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Plasmablastic Lymphoma: A Review of Current Knowledge and Future Directions.

Elyamany G, Al Mussaed E, Alzahrani AM - Adv Hematol (2015)

Bottom Line: There is no standard chemotherapy protocol for treatment of PBL.Cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) or CHOP-like regimens have been the backbone while more intensive regimens such as cyclophosphamide, vincristine, doxorubicin, high-dose methotrexate/ifosfamide, etoposide, high-dose cytarabine (CODOX-M/IVAC), or dose-adjusted etoposide, prednisone, vincristine, cyclophosphamide, and doxorubicin (DA-EPOCH) are possible options.Recently, a few studies have reported the potential value of the proteasome inhibitor bortezomib and thalidomide in PBL patients.

View Article: PubMed Central - PubMed

Affiliation: Department of Pathology and Blood Bank, Prince Sultan Military Medical City, P.O. Box 7897, Riyadh 11159, Saudi Arabia ; Department of Hematology, Theodor Bilharz Research Institute, Egypt.

ABSTRACT
Plasmablastic lymphoma (PBL) is an aggressive subtype of non-Hodgkin's lymphoma (NHL), which frequently arises in the oral cavity of human immunodeficiency virus (HIV) infected patients. PBL shows diffuse proliferation of large neoplastic cells resembling B-immunoblasts/plasmablasts, or with plasmacytic features and an immunophenotype of plasma cells. PBL remains a diagnostic challenge due to its peculiar morphology and an immunohistochemical profile similar to plasma cell myeloma (PCM). PBL is also a therapeutic challenge with a clinical course characterized by a high rate of relapse and death. There is no standard chemotherapy protocol for treatment of PBL. Cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) or CHOP-like regimens have been the backbone while more intensive regimens such as cyclophosphamide, vincristine, doxorubicin, high-dose methotrexate/ifosfamide, etoposide, high-dose cytarabine (CODOX-M/IVAC), or dose-adjusted etoposide, prednisone, vincristine, cyclophosphamide, and doxorubicin (DA-EPOCH) are possible options. Recently, a few studies have reported the potential value of the proteasome inhibitor bortezomib and thalidomide in PBL patients. The introduction of genes encoding artificial receptors called chimeric antigen receptors (CARs) and CAR-modified T cells targeted to the B cell-specific CD19 antigen have demonstrated promising results in multiple early clinical trials. The aim of this paper is to review the recent advances in epidemiology; pathophysiology; clinical, pathologic, and molecular characteristics; therapy; and outcome in patients with PBL.

No MeSH data available.


Related in: MedlinePlus

Selected immunophenotype of PBL: the PBL cells demonstrate immunoreactivity to CD138 (a), lambda light chain, ISH (b), and HHV8 (c) and negativity for CD20 (d) and CD56 (e). Proliferation index is high (f).
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fig2: Selected immunophenotype of PBL: the PBL cells demonstrate immunoreactivity to CD138 (a), lambda light chain, ISH (b), and HHV8 (c) and negativity for CD20 (d) and CD56 (e). Proliferation index is high (f).

Mentions: PBL is a high-grade B-cell lymphoma that arises from postgerminal center B-cell. The hallmark immunohistochemical staining pattern of PBL is that of terminally differentiated B-cell. PBL demonstrates little to no expression of leukocyte common antigen (LCA) or the B-cell markers CD20, CD79a, and PAX5. However, the plasma cell markers VS38c, CD38, multiple myeloma oncogene-1 (MUM1), and CD138 (syndecan-1) seem to be almost universally expressed [3, 16, 32]. PBL is characterized by a high proliferation index reflected by Ki67 expression, usually >80% (Figure 2).


Plasmablastic Lymphoma: A Review of Current Knowledge and Future Directions.

Elyamany G, Al Mussaed E, Alzahrani AM - Adv Hematol (2015)

Selected immunophenotype of PBL: the PBL cells demonstrate immunoreactivity to CD138 (a), lambda light chain, ISH (b), and HHV8 (c) and negativity for CD20 (d) and CD56 (e). Proliferation index is high (f).
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4555447&req=5

fig2: Selected immunophenotype of PBL: the PBL cells demonstrate immunoreactivity to CD138 (a), lambda light chain, ISH (b), and HHV8 (c) and negativity for CD20 (d) and CD56 (e). Proliferation index is high (f).
Mentions: PBL is a high-grade B-cell lymphoma that arises from postgerminal center B-cell. The hallmark immunohistochemical staining pattern of PBL is that of terminally differentiated B-cell. PBL demonstrates little to no expression of leukocyte common antigen (LCA) or the B-cell markers CD20, CD79a, and PAX5. However, the plasma cell markers VS38c, CD38, multiple myeloma oncogene-1 (MUM1), and CD138 (syndecan-1) seem to be almost universally expressed [3, 16, 32]. PBL is characterized by a high proliferation index reflected by Ki67 expression, usually >80% (Figure 2).

Bottom Line: There is no standard chemotherapy protocol for treatment of PBL.Cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) or CHOP-like regimens have been the backbone while more intensive regimens such as cyclophosphamide, vincristine, doxorubicin, high-dose methotrexate/ifosfamide, etoposide, high-dose cytarabine (CODOX-M/IVAC), or dose-adjusted etoposide, prednisone, vincristine, cyclophosphamide, and doxorubicin (DA-EPOCH) are possible options.Recently, a few studies have reported the potential value of the proteasome inhibitor bortezomib and thalidomide in PBL patients.

View Article: PubMed Central - PubMed

Affiliation: Department of Pathology and Blood Bank, Prince Sultan Military Medical City, P.O. Box 7897, Riyadh 11159, Saudi Arabia ; Department of Hematology, Theodor Bilharz Research Institute, Egypt.

ABSTRACT
Plasmablastic lymphoma (PBL) is an aggressive subtype of non-Hodgkin's lymphoma (NHL), which frequently arises in the oral cavity of human immunodeficiency virus (HIV) infected patients. PBL shows diffuse proliferation of large neoplastic cells resembling B-immunoblasts/plasmablasts, or with plasmacytic features and an immunophenotype of plasma cells. PBL remains a diagnostic challenge due to its peculiar morphology and an immunohistochemical profile similar to plasma cell myeloma (PCM). PBL is also a therapeutic challenge with a clinical course characterized by a high rate of relapse and death. There is no standard chemotherapy protocol for treatment of PBL. Cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) or CHOP-like regimens have been the backbone while more intensive regimens such as cyclophosphamide, vincristine, doxorubicin, high-dose methotrexate/ifosfamide, etoposide, high-dose cytarabine (CODOX-M/IVAC), or dose-adjusted etoposide, prednisone, vincristine, cyclophosphamide, and doxorubicin (DA-EPOCH) are possible options. Recently, a few studies have reported the potential value of the proteasome inhibitor bortezomib and thalidomide in PBL patients. The introduction of genes encoding artificial receptors called chimeric antigen receptors (CARs) and CAR-modified T cells targeted to the B cell-specific CD19 antigen have demonstrated promising results in multiple early clinical trials. The aim of this paper is to review the recent advances in epidemiology; pathophysiology; clinical, pathologic, and molecular characteristics; therapy; and outcome in patients with PBL.

No MeSH data available.


Related in: MedlinePlus