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Linda M. Smith Resar

Linda M. Smith Resar, MD

Hematologic Malignancy

Accepting New Patients
Johns Hopkins Affiliations:
  • Johns Hopkins School of Medicine Faculty

Languages

  • French
  • English

14 Insurances Accepted

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Gender

Female

About Linda M. Smith Resar

Primary Academic Title

Professor of Medicine

Background

Dr. Resar's studies molecular mechanisms leading to cancer, blood diseases, sickle cell anemia, hemophilia and other coagulopathies. Her research focuses on the HMG-I/Y gene family, which is widely overexpressed and functions as oncogenes in human cancers. Her laboratory recently developed transgenic mice overexpressing HMG-I; 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. Translational studies are underway to determine if overexpression of HMG-I is a marker for more aggressive human cancers. Resar's long-term goal is to develop more rational therapies that interfere with HMG-I/Y function in neoplastic transformation.

Centers and Institutes

Cell Engineering, Institute for

Additional Academic Titles

Professor of Pathology, Professor of Oncology

Research Interests

Basic research focus is hematologic malignancy and molecular mechanisms that lead to cancer, Clinical research interests include sickle cell anemia.

Lab Website

Linda Smith-Resar Lab - Lab Website

  • The Linda Smith-Resar Lab primarily investigates hematologic malignancy and molecular mechanisms that lead to cancer as well as sickle cell anemia. Recent studies suggest that education is an important and effective component of a patient blood management program and that computerized provider order entry algorithms may serve to maintain compliance with evidence-based transfusion guidelines. Another recent study indicated that colonic epithelial cells undergo metabolic reprogramming during their evolution to colorectal cancer, and the distinct metabolites could serve as diagnostic tools or potential targets in therapy or primary prevention.

Research Summary

Dr. Resar's studies molecular mechanisms leading to cancer, blood diseases, sickle cell anemia, hemophilia and other coagulopathies. Her research focuses on the HMG-I/Y gene family, which is widely overexpressed and functions as oncogenes in human cancers. Her laboratory recently developed transgenic mice overexpressing HMG-I; 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. Translational studies are underway to determine if overexpression of HMG-I is a marker for more aggressive human cancers. Resar's long-term goal is to develop more rational therapies that interfere with HMG-I/Y function in neoplastic transformation.

Selected Publications

  • Resar, L.M. The high mobility group A1 gene: transforming inflammatory signals into cancer? Cancer Res. 2010 Jan 15;70(2):436-439

  • Di Cello, F.; Hillion, J.; Hristov, A.; Wood, L.J.; Mukherjee, M.; Schuldenfrei, A.; Kowalski, J.; Bhattacharya, R.; Ashfaq, R.; Resar, L.M. HMGA2 participates in transformation in human lung cancer. Mol Cancer Res. 2008 May;6(5):743-750

  • Di Cello, F.; Hillion, J.; Kowalski, J.; Ronnett, B.M.; Aderinto, A.; Huso, D.L.; Resar, L.M. Cyclooxygenase inhibitors block uterine tumorigenesis in HMGA1a transgenic mice and human xenografts. Mol Cancer Ther. 2008 Jul;7(7):2090-2095

  • Hillion, J.; Dhara, S.; Sumter, T.F.; Mukherjee, M.; Di Cello, F.; Belton, A.; Turkson, J.; Jaganathan, S.; Cheng, L.; Ye, Z.; Jove, R.; Aplan, P.; Lin, Y.W.; Wertzler, K.; Reeves, R.; Elbahlouh, O.; Kowalski, J.; Bhattacharya, R.; Resar, L.M. The high-mobility group A1a/signal transducer and activator of transcription-3 axis: an Achilles heel for hematopoietic malignancies Cancer Res. 2008 Dec 15;68(24):10121-10127

  • Hillion, J.; Wood, L.J.; Mukherjee, M.; Bhattacharya, R.; Di Cello, F.; Kowalski, J.; Elbahloul, O.; Segal, J.; Poirier, J.; Rudin, C.M.; Dhara, S.; Belton, A.; Joseph, B.; Zucker, S.; Resar, L.M. Upregulation of MMP-2 by HMGA1 promotes transformation in undifferentiated, large-cell lung cancer. Mol Cancer Res. 2009 Nov;7(11):1803-1812

