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Feyruz V. Rassool

Feyruz V. Rassool Ph.D.

Academic Title: Associate Professor
Primary Appointment: Radiation Oncology
Location: BRB 8-037
Phone: (410) 706-5337
Fax: (410) 706-6666
Lab: (410) 706-5338

Personal History:


BSc Hons, Human Genetics
University College London , June, 1983.

Ph.D., Biological Sciences
University of London , Jan, 1990.
Royal Postgraduate Medical School
Title: Human Leukemia and the BCR Gene (Supervisor: Prof. John Goldman)


Postdoctoral Fellow, Section of Hematology/Oncology, University of Chicago
10/89-6/94. (Mentors: Professors Michelle Le Beau and Timothy McKeithan)

Research Associate, Section of Hematology/Oncology, University of Chicago
7/94 –5/96

Research Associate (Assistant Prof.), Section of Hematology/Oncology, University of Chicago
5/96- 4/98

Lecturer, Guy’s, King’s, Thomas’s School of Medicine, London, UK.,

Head of Genomic Instability Laboratory, 5/98-1/05

Associate Professor, University of Maryland School of Medicine, Baltimore, US , 1/05-present

Research Interests:

Chromosomal instability is a characteristic feature of myeloid malignancies and the preleukemic syndromes that predispose to these leukemias. My primary research interest is to elucidate the molecular basis for genomic instability in these diseases. We have accrued evidence that genomic instability in myeloid malignancies may be driven by a combination of ongoing constitutive DNA damage coupled with increased activity of the error-prone non homologous end-joining (NHEJ) pathway which results in improper repair of double strand breaks (DSB). This cycle of DNA damage and misrepair is driven by endogenous reactive oxygen species production, a likely source for genomic instability in myeloid leukemias and premalignant syndromes that introduces genomic changes into DNA and drives disease progression.

My group is actively pursuing the following goals:

(1) To identify and characterize the protein complexes pre- and -post DNA damage at DSB in inherited preleukemic syndromes and acute myeloid leukemias.
(2) To determine the signal transduction pathways important in the creation of oxygen radicals in myeloid malignancies
(3) To determine whether error-prone NHEJ is associated with acquisition of
chromosomal abnormalities in models for myeloid leukemic progression in i) mice and ii) human preleukemic syndromes.
(4) To determine the role histone deacetylase inhibitors and demethylating agents in abnormal DNA damage in cancer.

Clinical Speciality:

Myeloid leukemias: CML and AML

Lab Techniques and Equipment:

* Immunostaining for DNA damage and repair proteins
* General molecular biology
* General biochemistry techniques
* Functional DNA repair assays

* General equipment for molecular biology, biochemistry and tissue culture techniques
* Q-PCR machine
* Fluorescence microscope and CCD camera
* Cytospin machine
* ELISA reading device

Grants and Contracts:


2006-2010: Research Grant, LLS Translational Award. "The Role of WRN/Ligase III/XRCC1 in Genomic Instability in CML", Principal Investigator: Feyruz Rassool.
2007-2009: Research Grant, DOD. "The Role of 'Back-up Repair' in Genomic Instability in CML", Principal Investigator: Feyruz Rassool.
2007-2011: Grant Project, NIH. "Mechanisms of Combined Epigenetic Therapy in Myeloid Malignancies", Principal Investigator: Steve Gore (Johns Hopkins University), Role: Co-Investigator.
2008-2011: Research Grant, TEDCO (Maryland). "Dissecting the Genetic and Epigenetic Origins Underlying Tumorigenic Potential of Human Embryonic and Adult Stem Cells". Principal Investigator: Stephen Baylin, Role: Co- Principal Investigator.
2009-2012: Research Grant, V Foundation (Private Foundation). "DNA Repair Inhibitors in Leukemia", Principal Investigator: Feyruz Rassool.


2010-2015: Research Grant, NIH. "The Role of ROS in FLT3/ITD Leukemia", Principal Investigator: Feyruz Rassool and Donald Small (Johns Hopkins University)


Recent Publications

Gaymes TJ, North PS, Brady N, Hickson ID, Mufti GJ, Rassool FV.  Increased error-prone non homologous DNA end-joining - a proposed mechanism of chromosomal instability in Bloom's syndrome. Oncogene (2002). 21(16):2525-33.

