Waldenstrom Macroglobulinemia Medication: Corticosteroids, Antineoplastics, Tyrosine Kinase Inhibito
Waldenstrom Macroglobulinemia Medication: Corticosteroids, Antineoplastics, Tyrosine Kinase Inhibitor, Antineoplastics, Alkylating, Antineoplastics, Antimetabolite, Antineoplastics, Anthracycline, Antineoplastics, Monoclonal Antibody, Immunomodulators, Antineoplastics, Proteasome Inhibitors, ...
Various drugs, including corticosteroids (eg, prednisone), alkylating agents (eg, chlorambucil, melphalan, cyclophosphamide), biologic response modifiers (eg, interferon alfa, interferon gamma), and purine analogues (eg, fludarabine, 2-chlorodeoxyadenosine), are used in the treatment of Waldenström macroglobulinemia.
Salvage therapy for patients with resistant disease or relapse includes reuse or alternative use of front-line agent, combination therapy, thalidomide (with or without steroids), autologous transplantation, and monoclonal antibody (alemtuzumab).
These agents have anti-inflammatory properties and cause profound and varied metabolic effects. They modify the body's immune response to diverse stimuli.
Prednisone is an immunosuppressant used for the treatment of autoimmune disorders. It may decrease inflammation by reversing increased capillary permeability and suppressing polymorphonuclear leukocyte activity.
Tyrosine kinase enzymes are responsible for activating many proteins by signal transduction cascades, phosphorylation, and other mechanisms. Tyrosine kinase inhibitors block these functions.
Ibrutinib is a Bruton's tyrosine kinase (BTK) inhibitor. It forms a covalent bond with a cysteine residue in the BTK active site, leading to inhibition of BTK enzymatic activity. BTK is a signaling molecule of the B-cell antigen receptor (BCR) and cytokine receptor pathways. BTK's role in signaling through the B-cell surface receptors results in activation of pathways necessary for B-cell trafficking, chemotaxis, and adhesion. It is the first FDA-approved drug that is indicated for Waldenström macroglobulinemia.
These agents inhibit cell growth and proliferation. Many combinations of chemotherapeutic agents have been tried, with no evidence of clear superiority over single-agent chemotherapy with chlorambucil and considerably more toxicity.
This agent alkylates and cross-links strands of deoxyribonucleic acid (DNA), inhibiting DNA replication and ribonucleic acid (RNA) transcription. Chlorambucil is an important drug in the treatment of Waldenström macroglobulinemia. It is usually administered when extreme bone marrow infiltration, anemia, splenomegaly, lymphadenopathy, and bleeding are present.
Melphalan inhibits mitosis by cross-linking DNA strands; it ultimately disrupts nucleic acid function.
Cyclophosphamide 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 the growth of normal and neoplastic cells.
Antimetabolites inhibit cell growth and proliferation. Many combinations of chemotherapeutic agents have been tried, with no evidence of clear superiority over single-agent chemotherapy with chlorambucil and considerably more toxicity.
Cladribine is a synthetic antineoplastic agent for continuous intravenous (IV) infusion. The enzyme deoxycytidine kinase phosphorylates this compound into an active 5+-triphosphate derivative, which, in turn, breaks DNA strands and inhibits DNA synthesis. Cladribine disrupts cell metabolism, causing death to resting and dividing cells.
Fludarabine is a nucleotide analogue of vidarabine converted to 2-fluoro-ara-A, which enters the cell and is phosphorylated to form active metabolite 2-fluoro-ara-adenosine triphosphate (ATP). It inhibits DNA synthesis.
These agents immunomodulate the response to malignant cells.
Doxorubicin inhibits topoisomerase II and produces free radicals, which may cause destruction of DNA. The combination of these 2 events can, in turn, inhibit the growth of neoplastic cells. Doxorubicin may be effective in chlorambucil-refractory Waldenström macroglobulinemia.
These agents immunomodulate the response to malignant cells.
Rituximab is a genetically engineered human monoclonal antibody directed against the CD20 antigen found on the surface of normal and malignant B lymphocytes.
Immunomodulators modulate processes that promote immune reactions resulting from diverse stimuli.
This is a protein product manufactured by recombinant DNA technology. It possesses complex antiviral, antineoplastic, and immunomodulating activities.
