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Burkitt Lymphoma and Burkitt-like Lymphoma Medication

  • Author: Ali H Kanbar, MD; Chief Editor: Emmanuel C Besa, MD  more...
 
Updated: Apr 08, 2016
 

Medication Summary

Intensive systemic chemotherapy is the treatment of choice for this aggressive disease in all its stages.[31] Supportive medications are used to help control the adverse effects of chemotherapy, such as nausea, vomiting, tumor lysis syndrome, and infections.

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Alkylating Agents

Class Summary

Alkylating agents inhibit cell growth and proliferation.

Cyclophosphamide (Cytoxan)

 

Cyclophosphamide is cell cycle nonspecific and involves hepatic metabolism. This agent is chemically related to nitrogen mustards. As an alkylating agent, the mechanism of action of the active metabolites may involve cross-linking of DNA, which may interfere with growth of normal and rapidly proliferating malignant cells.

Ifosfamide (Ifex)

 

Ifosfamide is chemically related to nitrogen mustards and is a synthetic analogue of cyclophosphamide. This agent requires metabolic activation in the liver. The alkylated metabolites of ifosfamide have been shown to react with cellular DNA. This agent inhibits DNA and protein synthesis and, thus, cell proliferation by causing DNA cross-linking and denaturation of double helix.

Vincristine (Oncovin)

 

The mechanism of action of vincristine is uncertain. This agent is cell cycle specific at the M and S phases and inhibits microtubule assembly at metaphase, resulting in cell division arrest. Approximately 80% of vincristine is excreted by the liver. This agent may cause a decrease in reticuloendothelial cell function or an increase in platelet production.

Methotrexate (Folex PFS)

 

Methotrexate is cell cycle S-phase specific. This agent inhibits enzyme dihydrofolate reductase (DHFR), resulting in decreased conversion of folic acid to tetrahydrofolate, which is essential for DNA synthesis. Methotrexate is metabolized in the liver, and most of the drug is excreted unchanged in urine. This agent crosses the blood-brain barrier and placenta.

Cytarabine (Ara-C)

 

Cytarabine (Ara-C) is cell-cycle S-phase specific, blocking the progression from G1 to S phase. This agent is converted intracellularly to the active compound cytarabine-5'-triphosphate, which inhibits DNA polymerase. This inhibition, in turn, halts viral replication.

Doxorubicin (Adriamycin)

 

Doxorubicin is an anthracycline antibiotic that can intercalate with DNA and affects many DNA functions, including synthesis. This agent forms DNA-cleavable complexes by interacting with topoisomerase II, which is responsible for the cytocidal activity of the drug.

Doxorubicin is administered intravenously and distributes widely into body tissues, including the heart, kidneys, lungs, liver, and spleen; however, it does not cross the blood-brain barrier and is excreted primarily in bile.

Rituximab (Rituxan)

 

Rituximab is a genetically engineered, chimeric, murine/human monoclonal antibody directed against the CD20 antigen found on the surface of normal and malignant B lymphocytes. This antibody is an immunoglobulin (Ig) G1 kappa immunoglobulin that contains murine light- and heavy-chain variable region sequences and human constant region sequences.

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Glucocorticoids

Class Summary

The pharmacologic properties of glucocorticoid agents are therapeutically effective in various diseases, including neoplasms.

Prednisone (Sterapred)

 

Glucocorticoids have a lympholytic effect, although mechanism of this action is not clear.

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Urate-Oxidase Enzymes

Class Summary

Urate-oxidase enzymes can be used to treat hyperuricemia associated with malignancy.

Rasburicase (Elitek)

 

Rasburicase is a recombinant form (derived from Saccharomyces cervisiae-synthesized, Aspergillus flavus) of the enzyme urate oxidase, which oxidizes uric acid to allantoin. This agent is indicated for the treatment and prophylaxis of severe hyperuricemia associated with the treatment of malignancy and has an elimination half-life of 18 hours. Hyperuricemia causes a precipitant in the kidneys, which leads to acute renal failure. Unlike uric acid, allantoin is soluble and easily excreted by the kidneys.

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Contributor Information and Disclosures
Author

Ali H Kanbar, MD Medical Oncologist/Hematologist, Dayton Cancer Center

Ali H Kanbar, MD is a member of the following medical societies: American College of Physicians, American Society of Hematology, American Society of Clinical Oncology

Disclosure: Nothing to disclose.

Coauthor(s)

Ronald A Sacher, MB, BCh, FRCPC, DTM&H Professor, Internal Medicine and Pathology, Director, Hoxworth Blood Center, University of Cincinnati Academic Health Center

Ronald A Sacher, MB, BCh, FRCPC, DTM&H is a member of the following medical societies: American Association for the Advancement of Science, American Association of Blood Banks, American Society for Clinical Pathology, American Society of Hematology, College of American Pathologists, International Society on Thrombosis and Haemostasis, Royal College of Physicians and Surgeons of Canada, American Clinical and Climatological Association, International Society of Blood Transfusion

Disclosure: Serve(d) as a speaker or a member of a speakers bureau for: GSK Pharmaceuticals,Alexion,Johnson & Johnson Talecris,,Grifols<br/>Received honoraria from all the above companies for speaking and teaching.

