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Linda Resar, M.D.

Associate Professor of Medicine,
Oncology & Pediatrics
 

Contact Information:

To Make an Appointment: 

New Patients

410-955-3142

Return Patients

410-955-3142

Administrative Office:

410-614-0167

Email  

lresar@jhmi.edu


 

Dr. Linda M.S. Resar

 

 

 

 

 

 

Clinical/Academic Interests
The molecular mechanisms leading to cancer, blood diseases in young adults, sickle cell anemia and other hemoglobinopathies, hemophilia and other coagulopathies.

   

  

Academic Positions
1986 - 1989

Internship and Residency in Pediatrics,
The Johns Hopkins University
School of Medicine,
Baltimore, Maryland

1989 - 1992

Hematology Oncology Fellowship, The Johns Hopkins University
School of Medicine,
Baltimore, Maryland

1992 - 1993

Instructor in Pediatrics, The Johns Hopkins University
School of Medicine,Baltimore,Maryland

1993 - 2001

Assistant Professor in Pediatrics, The Johns Hopkins University
School of Medicine, Baltimore, Maryland

1994 - 2001

Assistant Professor in Oncology, The Johns Hopkins University
School of Medicine,Baltimore,Maryland

2000 – Present

Adjunct Investigator, Pediatric Oncology Branch,
The National Cancer Institute,
National Institutes of Health

2001 - PresentAssociate Professor in Pediatrics & Oncology, The Johns Hopkins University School of Medicine, Baltimore, Maryland
2004 – Present

Associate Professor of Medicine, The Johns Hopkins University
School of Medicine, Baltimore, Maryland



 

 

 

 

 

 

 

 

 

Selected Publications

  • Resar LMS, Oski FA.  Cold water exposure and vaso-occlusive crises in sickle cell disease.  J Pediatr. 1991, 118:407-409.

  • Resar LMS, Dolde C, Barrett JF, Dang CV.  B-Myc inhibits neoplastic transformation and transcriptional activation by c-Myc. Mol Cell Biol. 1993, 13:1130-1136. 

  • Resar LMS, Phillips PC, Kastan MB, Leventhal BG, Civin CI, Bowman PW.  Acute neurotoxicity after intrathecal cytosine arabinoside in 2 adolescents with acute lymphoblastic leukemia of B-cell type. Cancer. 1993, 71:117-123. 

  • Wood LJ, Mukherjee M, Dolde CE, Xu Y, Bunton T, Maher J, Williams JB, Resar LMS.   HMG-I/Y: A new c-Myc target gene and potential human oncogene. Mol Cell Biol. 2000, 20:5490-5502.  (Cited in Science STRIKE publication for papers of significance)

  • Wood LJ, Maher J, Bunton TE, Resar LMS. The oncogenic properties of the HMG-I gene family. Cancer Res. 2000, 60:4256-4261.

  • Dolde CE, Mukherjee M, Cho C, Resar LMS.  The role of HMG-I/Y in the human breast cancer. Breast Cancer Res Treat. 2002, 71:181-191.

  • Resar LMS, Fitzpatrick LK, Friedmann AM, Brusilow SW, Dover GJ.  Induction of fetal hemoglobin synthesis in children with sickle cell anemia on oral sodium phenylbutyrate. J Pediatr Hematol Oncol. 2002, 24:737-741.

  • Dhar A, Hu J, Reeves R, Resar L, Colburn N. Dominant negative c-Jun (TAM67) target genes: HMGA1 is required for tumor promoter-induced transformation. Oncogene 2004, 23:4466-4476.

  • Xu Y, Sumter Felder T, Bhattacharya R, Tesfaye A, Wood, LJ, Fuchs E, Huso D, Resar LMS. The HMG-I oncogene causes highly penetrant, metastatic lymphoid malignancy in transgenic mice and is overexpressed in human lymphoid malignancy. Cancer Res. 2004, 64:3371-3375.

Research Interests
Dr. Resar’s laboratory is directed at understanding the molecular mechanisms involved in cancer.  Her research has focused on the HMG-I/Y gene family, which is widely overexpressed in human cancers.  Dr. Resar’s work established that these genes function as oncogenes in vivo.  Her laboratory recently developed transgenic mice overexpressing HMG-I and all mice develop aggressive lymphoid malignancy similar to leukemia and lymphoma in humans.  Her studies also demonstrate that this gene is overexpressed in human lymphoid and other malignancies, indicating that this mouse model is relevant to human tumors.  Translational studies are underway to determine if overexpression of this gene is a marker for more aggressive cancer in humans.  Studies are also ongoing to identify the molecular pathways important in cancers with overexpression of HMG-I/Y genes.  The long-term goal is to develop more rational therapies that interfere with HMG-I/Y function in neoplastic transformation.  Because increased HMG-I/Y expression occurs in a wide range of aggressive human cancers, these studies will be relevant to human cancer arising from diverse tissues.

Education:
1979 - 1983B.S., Medical Sciences, University of Wisconsin, Milwaukee, Wisconsin
1982 - 1986M.D., Medical College of Wisconsin, Milwaukee, Wisconsin

 

 

 
 
 
 
 

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