Interferon gamma-1b is a single-chain polypeptide containing 140 amino acids. It is produced by fermentation of genetically engineered Escherichia coli bacterium containing DNA that encodes for the human protein.
Thalidomide is a derivative of glutethimide. Its mode of action for immunosuppression is unclear. Inhibition of neutrophil chemotaxis and decreased monocyte phagocytosis may occur. Thalidomide may cause a 50-80% reduction of tumor necrosis factor–alpha.
Proteosome inhibitors inhibit cell growth and proliferation.
Bortezomib was the first of the anticancer agents known as proteasome inhibitors to be approved. The proteasome pathway is an enzyme complex existing in all cells. This complex degrades ubiquitinated proteins that control the cell cycle and cellular processes and maintains cellular homeostasis. Reversible proteasome inhibition disrupts pathways supporting cell growth, thus decreasing cancer cell survival.
These antineoplastic agents have antiproliferative and antiangiogenic properties.
Everolimus is a mammalian target of rapamycin (mTOR) inhibitor that is approved by the US Food and Drug Administration for the treatment of renal cell cancer, subependymal giant cell astrocytoma, and advanced neuroendocrine tumors of pancreatic origin. It is a kinase inhibitor that inhibits antigenic and interleukin (IL-2 and IL-5)–stimulated activation and proliferation of T and B lymphocytes. Phase II studies demonstrate activity in relapsed Waldenström macroglobulinemia.
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, American Society of Hematology
Disclosure: Received honoraria from Novartis for speaking and teaching; Received consulting fee from Novartis for speaking and teaching; Received honoraria from Ariad for speaking and teaching; Received honoraria from Celgene for speaking and teaching.
Coauthor(s)
Doris Ponce, MD Fellow, Department of Hematology/Oncology, New York Medical College
Doris Ponce, MD is a member of the following medical societies: American College of Physicians, American Medical Association, American Society of Hematology, American Society of Clinical Oncology
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
Acknowledgements
Wendy Hu, MD Consulting Staff, Department of Hematology/Oncology and Bone Marrow Transplantation, Huntington Memorial Medical Center
Wendy Hu, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, American Society for Blood and Marrow Transplantation, American Society of Hematology, and Physicians for Social Responsibility
Disclosure: Nothing to disclose.
Koyamangalath Krishnan, MD, FRCP, FACP Paul Dishner Endowed Chair of Excellence in Medicine, Professor of Medicine and Chief of Hematology-Oncology, James H Quillen College of Medicine at East Tennessee State University
Koyamangalath Krishnan, MD, FRCP, FACP is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, American Society of Hematology, and Royal College of Physicians
Disclosure: Nothing to disclose.
Vijay Ramu, MBBS Staff Physician, Department of Internal Medicine, East Tennessee State University
Vijay Ramu, MBBS is a member of the following medical societies: American College of Physicians
Disclosure: Nothing to disclose.
Paul Schick, MD Emeritus Professor, Department of Internal Medicine, Jefferson Medical College of Thomas Jefferson University; Research Professor, Department of Internal Medicine, Drexel University College of Medicine; Adjunct Professor of Medicine, Lankenau Hospital
Paul Schick, MD is a member of the following medical societies: American College of Physicians, American Heart Association, American Society of Hematology, International Society on Thrombosis and Haemostasis, and New York Academy of Sciences
Disclosure: Nothing to disclose.
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
Harsha Vyas, MD Fellow, Section of Hematology and Oncology, Wake Forest University School of Medicine
Harsha Vyas, MD 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.
References
Medication Summary
Various drugs, including corticosteroids (eg, prednisone), alkylating agents (eg, chlorambucil, melphalan, cyclophosphamide), biologic response modifiers (eg, interferon alfa, interferon gamma), and purine analogues (eg, fludarabine, 2-chlorodeoxyadenosine), are used in the treatment of Waldenström macroglobulinemia.
Salvage therapy for patients with resistant disease or relapse includes reuse or alternative use of front-line agent, combination therapy, thalidomide (with or without steroids), autologous transplantation, and monoclonal antibody (alemtuzumab).
Corticosteroids
Class Summary
These agents have anti-inflammatory properties and cause profound and varied metabolic effects. They modify the body's immune response to diverse stimuli.
