[论坛推荐]内华达州肿瘤中心骨髓获取及移植研究博士后岗位
来源：丁香人才网
日期：2008-03-20
Institution
Ma’s Progenitor Cell Lab
Yupo Ma, M.D., M.S., Ph.D.
Chief of Hematopathology
Medical Director of Flow Cytometry Lab
Dr. Ma earned his medical degree from Jinan University (P.R. China),College of Medicine and a Ph.D. from the University Of South AlabamaCollege Of Medicine. He completed a residency in Pathology at BrownUniversity, clinical fellowship in Hematopathology at M.D. AndersonCancer Center and has conducted Post Doctoral Training in Pathology atHarvard Medical School. Dr. Ma specializes in the diagnosis of leukemiaand lymphoma. Formerly Dr. Ma was an assistant professor and director ofthe Flow Cytometry Lab at the University of Arkansas.
Dr. Ma joined the Nevada Cancer Institute's Division of Pathology andLaboratory Development in 2005.
Laboratory Members
Zaida Alipio, B.S.
Taylor Fowles. B.S.
Jianchang Yang, M.D., Ph.D.
Jennifer Xu, M.S., Ph.D.
Chaoyong Zhu, M.D., Ph.D.
Description
Research Interests
Dr. Ma’s lab focuses on the role of SALL4 in embryonic/adult progenitorcells and leukemic progenitor cells. The SALL gene family is themammalian homologue of Drosophila gene Spalt (sal). In Drosophila, salmutation can lead to the incomplete separation of the head and trunk ofthe fly. In the human, heterogenous mutation of SALL1 causesTownes-Brock Syndrome with renal, cardiac, genital malformation.Heterogenous mutation of SALL4 in human is associated with OkihiroSyndrome with limitation of eye abduction, deafness and digitmalformation. SALL4 is able to bind to Oct 4 and Nanog. SALL4 plays animportant role in the maintenance of ES cell pluripotent properties andself renewal. The loss of expression results in ES cell differentiation.
We have demonstrated that SALL4 is constitutively expressed in acutemyeloid leukemias (AML) and fails to turn off in nearly all human AMLs.A fundamental unanswered question: is constitutive expression of SALL4sufficient to induce AML? In addition, what mechanisms of SALL4 induceAML? How does SALL4 promoter leukemic progenitor cell self renewal? Wehave chosen a mammalian model system to approach these questions. Thisshould allow us to test directly leukemogenic potential of constitutiveexpression of SALL4 in a mammalian model. A mammalian modeloverexpressing SALL4 develops hematopoietic disorders includingmyelodysplastic-like symptoms and subsequently acute myeloid leukemia.The constitutive expression of SALL4 is causal to the leukemic phenotypeand SALL4 may interact with the Wnt/β-catenin pathway in theleukemogenesis. Our mammalian models should provide a useful platform toanalyze the effect of SALL4 on hematopoiesis and its potentialcooperation with Wnt/β-catenin pathway in the pathogenesis of leukemiaprogenitor cells. Leukemic progenitor cells are aberrant cells thatmaintain and propagate blood cancers. Leukemic progenitor cells are notthe same as progenitor cells and they can turn into blood cancer cells.
A parallel project involves an investigation of the SALL4 function indevelopment and hematopoiesis. We are creating a loss of function modelfor SALL4 using conventional and conditional knockout approaches. Incharacterizing the phenotype of SALL4 deficient models, we are focusingon the role of SALL4 in regulating hematopoiesis and hematopoieticprogenitor cell function.
My other research interest is somatic cell reprogramming, with mucheffort towards the goal of generation of patient-specific pluripotentprogenitor cells (hESC-like cells) for clinical therapies including bonemarrow transplantation. Because these hESC-like cells would begenetically identical to the other cells in the patient, they would notbe rejected when transplanted. This research may make it possible tocreate better progenitor cells and could lead to technologies that makeit possible to create new hESC-like cells from virtually any cell in apatient without the need for harvesting human embryos.
Current Publications
1. L Chai, Yang J, Di C, Cui W, Lai R, and Ma Y. Transcriptionalactivation of the SALL1 by the human SIX1 domain. 2006, J. Biol. Chem. 14;281(28):18918-26.