  • Hines, P.; Dover, G.J.; Resar, L.M. Pulsed-dosing with oral sodium phenylbutyrate increases hemoglobin F in a patient with sickle cell anemia. Pediatr Blood Cancer. 2008 Feb;50(2):357-359

  • Hristov, A.C.; Cope, L.; Di Cello, F.; Reyes, M.D.; Singh, M.; Hillion, J.A.; Belton, A.; Joseph, B.; Schuldenfrei, A.; Iacobuzio-Donahue, C.A.; Maitra, A.; Resar, L.M. HMGA1 correlates with advanced tumor grade and decreased survival in pancreatic ductal adenocarcinoma. Mod Pathol. 2010 Jan;23(1):98-104

  • Hristov, A.C.; Cope, L.; Reyes, M.D.; Singh, M.; Iacobuzio-Donahue, C.; Maitra, A.; Resar, L.M. HMGA2 protein expression correlates with lymph node metastasis and increased tumor grade in pancreatic ductal adenocarcinoma. Mod Pathol. 2009 Jan;22(1):43-49

  • Karp, J.E.; Smith, B.D.; Resar, L.S.; Greer, J.M.; Blackford, A.; Zhao, M.; Moton-Nelson, D.; Alino, K.; Levis, M.J.; Gore, S.D.; Joseph, B.; Carraway, H.; McDevitt, M.A.; Bagain, L.; Mackey, K.; Briel, J.; Doyle, L.A.; Wright, J.J.; Rudek, M.A. Phase I and pharmacokinetic study of bolus-infusion flavopiridol followed by cytosine arabinoside and mitoxantrone for acute leukemias. Blood. 2011 Jan 14;Epub 1/18/11

  • Mazaheri, P.; Nadkarni, G.; Lowe, E.; Hines, P.; Vuica, M.; Griffin, M.; Resar, L.M. Ghosal hematodiaphyseal dysplasia: a rare cause of a myelophthisic anemia. Pediatr Blood Cancer. 2010 Dec 1;55(6):1187-1190

  • Savage, W.J.; DeRusso, P.A.; Resar, L.M.; Chen, A.R.; Higman, M.A.; Loeb, D.M.; Jones, R.J.; Brodsky, R.A. Treatment of hepatitis-associated aplastic anemia with high-dose cyclophosphamide. Pediatr Blood Cancer. 2007 Dec;49(7):947-951

  • Tesfaye, A.; Di Cello, F.; Hillion, J.; Ronnett, B.M.; Elbahloul, O.; Ashfaq, R.; Dhara, S.; Prochownik, E.; Tworkoski, K.; Reeves, R.; Roden, R.; Ellenson, L.H.; Huso, D.L.; Resar, L.M. The high-mobility group A1 gene up-regulates cyclooxygenase 2 expression in uterine tumorigenesis. Cancer Res. 2007 May 1;67(9):3998-4004

Locations

  1. Johns Hopkins Outpatient Center
    • 601 North Caroline Street, Floor 7, Baltimore, MD 21287

    Expertise

    Education

    Johns Hopkins University School of Medicine

    Fellowship, Pediatrics, 1992

    Johns Hopkins University School of Medicine

    Residency, Pediatrics, 1989

    Medical College of Wisconsin

    Medical Education, MD, 1986

    Board Certifications

    Pediatric Hematology-Oncology

    American Board of Pediatrics, 1996

    Insurance

    Johns Hopkins providers accept various commercial health insurance plans. However, they may not be included in all of an insurance company's plans or offerings. This may include Exchange, Medicaid, Medicare, and specific limited benefit plans. Exceptions to participation also exist based on your employer’s benefits package and the provider's location or specialty. Please contact your insurer directly to make sure your doctor is covered by your plan. For more details, please review our Insurance Information.
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    • Aetna
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    • Johns Hopkins Health Plans
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    • Pennsylvania's Preferred Health Networks (PPHN)
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    • Private Healthcare Systems (PHCS)
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    • Veteran Affairs Community Care Network (Optum-VACCN)