Prednisone
Prednisone is an immunosuppressant used for the treatment of autoimmune disorders. It may decrease inflammation by reversing increased capillary permeability and suppressing polymorphonuclear leukocyte activity.
Antineoplastics, Tyrosine Kinase Inhibitor
Class Summary
Tyrosine kinase enzymes are responsible for activating many proteins by signal transduction cascades, phosphorylation, and other mechanisms. Tyrosine kinase inhibitors block these functions.
Ibrutinib (Imbruvica)
Ibrutinib is a Bruton's tyrosine kinase (BTK) inhibitor. It forms a covalent bond with a cysteine residue in the BTK active site, leading to inhibition of BTK enzymatic activity. BTK is a signaling molecule of the B-cell antigen receptor (BCR) and cytokine receptor pathways. BTK's role in signaling through the B-cell surface receptors results in activation of pathways necessary for B-cell trafficking, chemotaxis, and adhesion. It is the first FDA-approved drug that is indicated for Waldenström macroglobulinemia.
Antineoplastics, Alkylating
Class Summary
These agents inhibit cell growth and proliferation. Many combinations of chemotherapeutic agents have been tried, with no evidence of clear superiority over single-agent chemotherapy with chlorambucil and considerably more toxicity.
Chlorambucil (Leukeran)
This agent alkylates and cross-links strands of deoxyribonucleic acid (DNA), inhibiting DNA replication and ribonucleic acid (RNA) transcription. Chlorambucil is an important drug in the treatment of Waldenström macroglobulinemia. It is usually administered when extreme bone marrow infiltration, anemia, splenomegaly, lymphadenopathy, and bleeding are present.
Melphalan (Alkeran)
Melphalan inhibits mitosis by cross-linking DNA strands; it ultimately disrupts nucleic acid function.
Cyclophosphamide
Cyclophosphamide 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 the growth of normal and neoplastic cells.
Antineoplastics, Antimetabolite
Class Summary
Antimetabolites inhibit cell growth and proliferation. Many combinations of chemotherapeutic agents have been tried, with no evidence of clear superiority over single-agent chemotherapy with chlorambucil and considerably more toxicity.
Cladribine (Leustatin)
Cladribine is a synthetic antineoplastic agent for continuous intravenous (IV) infusion. The enzyme deoxycytidine kinase phosphorylates this compound into an active 5+-triphosphate derivative, which, in turn, breaks DNA strands and inhibits DNA synthesis. Cladribine disrupts cell metabolism, causing death to resting and dividing cells.
Fludarabine (Fludara)
Fludarabine is a nucleotide analogue of vidarabine converted to 2-fluoro-ara-A, which enters the cell and is phosphorylated to form active metabolite 2-fluoro-ara-adenosine triphosphate (ATP). It inhibits DNA synthesis.
Antineoplastics, Anthracycline
Class Summary
These agents immunomodulate the response to malignant cells.
Doxorubicin (Adriamycin)
Doxorubicin inhibits topoisomerase II and produces free radicals, which may cause destruction of DNA. The combination of these 2 events can, in turn, inhibit the growth of neoplastic cells. Doxorubicin may be effective in chlorambucil-refractory Waldenström macroglobulinemia.
Antineoplastics, Monoclonal Antibody
Class Summary
These agents immunomodulate the response to malignant cells.
Rituximab (Rituxan)
Rituximab is a genetically engineered human monoclonal antibody directed against the CD20 antigen found on the surface of normal and malignant B lymphocytes.
Immunomodulators
Class Summary
Immunomodulators modulate processes that promote immune reactions resulting from diverse stimuli.
Interferon alfa-2b (Intron A)
This is a protein product manufactured by recombinant DNA technology. It possesses complex antiviral, antineoplastic, and immunomodulating activities.
Interferon gamma-1b (Actimmune)
Interferon gamma-1b is a single-chain polypeptide containing 140 amino acids. It is produced by fermentation of genetically engineered Escherichia coli bacterium containing DNA that encodes for the human protein.
Thalidomide (Thalomid)
Thalidomide is a derivative of glutethimide. Its mode of action for immunosuppression is unclear. Inhibition of neutrophil chemotaxis and decreased monocyte phagocytosis may occur. Thalidomide may cause a 50-80% reduction of tumor necrosis factor–alpha.
Antineoplastics, Proteasome Inhibitors
Class Summary
Proteosome inhibitors inhibit cell growth and proliferation.
