Yupo Ma M.D., M.S., Ph.D
CURRICULUM VITAE
PROFESSIONAL EXPERIENCE:
12/05 to Present
Adjunct Professor
UNLV Dental School
Las Vegas, NV
05/05 to Present
Nevada Cancer Institute
Physician/
Dept. of Pathology
Chief of Hematopathology Las Vegas NV
05/05 to Present
Physician/
Director for Clinical Lab
Nevada Cancer Institute
Dept. of Pathology
Las Vegas NV
05/05 to Present
Physician/
Director for Clinical Lab
Quest Diagnostics at Nevada Cancer Institute
Las Vegas NV
12/05 to Present
Multiple Academic Centers for Ontak Clinical Trial
Central Pathology Reviewer for T-cell Lymphomas (centers include Ohio State,
Hopkins, Emory, Penn, Texas A&M).
07/02- 05/05
University of Arkansas for Medical Sciences
Physician/Asst Professor Department of Pathology
Director of Flow Cytometry Hematopathologist
Hematopathologist
Little Rock, AR
EDUCATION:
07/01 to 06/02
Fellowship
MD Anderson Cancer Center
Houston TX
Hematopathology
07/97 to 06/01
Residency
Brown University
Providence RI
Pathology
Chief Resident 2000-2001
01/93 to 06/97
Postdoctoral Fellowship
Harvard Medical School
Boston MA
Pathology
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12/88 to 12/92
Ph.D.
University of South Alabama College of Medicine
Mobile AL
Anatomy
09/89 to 11/88
Masters of Science
University of Washington
Seattle WA,
Pathobiology
09/85 to 08/86
Internship (rotating)
Jinan University, Affiliated Hospital
Guangzhou, People's Republic of China
09/80 to 08/86
Doctor of Medicine
Jinan University College of Medicine
P.R. China
LANGUAGES SPOKEN:
Chinese and English
CITIZENSHIP:
U.S. Citizen
SOCIETY MEMBERSHIPS:

The College of American Pathology
AWARDS:
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Best Chinese Physician in the USA (2005)
NIH Career Development Award (2003-2008)
Principle Investigator of Brown University (1999-2001)
NIH Postdoctoral Research Fellowship (1991-1992)
Hospital Appointments:
 University of Arkansas for Medical Science (UAMS), 2002-2005
 Arkansas Children Hospital, Little Rock, 20002-2005
 Nevada Cancer Institute, Las Vegas, 2005-present
Licensure of Physician:
 Arkansas State, 2002-present
 Nevada State, 2005-present
 Nevada State, Licensed laboratory Director, 2005-present
Teaching Assignments:
 University of Arkansas for Medical Sciences (UAMS), 2002-2005
Resident and fellow teaching--leukemia and lymphoma
 Summer Student Research Advisor: Amalin, Kieber-emmons, 2004
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Postdoctoral Research Advisor: Drs. Jianchang Yang, Qianohua
Kang, Jun Qu and Fang Liu.
Clinical Hematopathology Fellow Advisor: Marwan Yared
Hemtaology-Oncology Grand Round Committee: 2002-2005

UNLV Dental School, Las Vegas, 2005 ( 5 hour lectures)
Medical student teaching----Leukemia and lymphoma

UNLV Dental School Student, Las Vegas: Matthew Mizukawa working
for a research project
Academic Services:
 University of Arkansas for Medical Sciences:
Medical Student Interview Committee, 2004
Pathology Resident Interview Committee, 2003-2005
Hematopathology Fellowship Committee, 2002-2005
 Nevada Cancer Institute:
Nevada Cancer Institute Animal Resources Advisory Committee, 2005present
 Clinical Trial Reviewing Committee at Nevada Cancer Institute,
2005-present
US PATENTS:
1. “Diagnosing and Treating Cancer Cells Using Sal2 ” ( Filed through
Harvard Medical School)
2. “Targeting of SALL4 for the treatment and diagnosis of proliferative
disorders associated with myelodysplastic syndrome (MDS)” (Filed
through NVCI)
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RESEARCH SUPPORT:
Inactive Grant:
1. NIH Research Fellowship
Ongoing Grants:
2. Role of Hsal 2 in Ovarian Cancer
NIH/K08/Principle Investigator
8/1/03-7/30/08, 75% effort, $135, 000/year
The overall research goal is to examine the functional roles and underlying
mechanisms of Hsal2 isoforms, as well as gene regulation, and to identify
upstream and downstream targets. Aim 1 will determine the role of altered Hsal2
isoform expression in ovarian cancer initiation and progression by studying the
effect of Hsal2 isoform overexpression on tumorigenicity, identifying target genes
that are subordinate to Hsal2 isoform expression, and characterizing upstream
regulators of Hsal2 isoforms. Aim 2 will determine the underlying mechanism of
altered Hsal2 isoform expression in ovarian cancer by delineating the use of
Hsal2 P1 and P2 promoters, measuring the methylation status of CpG islands in
Hsal2 isoform promoters, and correlating this with their expression in ovarian
cancer.
