Sectional Longitudinal Cohort Study in Saudi Arabia","authors":"Manar M. Ismail, Amal Zaghloul, AB AbdulateefNahla, Morsi Heba","doi":"10.4172/2329-6917.1000230","DOIUrl":"https://doi.org/10.4172/2329-6917.1000230","url":null,"abstract":"CD66 and its isoforms modulate several physiologic processes and have a role in aggressiveness of malignancies. We aimed at investigating pan CD66, CD66 a, b, and c expression and their clinical implication in acute leukemia. This study included 85 cases, 50 AML, 33 ALL and 2 mixed lineage leukemia from King Abdullah Medical City, Saudi Arabia. Pan CD66, CD66a, CD66b and CD66c were detected by flow cytometry at diagnosis and pan CD66 was reanalyzed at day28. Pan CD66 and CD66c expression rate was 51.8% in B-ALL and significantly correlated with BCR/ABL gene, P-value 0.037. CD66a was detected in 11.1% and significantly associated with shorter overall survival (OS), P-value 0.045. In AML, the expression rates were 40%, 28% and 32% for pan CD66, CD66b and CD66c respectively. CD66b was significantly correlated with favorable cytogenetic and prolonged OS, P-value 0.001 and 0.025 respectively. CD66c was correlated with CD25 positivity, P-value 0.003. The expression of pan CD66 at diagnosis and day 28, were significantly correlated, P-value <0.0001. Accordingly, pan CD66 could be added to the panel for MRD. Our data were encouraging to our center to follow other centers that already included CD66c in their panel for MRD detection. CD66c may be tried as a target for monoclonal antibody therapy in CD66c positive acute leukemia. Large-scale studies are needed to verify the association of CD66b expression with cytogenetics and survival in AML","PeriodicalId":90223,"journal":{"name":"Journal of leukemia (Los Angeles, Calif.)","volume":"5 1","pages":"1-9"},"PeriodicalIF":0.0,"publicationDate":"2017-04-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4172/2329-6917.1000230","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45316589","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 : 2017-04-05DOI: 10.4172/2329-6917.1000229
S. Thekkudan, Soniya Nityan
Development of psoriasis during Imatinib therapy has been described only as few case reports. Psoriasis developing during Nilotinib therapy is also rare, with only two cases reported. In psoriasis, the suppressor activity of T-regulatory cells is decreased, either due to a reduction in the number or due to a reduced ability of T-regulatory cells to produce suppressive cytokines. Imatinib and Nilotinib inhibited the proliferation and immunosuppressive effect of T-regulatory cells in a dose dependent manner. This is the first case report of Dasatinib causing worsening of Psoriasis vulgaris, possibly due to the more potent action of Dasatinib on T regs. Most cases can be managed without any dose reductions in tyrosine kinase inhibitor therapy along with topical therapies and oral methotrexate.
{"title":"Development of Psoriasis Vulgaris in a Chronic Myeloid Leukemia Patient on Second-Generation Tyrosine Kinase Inhibitor Therapy","authors":"S. Thekkudan, Soniya Nityan","doi":"10.4172/2329-6917.1000229","DOIUrl":"https://doi.org/10.4172/2329-6917.1000229","url":null,"abstract":"Development of psoriasis during Imatinib therapy has been described only as few case reports. Psoriasis developing during Nilotinib therapy is also rare, with only two cases reported. In psoriasis, the suppressor activity of T-regulatory cells is decreased, either due to a reduction in the number or due to a reduced ability of T-regulatory cells to produce suppressive cytokines. Imatinib and Nilotinib inhibited the proliferation and immunosuppressive effect of T-regulatory cells in a dose dependent manner. This is the first case report of Dasatinib causing worsening of Psoriasis vulgaris, possibly due to the more potent action of Dasatinib on T regs. Most cases can be managed without any dose reductions in tyrosine kinase inhibitor therapy along with topical therapies and oral methotrexate.","PeriodicalId":90223,"journal":{"name":"Journal of leukemia (Los Angeles, Calif.)","volume":" ","pages":"1-2"},"PeriodicalIF":0.0,"publicationDate":"2017-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4172/2329-6917.1000229","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48163339","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 : 2017-03-30DOI: 10.4172/2329-6917.1000228
Z. Tóth, G. Lukács, P. Rajnics, G. Bajzik, M. Egyed, Á. Kovács, I. Repa
Multiple myeloma is a hematologic malignancy characterized by a clonal proliferation of plasma cells. PET/MR is a new emerging hybrid imaging modality, its potential role in numerous different malignant diseases is under extensive evaluation. Our report describes PET/MR findings of a relapsed multiple myeloma case.