Bortezomib (Velcade)
Bortezomib was the first of the anticancer agents known as proteasome inhibitors to be approved. The proteasome pathway is an enzyme complex existing in all cells. This complex degrades ubiquitinated proteins that control the cell cycle and cellular processes and maintains cellular homeostasis. Reversible proteasome inhibition disrupts pathways supporting cell growth, thus decreasing cancer cell survival.
Antineoplastics, mTOr Kinase Inhibitor
Class Summary
These antineoplastic agents have antiproliferative and antiangiogenic properties.
Everolimus (Afinitor, Zortress)
Everolimus is a mammalian target of rapamycin (mTOR) inhibitor that is approved by the US Food and Drug Administration for the treatment of renal cell cancer, subependymal giant cell astrocytoma, and advanced neuroendocrine tumors of pancreatic origin. It is a kinase inhibitor that inhibits antigenic and interleukin (IL-2 and IL-5)–stimulated activation and proliferation of T and B lymphocytes. Phase II studies demonstrate activity in relapsed Waldenström macroglobulinemia.
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, American Society of Hematology
Disclosure: Received honoraria from Novartis for speaking and teaching; Received consulting fee from Novartis for speaking and teaching; Received honoraria from Ariad for speaking and teaching; Received honoraria from Celgene for speaking and teaching.
Coauthor(s)
Doris Ponce, MD Fellow, Department of Hematology/Oncology, New York Medical College
Doris Ponce, MD is a member of the following medical societies: American College of Physicians, American Medical Association, American Society of Hematology, American Society of Clinical Oncology
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
Acknowledgements
Wendy Hu, MD Consulting Staff, Department of Hematology/Oncology and Bone Marrow Transplantation, Huntington Memorial Medical Center
Wendy Hu, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, American Society for Blood and Marrow Transplantation, American Society of Hematology, and Physicians for Social Responsibility
Disclosure: Nothing to disclose.
Koyamangalath Krishnan, MD, FRCP, FACP Paul Dishner Endowed Chair of Excellence in Medicine, Professor of Medicine and Chief of Hematology-Oncology, James H Quillen College of Medicine at East Tennessee State University
Koyamangalath Krishnan, MD, FRCP, FACP is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, American Society of Hematology, and Royal College of Physicians
Disclosure: Nothing to disclose.
Vijay Ramu, MBBS Staff Physician, Department of Internal Medicine, East Tennessee State University
Vijay Ramu, MBBS is a member of the following medical societies: American College of Physicians
Disclosure: Nothing to disclose.
Paul Schick, MD Emeritus Professor, Department of Internal Medicine, Jefferson Medical College of Thomas Jefferson University; Research Professor, Department of Internal Medicine, Drexel University College of Medicine; Adjunct Professor of Medicine, Lankenau Hospital
Paul Schick, MD is a member of the following medical societies: American College of Physicians, American Heart Association, American Society of Hematology, International Society on Thrombosis and Haemostasis, and New York Academy of Sciences
Disclosure: Nothing to disclose.
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
Harsha Vyas, MD Fellow, Section of Hematology and Oncology, Wake Forest University School of Medicine
Harsha Vyas, MD 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.
References
- Vogt RF, Marti GE. Overview of monoclonal gammopathies of undetermined significance. Br J Haematol. 2007 Dec. 139(5):687-9. [Medline].
- Pasricha SR, Juneja SK, Westerman DA, Came NA. Bone-marrow plasma cell burden correlates with IgM paraprotein concentration in Waldenstrom macroglobulinaemia. J Clin Pathol. 2011 Jun. 64(6):520-3. [Medline].
- Adamia S, Pilarski PM, Belch AR, Pilarski LM. Genetic abnormalities in Waldenstrom's macroglobulinemia. Clin Lymphoma Myeloma. 2009 Mar. 9(1):30-2. [Medline].
- Ogmundsdottir HM, Einarsdottir HK, Steingrimsdottir H, Haraldsdottir V. Familial predisposition to monoclonal gammopathy of unknown significance, Waldenström's macroglobulinemia, and multiple myeloma. Clin Lymphoma Myeloma. 2009 Mar. 9(1):27-9. [Medline].