3. Mouse Model of Duane Radial Ray Syndrome (Okihiro Syndrome)
Tobacco Fund/Principle Investigator
7/1/03-6/30/05, $70, 000 totally
The overall research goal is to investigate the possibility of that SALL4 gene is a
tumor suppressor gene in a knockout mouse model. Specific Aim I: Generate null
and conditional mutant alleles of SALL4 by Cre/LoxP-mediated gene targeting.
Specific Aim II: Characterize developmental defects in the mutant mice. We
plan to use this mouse model to further our understanding of how the
malformations seen in this Duane radial ray syndrome develop and to test if
SALL 4 acts as a tumor suppressor gene like SALL2
4. Functional Analysis of Hsal2, A Novel Tumor Suppressor Associated
with p21Cip1/Waf in Human Cancer
American Cancer Society Institutional Research Grant /Principle Investigator
1/1/04-12/30/05, $20,000 totally
The overall research goal is to test our hypothesis that expression of Hsal2
protects against ovarian cancer initiation whereas loss of Hsal2 predisposes to
ovarian cancer, with subsequent genetic events promoting progression to overt
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cancer. We plan to demonstrate that (1) The loss of Hsal2 expression is present
as an early event in ovarian cancer (borderline tumor), with expression levels of
Hsal2 decreased slightly and decreased even more so in invasive serous
carcinoma; the reduced expression of Hsal 2 correlates with the loss of P21, and
(2) over-expressing Hsal2 isoforms in ovarian cancer cell lines induces
apoptosis, decreases colony formation in soft agar, and decreases tumorigenesis
in nude mice; and the effects of Hsal 2 tumor suppression occur through upregulation of p21.
5. Growth Control in Multiple Myeloma
NIH/P01/Core D, Cell Analysis and Sample Banking, Co-investigator
(collaboration with University of Arkansas)
6/30/04-7/1/09, 10% effort, $400,000/year
The Cell Analysis and Sample Banking Core are to provide support to the clinical
and basic projects by centralizing common procedures. These include sample
acquisition, characterization, and distribution and banking; cell sorting; analytical
flow cytometry; tissue microarrays; histology and Immunohistochemistry.
6. Functional Analysis of SALL4 in in Hematopoietic Differentiation and
Leukemogenesis
NIH/P20/subcontract, Project leader (Principle Investigator)
7/1/06-6/30/08, 20% effort, $200,000/year
The goal is to further our understanding of the mechanisms involved in
leukemogenesis by examining SALL4, a newly identified transcriptional repressor
in leukemia. Specific Aim I: Determine molecular mechanism(s) of SALL4
isoforms in the initiation and/or the progression of AML; Specific Aim II:
Determine how SALL4 isoforms affect signaling pathways, which initiate or cause
progression of AML
7. Development of novel vascular cell lines and xenograft mouse model for
infantile hemangioma
Vascular and Birthmarks Institute of New York at Roosevelt Hospital. 0%
effort,
2005, $40,000 (Co-principle Investigator wit Dr. Fink).
Pending Grants
1. Nevada Bioengineering and Bioinformatics Summer Institutes.
NSF summer student grant, 2005, 0% effort. Co-PI.
A multidisciplinary group of scientists from the University of Nevada Las Vegas
(UNLV) Colleges of Science and Engineering have joined with investigators from
the Nevada Cancer Institute (NCI) to establish a Nevada Bioengineering and
Bioinformatics Summer Institutes (NBBSI) to train the next generation of
multidisciplinary investigators in these fields (summer student working in a
research lab).