{"title":"PET/MR in Relapsed Multiple Myeloma","authors":"Z. Tóth, G. Lukács, P. Rajnics, G. Bajzik, M. Egyed, Á. Kovács, I. Repa","doi":"10.4172/2329-6917.1000228","DOIUrl":"https://doi.org/10.4172/2329-6917.1000228","url":null,"abstract":"Multiple myeloma is a hematologic malignancy characterized by a clonal proliferation of plasma cells. PET/MR is \u0000 a new emerging hybrid imaging modality, its potential role in numerous different malignant diseases is under \u0000 extensive evaluation. Our report describes PET/MR findings of a relapsed multiple myeloma case.","PeriodicalId":90223,"journal":{"name":"Journal of leukemia (Los Angeles, Calif.)","volume":"5 1","pages":"1-2"},"PeriodicalIF":0.0,"publicationDate":"2017-03-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42874761","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 : 2017-03-25DOI: 10.4172/2329-6917.1000227
Yongxin Zheng, F. Guo, Y. Zou, Wu Jun
The present study was undertaken to investigate the aberrant DNA ethymlation in P1 promoter region of p53 gene in acute leukemia patients. The aberrant DNA methylation of Tp53 gene in fresh leukemia cells obtained from 31 newly diagnosed patients as well as monocyte leukemia U937 cells were detected by using polymerase chain reaction (PCR). The results revealed that aberrant DNA methylation in P1 promoter region of Tp53 was detectable in 12 cases of 31 leukemia patients (38.7%) as well as in U937 cells, while no aberrant DNA methylation of this gene was detected in normal control group (11 healthy volunteers), indicating that there was significant difference between acute leukemia patients and healthy donors (P=0.0183, Fisher’s exact test). Furthermore, no significant difference was found in acute myeloid leukemia (AML) and acute lymphoid leukemia (ALL) patients (35.2% vs 42.8%, P=0.7241, Fisher’s exact test). Our results, for the first time to our knowledge, provide laboratory evidence that aberrant DNA methylation in P1 promoter region of Tp53 gene is an common phenomenon in both AML and ALL patients, and that the significance of this special DNA methylation in acute leukemia needs further and profound investigation.
本研究旨在探讨急性白血病患者p53基因P1启动子区DNA甲基化异常。应用聚合酶链式反应(PCR)检测31例新诊断白血病患者新鲜白血病细胞及单核细胞白血病U937细胞中Tp53基因的异常DNA甲基化。结果显示，在31例白血病患者(38.7%)和U937细胞中检测到Tp53 P1启动子区DNA甲基化异常，而在正常对照组(11例健康志愿者)中未检测到该基因的DNA甲基化异常，说明急性白血病患者与健康供者之间存在显著差异(P=0.0183, Fisher精确检验)。急性髓性白血病(AML)和急性淋巴性白血病(ALL)患者的外周血淋巴细胞密度差异无统计学意义(35.2% vs 42.8%， P=0.7241, Fisher精确检验)。我们的研究结果为我们所知的第一次提供了实验室证据，证明Tp53基因P1启动子区DNA甲基化异常在AML和ALL患者中都是一种普遍现象，这种特殊的DNA甲基化在急性白血病中的意义需要进一步深入研究。
{"title":"Aberrant DNA Methylation in P1 Promoter Region of Tp53 Gene in Acute Leukemia","authors":"Yongxin Zheng, F. Guo, Y. Zou, Wu Jun","doi":"10.4172/2329-6917.1000227","DOIUrl":"https://doi.org/10.4172/2329-6917.1000227","url":null,"abstract":"The present study was undertaken to investigate the aberrant DNA ethymlation in P1 promoter region of p53 gene in acute leukemia patients. The aberrant DNA methylation of Tp53 gene in fresh leukemia cells obtained from 31 newly diagnosed patients as well as monocyte leukemia U937 cells were detected by using polymerase chain reaction (PCR). The results revealed that aberrant DNA methylation in P1 promoter region of Tp53 was detectable in 12 cases of 31 leukemia patients (38.7%) as well as in U937 cells, while no aberrant DNA methylation of this gene was detected in normal control group (11 healthy volunteers), indicating that there was significant difference between acute leukemia patients and healthy donors (P=0.0183, Fisher’s exact test). Furthermore, no significant difference was found in acute myeloid leukemia (AML) and acute lymphoid leukemia (ALL) patients (35.2% vs 42.8%, P=0.7241, Fisher’s exact test). Our results, for the first time to our knowledge, provide laboratory evidence that aberrant DNA methylation in P1 promoter region of Tp53 gene is an common phenomenon in both AML and ALL patients, and that the significance of this special DNA methylation in acute leukemia needs further and profound investigation.","PeriodicalId":90223,"journal":{"name":"Journal of leukemia (Los Angeles, Calif.)","volume":"5 1","pages":"1-4"},"PeriodicalIF":0.0,"publicationDate":"2017-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4172/2329-6917.1000227","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45737881","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 : 2017-03-20DOI: 10.4172/2329-6917.1000226
S. Taverna, C. Corrado
Nowadays cancer is one of the main reasons of death all over the world and it is estimated that deaths caused by cancer will grow dramatically in the next decades. Even if chemotherapy is the election therapy for solid tumors, as well as leukemias and lymphomas, cancer treatments are in continuous evolution trying to solve the problem of resistance mainly due to low accumulation of the drug in tumor cells (MDR). Natural compounds represent a valid alternative to treat several disease and recently the scientific community focus on these natural compounds and plant metabolites with therapeutic activities and low toxicities compared with synthetic ones. A combination therapy, that join conventional chemotherapy with natural plant metabolites, is now considered a new promising strategy to overcome MDR and reduce cellular toxicity; in particular, in leukemia due to its very complex origin and development of leukemogenesis. Here, we want to summarize and update the recent applications of natural compounds in the treatment of leukemia.