2. Ma Y, Wei C, Yang J, Qu J, Di C , Amin HM, Lai R, Ritz J, Krause DS,and L Chai. SALL4, a novel oncogene, is constitutively expressed inacute myeloid leukemia (AML) and is sufficient to induce AML intransgenic mice. 2006, Blood , Oct 15;108Musical Note:2726-35.
3. Zhang J, Tam W, Tong GQ, Wu Q, Chan BS, Lou Y, Yang J, Ma Y, Chai L,Ng H, Lufkin T, Robson P and B Lim. Sall4 modulates embryonic stem cellpluripotency and early embryonic development by the transcriptionalregulation of Pou5f1. 2006 Nature Cell Biology, 2006 Oct;8(10): 1114.
4. Lai R, Lefresne SV, Franko B, Hui D, Hanson J, Mirza I, Mansoor A,Amin HM, Ma Y. Immunoglobin Vh somatic hypermutation in mantle celllymphoma- mutated genotype correlates with better clinical outcome 2006Modern Pathology 2006 Nov;19(11):1498-505.
5. Wei C, Nikki Kong, Ma Y, N, Yang J, Amin HM, Lai R and L Chai.Expression analysis of a novel oncogene, SALL4, in lymphoma, multiplemyeloma, and acute lymphoblastic leukemia. 2006 Modern Pathology, 2006 Dec;19(12):1585-92.
6. Yang J, Chai L, Liu F, Flink L,Pei L, Siberstain L, Amin, HM, Ward D,and Ma Y. Bmi-1 is a SALL4 Target Gene for SALL4 in Hematopoietic andLeukemic Cells. 2007, Proc. Natl. Acad. Sci. USA. 2007;104:10494-10499
Current Federal Grants:
1. NIH/K08/Principle Investigator
2. NIH/P20/subcontract, Project leader (Principle Investigator)
3. NIH/R01/Principle Investigator
4. VA Merit Award/Principle Investigator
Others
5. Birth Mark Foundation
6. ASH FELLOWSHIP Award (to Jianchang Yang)
Contact
老板现在急需要一名熟练骨髓获取及移植的博士后，最好能作小鼠肝脏或脾脏的细胞移植。给H1B签证，能在2个月后来美。
请将CV发至dxu@nvcancer.org.
Ma’s Progenitor Cell Lab
Yupo Ma, M.D., M.S., Ph.D.
Chief of Hematopathology
Medical Director of Flow Cytometry Lab
Dr. Ma earned his medical degree from Jinan University (P.R. China),College of Medicine and a Ph.D. from the University Of South AlabamaCollege Of Medicine. He completed a residency in Pathology at BrownUniversity, clinical fellowship in Hematopathology at M.D. AndersonCancer Center and has conducted Post Doctoral Training in Pathology atHarvard Medical School. Dr. Ma specializes in the diagnosis of leukemiaand lymphoma. Formerly Dr. Ma was an assistant professor and director ofthe Flow Cytometry Lab at the University of Arkansas.
Dr. Ma joined the Nevada Cancer Institute's Division of Pathology andLaboratory Development in 2005.
Laboratory Members
Zaida Alipio, B.S.
Taylor Fowles. B.S.
Jianchang Yang, M.D., Ph.D.
Jennifer Xu, M.S., Ph.D.
Chaoyong Zhu, M.D., Ph.D.
Description
Research Interests
Dr. Ma’s lab focuses on the role of SALL4 in embryonic/adult progenitorcells and leukemic progenitor cells. The SALL gene family is themammalian homologue of Drosophila gene Spalt (sal). In Drosophila, salmutation can lead to the incomplete separation of the head and trunk ofthe fly. In the human, heterogenous mutation of SALL1 causesTownes-Brock Syndrome with renal, cardiac, genital malformation.Heterogenous mutation of SALL4 in human is associated with OkihiroSyndrome with limitation of eye abduction, deafness and digitmalformation. SALL4 is able to bind to Oct 4 and Nanog. SALL4 plays animportant role in the maintenance of ES cell pluripotent properties andself renewal. The loss of expression results in ES cell differentiation.