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PUBLICATIONS:
M.S. Thesis:
Species-specific Monoclonal Antibodies against Surface Membrane
of Mycoplasma genitalium, 1989.
Ph.D. Thesis: Primary Structure of Murine Brain Spectrin ( Fodrin), 1993.
Original Articles
1. Zimmer, WE, Y. Ma, Goodman, SR. Tissue Distribution of Brain -Spectrin
mRNAs. Brain. Res. Bul. 1991;27:187-193.
2. Bloom, ML, Lee BR, Birkenmeier C, Ma Y, Zimmer WE, Goodman SR, Eicher
EM, Baker JE. The Gene for Brain Beta-Spectrin Isoform (235) Maps to
Mouse Chromosome 11 and Defines a New Region of Synteny to Human
Chromosome 2. Mammal. Genome 1992;3:293-295.
3. Ma, Y, Zimmer WE, Riderer BM, Goodman SR. The Complete Amino Acid
Sequence for Brain Spectrin ( Fodrin): Relationship to Globin Sequences.
Mol. Brain. Res. 1993;18:87-99.
4. Zimmer, WE, Ma Y, Zagon IS, Goodman SR. Developmental Expression of
Brain -Spectrin Isoform Messenger RNA. Brain. Res. 1992;594:75-83.
5. Warren, JC, Murdock, GL, Ma Y, Goodman, SR, Zimmer, WE. Molecular
Cloning of Testicular 20 -hydroxysteroid Dehydrogenase: Identity with
Aldose Reductase. Biochemistry. 1993;32:1401-1406.
6. Lengeling A, Zimmer WE, Goodman SR, Ma Y, Bloom ML, Bruneau G,
Krieger M, Thibault J, Kaupmann K, Jockusch H. Exclusion of Tow Candidate
Gene, Spnb-2 and Dcd, for the Wobbler Spinal Muscular Atrophy gene on
Proximal Mouse Chromosome 11. Mammal.Genome. 1994;5:163-166.
7. Clark MB, Ma Y, Bloom ML, Barker JE, Zagon IS, Zimmer WE, Goodman SR.
Brain Alpha Erythroid spectrin: Identification, Compartmentalization, and Beta
Spectrin Associations. Brain. Res. 1994;663:223-236.
8. Lukacher AE, Ma Y, Carroll JP, Abromson-Leeman, SR, Laning JC, Dorf ME,
Benjamin TL. Susceptibility to Tumors Induced by Polyoma Virus is Conferred
by Endogenous Mouse Mammary Tumor Virus Superantigen. J. Exp. Med.
1995;181:1683-1692.
9. Ma Y, Gozman A, Chai L, Steinhoff MM, Hansen K, Maizel AL. Hsal 1 is
Related to Kidney and Gonad Development and is Expressed in Wilms
Tumor. Pediatri Nephron. 2001;16:701-709.
10. Ma Y, Li D, Chai L, Maizel AL. Cloning and Characterization of Two
Promoters for Human Hsal 2 Gene and Their Transcriptional Repression by
the Wilms Tumor Suppressor Gene Product. J. Biol. Chem.
2001;276:48223-48230.
11. Li D, Dower K, Ma Y, Benjamin TL. A ‘Tumor Host Range’ Selection
procedure identifies p150 Sal 2 as a target of polyoma large T antigen. Proc.
Natl. Acad. Sci. USA. 2001 ;98:14619-14624.
12. Ma Y, Chai L, Cortez SC, Sopa EG, Steinhoff MM, Ford D, Morgan J. Maizel
AL. SALL1 Expression in the Human Pituitary-Adrenal/Gonadal Axis. J.
Endocrinol. 2002;173 (3):437-48.
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13. Amin HM, Medeiros J, Ma Y, McDonnel TJ, Feretzaki M, Levataki V,
Rassidakis GZ, O’Connonr SL, Lai R. Inhibition of JAK3 induces Apoptosis
and Decreases Anaplastic lLmphoma Kinase Activity in Anaplastic Large Cell
Lymphoma. Oncogene. 2003; 22:5399-407
14. Tian E, Zhang F, Walker R, Rasmussen E, Ma Y, Barlogie B and
Shaughnessy JD. The Role of the Wnt/-catenin Signaling Antagonist DKK1
in Development of Osteolytic Lesions in Multiple Myeloma. New Engl J.
MED. 2003, Dec 25; 349(26): 2483-94.