- Wang H, Chen Y, Li F, Delasalle K, Wang J, Alexanian R, et al. Temporal and geographic variations of Waldenstrom macroglobulinemia incidence: A large population-based study. Cancer. 2011 Dec 2. [Medline].
- Kastritis E, Zervas K, Repoussis P, et al. Prognostication in young and old patients with Waldenstrom's macroglobulinemia: importance of the International Prognostic Scoring System and of serum lactate dehydrogenase. Clin Lymphoma Myeloma. 2009 Mar. 9(1):50-2. [Medline].
- Kastritis E, Kyrtsonis MC, Hatjiharissi E, et al. No significant improvement in the outcome of patients with Waldenström's macroglobulinemia treated over the last 25 years. Am J Hematol. 2011 Jun. 86(6):479-83. [Medline].
- Castillo JJ, Olszewski AJ, Cronin AM, Hunter ZR, Treon SP. Survival trends in Waldenström macroglobulinemia: an analysis of the Surveillance, Epidemiology and End Results database. Blood. 2014 Jun 19. 123(25):3999-4000. [Medline].
- Treon SP, Cao Y, Xu L, Yang G, Liu X, Hunter ZR. Somatic mutations in MYD88 and CXCR4 are determinants of clinical presentation and overall survival in Waldenstrom macroglobulinemia. Blood. 2014 May 1. 123(18):2791-6. [Medline].
- Merlini G, Baldini L, Broglia C, Comelli M, Goldaniga M, Palladini G, et al. Prognostic factors in symptomatic Waldenstrom's macroglobulinemia. Semin Oncol. 2003 Apr. 30(2):211-5. [Medline].
- Menke MN, Feke GT, McMeel JW, Treon SP. Ophthalmologic techniques to assess the severity of hyperviscosity syndrome and the effect of plasmapheresis in patients with Waldenström's macroglobulinemia. Clin Lymphoma Myeloma. 2009 Mar. 9(1):100-3. [Medline].
- Varghese AM, Rawstron AC, Ashcroft AJ, Moreton P, Owen RG. Assessment of bone marrow response in Waldenstrom's macroglobulinemia. Clin Lymphoma Myeloma. 2009 Mar. 9(1):53-5. [Medline].
- Katzmann JA, Kyle RA, Benson J, et al. Screening panels for detection of monoclonal gammopathies. Clin Chem. 2009 Aug. 55(8):1517-22. [Medline].
- Poulain S, Ertault M, Leleu X, et al. SDF1/CXCL12 (-801GA) polymorphism is a prognostic factor after treatment initiation in Waldenstrom macroglobulinemia. Leuk Res. 2009 Sep. 33(9):1204-7. [Medline].
- Hunter ZR, Xu L, Yang G, Zhou Y, Liu X, Cao Y, et al. The genomic landscape of Waldenstrom macroglobulinemia is characterized by highly recurring MYD88 and WHIM-like CXCR4 mutations, and small somatic deletions associated with B-cell lymphomagenesis. Blood. 2014 Mar 13. 123(11):1637-46. [Medline].
- Jonhson SA, Birchall J, Luckie C. Guidelines on the management of waldenstrom macroglobulinaemia. British Society for Haematol. 2006. 132:683-97.
- [Guideline] Dimopoulos MA, Kastritis E, Owen RG, Kyle RA, Landgren O, Morra E, et al. Treatment recommendations for patients with Waldenström macroglobulinemia (WM) and related disorders: IWWM-7 consensus. Blood. 2014 Aug 28. 124(9):1404-1411. [Medline].
- Menke MN, Feke GT, McMeel JW, Treon SP. Effect of plasmapheresis on hyperviscosity-related retinopathy and retinal hemodynamics in patients with Waldenstrom's macroglobulinemia. Invest Ophthalmol Vis Sci. 2008 Mar. 49(3):1157-60. [Medline]. [Full Text].
- Leleu X, Tamburini J, Roccaro A, et al. Balancing risk versus benefit in the treatment of Waldenstrom's macroglobulinemia patients with nucleoside analogue-based therapy. Clin Lymphoma Myeloma. 2009 Mar. 9(1):71-3. [Medline].