We have demonstrated that SALL4 is constitutively expressed in acutemyeloid leukemias (AML) and fails to turn off in nearly all human AMLs.A fundamental unanswered question: is constitutive expression of SALL4sufficient to induce AML? In addition, what mechanisms of SALL4 induceAML? How does SALL4 promoter leukemic progenitor cell self renewal? Wehave chosen a mammalian model system to approach these questions. Thisshould allow us to test directly leukemogenic potential of constitutiveexpression of SALL4 in a mammalian model. A mammalian modeloverexpressing SALL4 develops hematopoietic disorders includingmyelodysplastic-like symptoms and subsequently acute myeloid leukemia.The constitutive expression of SALL4 is causal to the leukemic phenotypeand SALL4 may interact with the Wnt/β-catenin pathway in theleukemogenesis. Our mammalian models should provide a useful platform toanalyze the effect of SALL4 on hematopoiesis and its potentialcooperation with Wnt/β-catenin pathway in the pathogenesis of leukemiaprogenitor cells. Leukemic progenitor cells are aberrant cells thatmaintain and propagate blood cancers. Leukemic progenitor cells are notthe same as progenitor cells and they can turn into blood cancer cells.
A parallel project involves an investigation of the SALL4 function indevelopment and hematopoiesis. We are creating a loss of function modelfor SALL4 using conventional and conditional knockout approaches. Incharacterizing the phenotype of SALL4 deficient models, we are focusingon the role of SALL4 in regulating hematopoiesis and hematopoieticprogenitor cell function.
My other research interest is somatic cell reprogramming, with mucheffort towards the goal of generation of patient-specific pluripotentprogenitor cells (hESC-like cells) for clinical therapies including bonemarrow transplantation. Because these hESC-like cells would begenetically identical to the other cells in the patient, they would notbe rejected when transplanted. This research may make it possible tocreate better progenitor cells and could lead to technologies that makeit possible to create new hESC-like cells from virtually any cell in apatient without the need for harvesting human embryos.
Current Publications
1. L Chai, Yang J, Di C, Cui W, Lai R, and Ma Y. Transcriptionalactivation of the SALL1 by the human SIX1 domain. 2006, J. Biol. Chem. 14;281(28):18918-26.
2. Ma Y, Wei C, Yang J, Qu J, Di C , Amin HM, Lai R, Ritz J, Krause DS,and L Chai. SALL4, a novel oncogene, is constitutively expressed inacute myeloid leukemia (AML) and is sufficient to induce AML intransgenic mice. 2006, Blood , Oct 15;108Musical Note:2726-35.
3. Zhang J, Tam W, Tong GQ, Wu Q, Chan BS, Lou Y, Yang J, Ma Y, Chai L,Ng H, Lufkin T, Robson P and B Lim. Sall4 modulates embryonic stem cellpluripotency and early embryonic development by the transcriptionalregulation of Pou5f1. 2006 Nature Cell Biology, 2006 Oct;8(10): 1114.
4. Lai R, Lefresne SV, Franko B, Hui D, Hanson J, Mirza I, Mansoor A,Amin HM, Ma Y. Immunoglobin Vh somatic hypermutation in mantle celllymphoma- mutated genotype correlates with better clinical outcome 2006Modern Pathology 2006 Nov;19(11):1498-505.
5. Wei C, Nikki Kong, Ma Y, N, Yang J, Amin HM, Lai R and L Chai.Expression analysis of a novel oncogene, SALL4, in lymphoma, multiplemyeloma, and acute lymphoblastic leukemia. 2006 Modern Pathology, 2006 Dec;19(12):1585-92.
6. Yang J, Chai L, Liu F, Flink L,Pei L, Siberstain L, Amin, HM, Ward D,and Ma Y. Bmi-1 is a SALL4 Target Gene for SALL4 in Hematopoietic andLeukemic Cells. 2007, Proc. Natl. Acad. Sci. USA. 2007;104:10494-10499
Current Federal Grants:
1. NIH/K08/Principle Investigator
2. NIH/P20/subcontract, Project leader (Principle Investigator)
3. NIH/R01/Principle Investigator
4. VA Merit Award/Principle Investigator
Others
5. Birth Mark Foundation
6. ASH FELLOWSHIP Award (to Jianchang Yang)
Contact
老板现在急需要一名熟练骨髓获取及移植的博士后，最好能作小鼠肝脏或脾脏的细胞移植。给H1B签证，能在2个月后来美。
请将CV发至dxu@nvcancer.org.
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