{"title":"Natural Compounds: Molecular Weapons against Leukemia’s","authors":"S. Taverna, C. Corrado","doi":"10.4172/2329-6917.1000226","DOIUrl":"https://doi.org/10.4172/2329-6917.1000226","url":null,"abstract":"Nowadays cancer is one of the main reasons of death all over the world and it is estimated that deaths caused by cancer will grow dramatically in the next decades. Even if chemotherapy is the election therapy for solid tumors, as well as leukemias and lymphomas, cancer treatments are in continuous evolution trying to solve the problem of resistance mainly due to low accumulation of the drug in tumor cells (MDR). Natural compounds represent a valid alternative to treat several disease and recently the scientific community focus on these natural compounds and plant metabolites with therapeutic activities and low toxicities compared with synthetic ones. A combination therapy, that join conventional chemotherapy with natural plant metabolites, is now considered a new promising strategy to overcome MDR and reduce cellular toxicity; in particular, in leukemia due to its very complex origin and development of leukemogenesis. Here, we want to summarize and update the recent applications of natural compounds in the treatment of leukemia.","PeriodicalId":90223,"journal":{"name":"Journal of leukemia (Los Angeles, Calif.)","volume":"5 1","pages":"1-7"},"PeriodicalIF":0.0,"publicationDate":"2017-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41820290","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 : 2017-02-25DOI: 10.4172/2329-6917.1000I101
Joshua P. Sasine, Thomas D Lee, Rena R. Xian, G. Schiller
A 69-year-old man presented to an outside hospital with fatigue, fevers, altered mental status, and dyspnea. Laboratory testing revealed a white blood cell count of 231 × 103/μL with 88% blasts, hemoglobin of 6.2 g/dL, and platelet count of 80 × 103/μL. Bone marrow biopsy confirmed a diagnosis of acute myeloid leukemia (AML) with flow cytometric analysis demonstrating two abnormal myeloblast populations, the first expressing CD11b (partial), CD13, CD33, CD45 (dim), CD64, CD117, and HLA-DR and the other CD10, CD11b, CD13 (subset), CD14, CD15, CD33, CD45 (moderate to bright), CD64, and HLA-DR. Both populations showed heterogeneous expression of myeloperoxidase and were negative for CD34 expression. Karyotype and FISH studies revealed no chromosomal abnormalities.
{"title":"Acute Myeloid Leukemia with Cup-Like Nuclear Inclusions, and FLT3-ITD andNPM1 Mutations","authors":"Joshua P. Sasine, Thomas D Lee, Rena R. Xian, G. Schiller","doi":"10.4172/2329-6917.1000I101","DOIUrl":"https://doi.org/10.4172/2329-6917.1000I101","url":null,"abstract":"A 69-year-old man presented to an outside hospital with fatigue, fevers, altered mental status, and dyspnea. Laboratory testing revealed a white blood cell count of 231 × 103/μL with 88% blasts, hemoglobin of 6.2 g/dL, and platelet count of 80 × 103/μL. Bone marrow biopsy confirmed a diagnosis of acute myeloid leukemia (AML) with flow cytometric analysis demonstrating two abnormal myeloblast populations, the first expressing CD11b (partial), CD13, CD33, CD45 (dim), CD64, CD117, and HLA-DR and the other CD10, CD11b, CD13 (subset), CD14, CD15, CD33, CD45 (moderate to bright), CD64, and HLA-DR. Both populations showed heterogeneous expression of myeloperoxidase and were negative for CD34 expression. Karyotype and FISH studies revealed no chromosomal abnormalities.","PeriodicalId":90223,"journal":{"name":"Journal of leukemia (Los Angeles, Calif.)","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2017-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47226386","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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