Chief Editor

Emmanuel C Besa, MD Professor Emeritus, Department of Medicine, Division of Hematologic Malignancies and Hematopoietic Stem Cell Transplantation, Kimmel Cancer Center, Jefferson Medical College of Thomas Jefferson University

Emmanuel C Besa, MD is a member of the following medical societies: American Association for Cancer Education, American Society of Clinical Oncology, American College of Clinical Pharmacology, American Federation for Medical Research, American Society of Hematology, New York Academy of Sciences

Disclosure: Nothing to disclose.

Acknowledgements

Patturajah Anbumani, MD, MBBS, MS, MCh Associate Medical Director, Best Medical Care; Former Associate Medical Director, Jeanes Hospital, Temple University Health System; Former Adjunct Clinical Assistant Professor, New York College of Osteopathic Medicine; Former Clinical Assistant Professor, Department of Medicine, State University of New York-Downstate

Patturajah Anbumani, MD, MBBS, MS, MCh is a member of the following medical societies: American College of Physicians, American Medical Association, and American Medical Women’s Association

Disclosure: Nothing to disclose.

Samer A Bleibel, MD Staff Physician, Department of Internal Medicine, Wayne State University School of Medicine, St John's Hospital and Medical Centers

Samer A Bleibel, MD is a member of the following medical societies: American College of Physicians

Disclosure: Nothing to disclose.

Asher A Chanan-Khan, MD Assistant Professor, Department of Medicine, Division of Lymphoma and Bone Marrow Transplantation, Roswell Park Cancer Institute, State University of New York at Buffalo

Asher A Chanan-Khan, MD is a member of the following medical societies: American College of Physicians, American Medical Association, and American Society of Hematology

Disclosure: Nothing to disclose.

Hanxian Huang, MD, PhD Staff Physician, Department of Internal Medicine, Leesburg Regional Medical Center, The Villages Regional Hospital

Hanxian Huang, MD, PhD is a member of the following medical societies: American College of Physicians-American Society of Internal Medicine

Disclosure: Nothing to disclose.

Anand B Karnad, MBBS Program Director, Fellowship Programs in Hematology-Oncology, Professor of Medicine, Division of Medical Oncology, Department of Medicine, University of Texas Health Sciences Center, San Antonio

Anand B Karnad, MBBS is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American Osler Society, American Society of Hematology, Assocation of Subspecialty Professors, and Massachusetts Medical Society

Disclosure: Nothing to disclose.

Olga Kozyreva, MD Attending Physician, Division of Hematology-Oncology, St Elizabeth's Medical Center; Assistant Professor, Tufts University School of Medicine

Disclosure: Nothing to disclose.

Sarah K May, MD Consulting Staff, Department of Hematology-Oncology, Caritas Carney Hospital, Commonwealth Hematology-Oncology PC

Disclosure: Nothing to disclose.

from Memorial Sloan-Kettering - Philip Schulman, MD Chief, Medical Oncology, Department of Medicine, Memorial Sloan-Kettering Cancer Center; Clinical Professor, Department of Medicine, New York University School of Medicine

Philip Schulman, MD is a member of the following medical societies: American Association for Cancer Research, American College of Physicians, American Society of Hematology, and Medical Society of the State of New York

Disclosure: Nothing to disclose.

Karen Seiter, MD Professor, Department of Internal Medicine, Division of Oncology/Hematology, New York Medical College

Karen Seiter, MD is a member of the following medical societies: American Association for Cancer Research, American College of Physicians, and American Society of Hematology

Disclosure: Novartis Honoraria Speaking and teaching; Schering Honoraria Speaking and teaching; Cephalon Honoraria Speaking and teaching; Celgene Honoraria Speaking and teaching

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Yubao Wang, MD, PhD Fellow, Division of Hematology/Medical Oncology, University of Texas Health Science Center, San Antonio

Yubao Wang, MD, PhD is a member of the following medical societies: American College of Physicians, American Society of Clinical Oncology, and American Society of Hematology

Disclosure: Nothing to disclose.

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Computed tomography scan in a patient with a large, left-sided axillary mass from which a biopsy was obtained. Biopsy findings were consistent with small noncleaved cell non-Hodgkin lymphoma.
Postchemotherapy computed tomography scan in a patient diagnosed with small noncleaved cell lymphoma (SNCCL) (same patient as in previous image). This image shows regression of a left axillary mass.
Coronal magnetic resonance imaging (MRI) section in a patient with large neck mass (same patient as in previous image). Biopsy findings showed Burkitt-like non-Hodgkin lymphoma (NHL). MRI was performed to assess for cord involvement.
Sagittal magnetic resonance imaging (MRI) section of the neck area showing a large mass invading the cervical spine with epidural encroachment (same patient as in the previous image). MRI was performed to rule out cord compression. The first image shows the gallium scan of this patient that correlates with the site of the tumor.
Right-sided pleural effusion in a patient with small noncleaved cell lymphoma (SNCCL) non-Hodgkin lymphoma.
Hematoxylin and eosin (H&E) stain. Sheets of monotonous-appearing lymphoid cells with one or more prominent nucleoli and an area of pale staining resulting from the presence of benign macrophages reveal a starry sky pattern.
The 2-dimensional flow cytometry demonstrates the highlighted cells to be CD5 negative and CD23 negative as well as lambda negative. Small noncleaved cell lymphoma (SNCCL) cells are typically CD19+, CD20+, CD22+, and CD10+.
 
 
 
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