Gaymes TJ, Mufti GJ, Rassool FV. Myeloid Leukemias have Increased Activity of the Non Homologous End-Joining Pathway and Concomitant DNA Misrepair that is Dependant on the Ku70/86 Heterodimer. Cancer Research (2002) 62, 2791-2797.

Cameron E, Mijovic A, Herman J, Baylin S, Pradhan A, Mufti GJ, and Rassool FV. P15INK4B is not mutated in adult familial myelodysplastic syndromes. Brit. J Haematology (2002) 119, 277-279.

Aktas D, Arno M, ,Mufti GJ, Rassool FV. Analysis of Chk2 in patients with myelodysplastic syndromes. Leukemia Research (2002) 26, 985-987.

Rassool FV. Double strand breaks and NHEJ pathways in leukemia. Cancer Letters (2003) 193, 1-9.

Brady N, Gaymes TJ, Cheung M, Mufti GJ, Rassool FV. Increased NHEJ Activity in Myeloid Leukemias is Associated with Ongoing or Induced DNA Damage at Sites that Recruit Key NHEJ Proteins. Cancer Research (2003) 63, 1798-1805.

Rassool FV, North PS, Mufti GJ, and Hickson ID. Constitutive DNA damage is linked to DNA replication abnormalities in Bloom’s syndrome cells. Oncogene (2003) 22, 8749-8757.

Pradhan A, Mijovic A, Mills K, Cumber P, Westwood N, Mufti GJ and Rassool FV. Differentially Expressed Genes in Adult Familial Myelodysplastic Syndromes (MDS). Leukemia (2004) 3, 449-59.

Rassool FV. Genetic rearrangements beget genomic instability. Blood 2004 104: 3424-3425.

Wei Y, Lin-Lee YC, Yang X, Dai W, Zhao S, Rassool FV, Elgart GW, Feun L, Savaraj N, Kuo MT. Molecular cloning of Chinese hamster 1q31 chromosomal fragile site DNA that is important to mdr1 gene amplification reveals a novel gene whose expression is associated with spermatocyte and adipocyte differentiation. Gene. 2006 May 10;372:44-52.

Gaymes TJ, Padua RA, Pla M, Orr S, Omidvar N, Chomienne C, Mufti GJ, Rassool FV. Histone deacetylase inhibitors (HDI) cause DNA damage in leukemia cells: a mechanism for leukemia-specific HDI-dependent apoptosis? Mol Cancer Res. 2006 Aug;4(8):563-73.

Rassool FV, Gaymes TJ, Omidvar N, Brady N, Beurlet S, Pla M, Reboul M, Lea N, Chomienne C, Thomas NSB, Mufti G, Padua RA. Reactive oxygen species, DNA damage and error-prone repair: a model for genomic instability with progression in myeloid leukemia? Cancer Res. (2007) 67, 8762-71.

Sallmyr A, Fan J, Datta K, Kim KT, Grosu D, Shapiro P, Small D, Rassool F. Internal tandem duplication of FLT3 (FLT3/ITD) induces increased ROS production, DNA damage, and misrepair: implications for poor prognosis in AML. Blood. 2008 Mar 15;111(6):3173-82. Epub 2008 Jan 11.

Sallmyr A, Fan J, Rassool FV. Genomic instability in myeloid malignancies: Increased reactive oxygen species (ROS), DNA double strand breaks (DSBs) and error-prone repair. Cancer Lett. 2008 May 6. [Epub ahead of print]

Maris Ranuncolo S, Wang L, Polo JM, Dell'oso T, Dierov J, Gaymes TJ, Rassool F, Carroll M, Melnick A. BCL6 mediated attenuation of DNA damage sensing triggers growth arrest and senescence through a 53-dependent pathway in a cell-context dependent manner. J Biol Chem. 2008 Jun 10. [Epub ahead of print]

Sallmyr A, Tomkinson AE, Rassool FV. Up-regulation of WRN and DNA ligase III{alpha} in chronic myeloid leukemia: consequences for the repair of DNA double strand breaks. Blood. 2008 Jun 4. [Epub ahead of print]