15. Amin HM, McDonnell TJ, Ma Y, Lin Q, Fujio Y, Kunisada K, Leventaki V, Das
P, Rassidakis GZ, Cutler C, Jeffrey Medeiros L, Lai R. Selective inhibition of
STAT3 induces apoptosis and G(1) cell cycle arrest in ALK-positive
anaplastic large cell lymphoma. Oncogene, 2004, June 7, 1-9
16. Li D, Tan Y, Mok S, Ma Y and Benjamin TL. p150Sal2 Is a p53-Independent
Regulator of p21WAF1/CIP . Mol. Cell. Bio . 2004. 24:3885-93.
17. Ma Y, Mansour A, Bekele BN, Zhou X, Keating MJ, O'Brien S, Giles FJ,
Albitar M. The clinical significance of large cells in bone marrow in patients
with chronic lymphocytic leukemia. 2004. Cancer. 100:2167-75.
18. CHAI L, YANG J, DI C, CUI W, LAI R, AND MA Y. Transcriptional activation of the
SALL1 by the human SIX1 domain. 2006 (Submitted to JBC, under revision)
19. Ma Y, Kang Q, Di C, Lai R, Theus J, and Chai L. Novel splicing variant of
Okihiro syndrome gene and its deregulation in transgenic mice associated
with cystic kidney and hydrocephulas.. 2006 (submitted).
20. 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 in acute
myeloid leukemia (AML) and is sufficient to induce AML in transgenic mice.
2006 (submitted to nature medicine)
21, Wei C, . Ma Y, Nikki Kong N, Yang J, Amin HM, Lai R
and L Chai. 2006. Expression analysis of a novel oncogene, SALL4, in
lymphoma, multiple myeloma, and acute lymphoblastic leukemia ( submitted
to American of Surgical Pathology)
Published Abstracts :
1. Ma Y, Zimmer WE, Goodman SR. Cloning and Nucleotide Sequence of
Mouse Brain -Spectrin cDNA. J. Cell. Biol. 1990;14F:28.
2. Zimmer WE, Melton CA, Ma Y, Zagon IS, Goodman SR. Differential
Regulation of  and  Spectrin mRNAs during Mouse Brain Development. J.
Cell. Bio 1990;11:505a.
3. Ma Y, Zimmer WE, Goodman SR. Cloning and Nucleotide Sequence of
Mouse Brain -Spectrin cDNA. J. Ala. Acad. of Sci. 1990;61:202.
4. Ma Y, Zimmer WE, Goodman SR. Cloning and Sequence of cDNAs
encoding a Mouse Brain -Spectrin. J. Cell. Biol. 1990;11:47a.
5. Ma Y, Zimmer WE, Rederer BM, Goodman SR. Primary Structure of Brain
Spectrin ( Fordrin). J. Ala. Acad. of Sci.1992;63:67.
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6. Ma Y, Zimmer WE, Rederer BM, Goodman SR. The Complete Sequence for
Brain -spectrin Indicates a Relationship with Heme Binding Proteins
(Globins). Society for Neuroscience. 1992;18:69.
7. Ma Y, Zimmer WE, Rederer BM, Goodman SR. The Complete Amino Acid
Sequence of Nonerythroid  Spectrin ( Fodrin): Indication of a Heme Binding
Domain. Society for Neuroscience 1992;3:264a.
8. Ma Y, Cho S, Riney C, Benjamin TL. 1997. Construction and Characterization
of a Polyoma Virus Mutant that Fails to Express Small T. Society for Tumor
Virus, Pg 16.
9. Ma Y, Schwartz S, Maizel AL, Singer DB. Townes-Brocks Syndrome: Hsal 1
Gene Mutation and New Manifestations. (In press in IAP Meeting, March
1998).
10. Ma Y, Gozman A, Li C, Steinhoff MM, Hansen K, Maizel AL. Identification of
the Townes-Brocks Syndrome Gene Product and Its Involvement of Kidney
and Gonad Development. Mod. Patho. 2000;13:106A.
11. Ma Y, Chai L, Stancu M, Steinhoff MM, Taylor W, Maizel AL. The TownesBrocks Syndrome Gene Product is Expressed at Multiple Levels of the
Reproductive Axis and Sex Hormone-producing Tumors. Mod. Patho.
2000;13:73.
