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Mariusz A. Wasik, MD

Mariusz A. Wasik, MD Physician

Professor of Pathology and Laboratory Medicine at the Hospital of the University of Pennsylvania

Dr. Wasik is a Penn Medicine employed physician.

Clinical Specialties

Specialties:

  • Pathology and Laboratory Medicine

Programs & Services:

  • Cancer
    • Bone Marrow Transplant and Stem Cell Transplant Program
    • Hematological Malignancies (Blood Cancer) Program
  • Pathology and Laboratory Medicine
    • Hematopathology
    • Immunobiology and Experimental Pathology
    • Laboratory Medicine

Board Certification:

  • Hematology, 1993
  • Pathology - Anatomic Pathology, 1991

Conditions & Treatments:

  • Blood Cancer
  • Bone Marrow and Stem Cell Transplantation
  • Bone Marrow Diseases
  • Cancer Screening and Diagnostics

Clinical Interests

Hematopathology (tissue biopsy and blood smear interpretation) including related flow cytometry immunophenotyping and molecular pathology.

Insurance Accepted

  • Aetna US Healthcare
  • Cigna
  • Cigna HealthSpring
  • Devon Health Services (Americare)
  • Gateway Health Plan
  • Geisinger Health Plan
  • HealthAmerica / HealthAssurance, a Coventry Plan
  • HealthPartners
  • HealthSmart
  • Highmark Blue Shield
  • Horizon Blue Cross Blue Shield of New Jersey
  • Humana / Choicecare
  • Independence Blue Cross (Keystone East)
  • Intergroup
  • Keystone First
  • Multiplan
  • NJ Medicaid
  • NJ Qualcare
  • Oxford Health Plan
  • PA Medicaid
  • PA Medicare
  • Preferred Care
  • Rail Road Medicare / Palmetto GBA
  • Tricare
  • United Healthcare
  • UnitedHealthcare Community Plan
  • US Family Health Plan

Education and Training

Medical School: Wroclaw Academy of Medicine
Fellowship:
Fellowship: Boston Medical Center (Formerly Boston City Hospital)
Fellowship: Dana-Farber Cancer Institute
Residency: Boston Medical Center (Formerly Boston City Hospital)
Fellowship: Beth Israel Deaconess Medical Center

Memberships

Academy of Clinical Laboratory Physicians and Scientists (1996- ), American Association for Advancement of Science (1987-88 and 1993-present) American Society for Investigative Pathology (1994- ), International Society for Cutaneous Lymphomas (1995- ), Society for Hematopathology (2000- ), University of Pennsylvania Cancer Center (1995- ), University of Pennsylvania Graduate Group in Cell and Molecular Biology, Local University of Pennsylvania Graduate Group in Immunology (1997- ), University of Pennsylvania Institute for Translational Medicine and Therapeutics (2005- present),

Affiliation

Dr. Wasik is a Penn Medicine employed physician.

Hospital Privileges:

  • Hospital of the University of Pennsylvania: Has privileges to treat patients in the hospital.
  • Penn Presbyterian Medical Center: Has privileges to treat patients in the hospital.
  • Pennsylvania Hospital: Has privileges to treat patients in the hospital.

Research

Research Interests:

Research Interests

Aberrant cell signaling and epigenetic regulation of gene expression in human lymphomas.

Research Summary

1. Role of the cytokine-signal transduction pathways and epigenetic gene silencing in pathogenesis of T-cell lymphoma.

Under this project my lab investigates the role of signals mediated through receptor for interleukin-2 (IL-2R) and functionally related cytokine receptors in malignant transformation of T lymphocytes. Part of the IL-2R, common chain ( c), is shared by receptors for several cytokines: IL-2, IL-4, IL-7, IL-9, IL-15, and IL-21. We found that cutaneous T-cell lymphoma cells display activation of the interleukin-2 receptor/cytokine common chain-associated Jak/STAT signal transduction pathway that is transient in the early stage of the lymphoma and constitutive in the late stage of the disease progression. More recently we determined that the constitutive Jak/STAT activation is due, at least in part, to the lack of expression of SHP-1 phosphatase, which normally down-regulates IL-2R/ c-mediated cell activating signals. Importantly, this work identified the mechanism underlying lack of SHP-1 expression as hypermethylation of the CpG DNA sequences within the SHP-1 promoter. This study may result in novel therapies for lymphoma based on selective inhibition of the elements of the IL-2R signal transduction pathway(s) which are preferentially utilized by malignant T cells and/or on induction of re-expression of the epigenetically-silenced SHP-1 gene. Our most recent work focuses on the molecular mechanisms of the aberrant gene silencing in the malignant lymphoid cells.

2. TOR signaling in posttransplant lymphoproliferative disorders (PTLDs) and other lymphoid malignancies.

Whereas the standard immunosuppressive agents foster development of PTLDs, the impact of novel immunosuppressive agents from the group of selective inhibitors of TOR serine/treonine kinase such as rapamycin and its derivatives including RAD remains undetermined. Our studies indicate that RAD has a strong inhibitory effect on PTLD-like and PTLD-derived B cells by suppressing their proliferation, blocking cell cycle progression and increasing apoptotic rate. In the in vivo SCID mouse xeno-transplant model, RAD markedly delayed growth or induced regression of established PTLD-related B-cell tumors. The drug completely eradicated or prevented tumor establishment in a subset of the treated mice at the doses matching the ones required to prevent graft rejection. These findings indicate that TOR inhibitors such as RAD may be effective in prevention and treatment of PTLDs and, possibly, other types of B-cell lymphoma. The molecular mechanism of this TOR inhibitor-mediated cell growth suppression is currently under investigation.

3. Mechanisms of malignant cell transformation by the chimeric NPM/ALK kinase.

Accumulating evidence indicates that expression of anaplastic lymphoma kinase (ALK) defines a distinct type of T-cell lymphoma. Expression of ALK in malignant T cells is typically due to the t(2;5) translocation resulting in formation of the fusion gene which encodes a 80-kDa hybrid protein that contains portion of the nuclear protein nucleophosmin (NPM) joined to the entire cytoplasmic portion of the receptor tyrosine kinase ALK. The NPM/ALK kinase is constitutively activated and highly oncogenic. Our studies concentrate on identification of downstream effector molecules triggered by the NPM/ALK kinase. They indicate that pathways involving STAT3, PI3K/AKT and, apparently, STAT5 are constitutively activated by this kinase. Regulation and function of STAT3 in the ALK+ T-cells and testing an ALK-inhibitor small molecule candidate are the main focus of the ongoing investigation.

Academic Contact Info

University of Pennsylvania Medical Center
7.106 Founders and 413 Stellar Chance
3400 Spruce St/4283

Philadelphia, PA 19104
Phone: (215) 662-3467
Fax: (215) 662-7529

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