- Treon SP, Tripsas CK, Yang G, Cao Y, Xu L, Hunter Z, et al. A prospective multicenter study Of The Bruton’s tyrosine kinase inhibitor ibrutinib in patients with relapsed or refractory Waldenström’s macroglobulinemia (abstract 251). Presented at the 55th American Society of Hematology Annual Meeting and Exposition. New Orleans, LA. December 7-10, 2013. [Full Text].
- Treon SP, Hansen M, Branagan AR. Polymorphisms in FcgammaRIIIA (CD16) receptor expression are associated with the clinical response to rituximab in waldenstrom's macroglobulinemia. J Clin Oncol. 2005. 23:474-81.
- Dhodapkar MV, Jacobson JL, Gertz MA. Prognostic factors and response to fludarabine therapy in patients with Waldenstrom macroglobulinemia: results of United States intergroup trial (Southwest Oncology Group S9003). Blood. 2001. 98:41-48.
- Johnson SA, Owen RG, Oscier DG. Phase III study of chlorambucil versus fludarabine as initial therapy for Waldenstrom's macroglobulinemia and related disorders. Clin Lymphoma. 2005. 4:294-97.
- Dimopoulos MA, Kastritis E, Roussou M, et al. Rituximab-based treatments in Waldenstrom's macroglobulinemia. Clin Lymphoma Myeloma. 2009 Mar. 9(1):59-61. [Medline].
- Kyle, RA, Treon SP, Alexanian R. Prognostic markers and criteria to initiate therapy in Waldenstrom's macroglobulinemia: consensus panel recommendations from the Second International Workshop on Waldenstrom's Macroglobulinemia. Seminars in Oncology. 2003. 30:116-120.
- Tedeschi A, Alamos SM, Ricci F, Greco A, Morra E. Fludarabine-based combination therapies for Waldenstrom's macroglobulinemia. Clin Lymphoma Myeloma. 2009 Mar. 9(1):67-70. [Medline].
- Treon SP, Hunter Z, Barnagan AR. CHOP plus rituximab therapy in Waldenstrom's macroblobulinemia. Clin Lymphoma. 2005. 4:273-7.
- Tedeschi A, Benevolo G, Varettoni M, Battista ML, Zinzani PL, Visco C, et al. Fludarabine plus cyclophosphamide and rituximab in Waldenstrom macroglobulinemia: An effective but myelosuppressive regimen to be offered to patients with advanced disease. Cancer. 2011 Jul 5. [Medline].
- Coleman M, Leonard J, Lyons L, Szelenyi H, Niesvizky R. Treatment of Waldenstrom's macroglobulinemia with clarithromycin, low-dose thalidomide, and dexamethasone. Semin Oncol. 2003 Apr. 30(2):270-4. [Medline].
- Ghobrial IM, Hong F, Padmanabhan S, et al. Phase II trial of weekly bortezomib in combination with rituximab in relapsed or relapsed and refractory Waldenstrom macroglobulinemia. J Clin Oncol. 2010 Mar 10. 28(8):1422-8. [Medline]. [Full Text].
- Ghobrial IM, Gertz M, Laplant B, et al. Phase II trial of the oral mammalian target of rapamycin inhibitor everolimus in relapsed or refractory Waldenstrom macroglobulinemia. J Clin Oncol. 2010 Mar 10. 28(8):1408-14. [Medline]. [Full Text].
- Treon SP, Soumerai JD, Hunter ZR, et al. Long-term follow-up of symptomatic patients with lymphoplasmacytic lymphoma/Waldenström macroglobulinemia treated with the anti-CD52 monoclonal antibody alemtuzumab. Blood. 2011 Jul 14. 118(2):276-81. [Medline]. [Full Text].
- Leblond V, Levy V, Maloisel F. Multicenter, randomized comparative trial of fludarabine and the combination of cyclophosphamide-doxorubicin-prednisone in 92 patients with Waldenstrom macroglobulinemia in first relapse or with primary refractory disease. Blood. 2001. 98:2640-4.
- Desikan R, Dhodapkar M, Siegel D, et al. High-dose therapy with autologous haemopoietic stem cell support for Waldenstrom's macroglobulinaemia. Br J Haematol. 1999 Jun. 105(4):993-6. [Medline].
- Treon SP, Morel P, Leblond V, Fermand JP. Report of the Third International Workshop on Waldenstrom's macroglobulinemia. Clin Lymphoma. 2005 Mar. 5(4):215-6. [Medline].
Source...