12. Ma Y, Mazel AL, Chai L, Taylor W, Stopa EG, Cortex S. Presence of Hsal 1,
A Downstream Component of Hedgehog/TGF- Signals in Human Pituitary,
Journal of Neuropathology and Experimental Neurology, 2000;59:452.
13. Chai, L, Ma Y, Krause D. Impairment of Myelopoiesis in Sall2-null mice.
Journal of the American Society of Hematology, 2003,102:334A.
14. Ferguson F, Oza K and Ma Y. Comparison of Syndecan-1 (CD138), PAS,
and H&E staining in Initial Evaluation of Monoclonal Gammopathies. Modern
Pathology, 2004, 17:247A.
15. Lee J, Ma Y, Franko B, Song X, Rassidakis, Amin H and Lai R. Expression a
SHP1 slicing Variant with Dominant Negative Effects in Malignant
Hematopoetic Neoplasm. Modern Pathology, 2004, 17:256A.
16. Theus J, Fender B, Waldron J, Zhan F, Shaughnessy and Ma Y. Dkk-1
Expression in Normal Lymphoid tissue and in Multiple Myelomas: Over
Expression of Dkk-1in Low and Medium Grade with Loss of Expression with
disease Progression. Modern Pathology, 2004,17: 273A
17. Huang Q, Zhang H, Ma Y, Schichman S, Scott M, Doglio L, Iannacone P,
Weiss L, and Fan CY. Development of Essential Thrombocythemia-Like
Myeloproliferative Disorder in Transgenic Mice.
Overexpressing a Human 8-Oxoguanine DNA-Glycosylase Gene. Blood, Nov
2004; 104: 791.
18. Chai L, Cui W, Yang J, Di C, Amin H, and Ma Y. SALL4, a novel oncogene
induces myelodysplastic syndrome and acute myeloid leukemia via Wnt/βcatenin pathway. Blood Nov. 2005; 106: 397a.
19. Rai R, Lefresne SV, Franko BC, Shi X, Hui D, Mansoor A, Amin HM, Ma Y.
Somatic Hypermatation of the Immunoglobulin Heavy Chain (IgH) Gene in
Mantle Cell Lymphoma. Laboratory Investigation, 2006, 86:235A.
Page 8 of 9
Research Interests in the laboratory
Dr. Ma’s lab focuses on the role of SALL4 in Human Development,
Leukemogenesis, and Hematopoiesis.
The SALL gene family is the mammalian homologue of Drosophila gene Spalt
(sal). In Drosophila, sal mutation can lead to the incomplete separation of the
head and trunk of the fly. In the human, heterogenous mutation of SALL1 causes
Townes-Brock Syndrome with renal, cardiac, genital malformation.
Heterogenous mutation of SALL4 in human is associated with Okihiro Syndrome
with limitation of eye abduction, deafness and digit malformation. SALL4 is able
to bind to Oct 4 and Nanog. SALL4 plays an important role in the maintenance of
ES cell pluripotent properties and self renewal. The loss of expression results in
ES cell differentiation.
We have demonstrated that SALL4 is constitutively expressed in acute myeloid
leukemias (AML) and fails to turn off in nearly all human AMLs. A fundamental
unanswered question: is constitutive expression of SALL4 sufficient to induce
AML? In addition, what mechanisms of SALL4 induce AML? How does SALL4
promoter leukemic stem cell self renewal?
We have chosen transgenic mice as a model system to approach these
questions. This should allow us to test directly leukemogenic potential of
constitutive expression of SALL4 in a murine model. Transgenic mice
overexpressing SALL4 develop hematopoietic disorders including
myelodysplastic-like symptoms and subsequently acute myeloid leukemia. The
constitutive expression of SALL4 is causal to the leukemic phenotype and SALL4
acts as an oncogene, probably through interaction with the Wnt/β-catenin
pathway in the leukemogenesis. Our murine model should provide a useful
platform to analyze the effect of SALL4 on hematopoiesis and its potential
cooperation with Wnt/β-catenin pathway in the pathogenesis of leukemia stem
cells.
A parallel project involves an investigation of the SALL4 function in development
and hematopoiesis. We are creating a loss of function model for SALL4 using
conventional and conditional knockout approaches. In characterizing the
phenotype of SALL4 deficient mice, we are focusing on the role of SALL4 in
regulating hematopoiesis and hematopoietic stem cell function.
.
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