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PubMed2002

Influence of host-recipient origin on clinical aspects of posttransplantation lymphoproliferative disorders in kidney transplantation.

BACKGROUND: Posttransplantation lymphoproliferative disorder (PTLD) is a well-known complication of immunosuppression associated with solid organ transplantation. The donor or host origin of PTLD may influence the outcome of the disease as it has been reported that a donor origin may be associated with a better prognosis. The aim of the study was to determine the origin (recipient or donor) of 12 PTLD occurring in kidney transplant recipients and to correlate the results with clinical findings. METHODS: Origin of PTLD was determined using HLA DRB1 molecular typing, analysis of multiple short-tandem repeat microsatellite loci, and HLA class I antigen expression by immunohistochemistry. RESULTS: Combining the three techniques, we found that eight cases originated from the recipient and four cases originated from the donor. The results of the three techniques were concordant and altogether assigned the origin of the tumors. All the donor-origin PTLD were strictly localized to the kidney graft, developed after a mean time of 5 months after transplantation, and regressed after reduction of immunosuppression. In contrast, seven of the eight recipient-origin PTLD presented as multisystemic disease, occurred a mean time of 75.7 months after the transplantation, and had a worse outcome (mortality, five deaths of eight patients, 62.5%). CONCLUSIONS: These results suggest that PTLD originating from the donor arise in the first year after transplantation into the graft, and that recipient-origin PTLD develop later as an invasive disease. Because it permits simultaneously the analysis of cell morphology and tumor origin, immunohistochemistry is a more reliable technique in the case of graft tumors associated with allograft rejection. The determination of the origin of the tumors seems to be of value in the management of PTLD to predict the outcome and to adapt therapy.

Adult↗

PubMed1999

Rational management of posttransplant lymphoproliferative disorder in pediatric recipients.

BACKGROUND/PURPOSE: Posttransplant lymphoproliferative disorder (PTLD) is a potentially lethal complication in the pediatric transplant patient secondary to Epstein-Barr virus (EBV) infection and potent immunosuppression. PTLD may develop in up to 10% of pediatric transplant recipients with mortality rates up to 80%. The authors report their experience with the diagnosis and efficacy of aggressive sequential management of PTLD in five patients under age 5 years. METHODS: A review of 75 pediatric liver transplant recipients on FK-506-based immunosuppression identified five biopsy-proven cases of PTLD and one probable case (8%). The probable case was a teenager, 6 months posttransplant in Spain, with mediastinal masses. No treatment or diagnosis was sought, and the patient died. The other five cases were managed with sequential therapy on an "intent-to-treat" basis with initial withdrawal of immunosuppression. If the disease progressed, patients were treated with four courses of intravenous cyclophosphamide, vincristine, Adriamycin, and intrathecal methotrexate and ara-C. RESULTS: Five children were anti-EBV titer negative at the time of transplant. Three of five received EBV-positive donor organs and two children received EBV-negative livers. Monoclonal PTLD developed between 2 and 31 months posttransplant (mean, 15.7 months). With onset of PTLD (four B cell lymphoma, one B cell leukemia) all patients had tapering or withdrawal of immunosuppression and initiation of highdose acyclovir. Two of five patients had complete remission and resumed immunosuppression. Two patients progressed and required chemotherapy. One patient with initial response relapsed 4 months later with B cell leukemia and required chemotherapy. All five patients are alive 10 to 38 months postdiagnosis (mean, 29 months). Three patients had rejection requiring resumption of FK-506 therapy. Two patients are maintained on low-dose alternate-day prednisone and no FK-506. All patients have normal liver function. Central nervous system lymphoma developed in one child with significant neurological sequelae. CONCLUSIONS: PTLD can develop in pediatric liver transplant recipients. Early withdrawal of immunosuppression and aggressive chemotherapy enabled us to achieve 100% patient and graft survival.

Algorithms↗

PubMed1999

Interleukin-10 and posttransplant lymphoproliferative disorder after kidney transplantation.

BACKGROUND: Posttransplant lymphoproliferative disorder (PTLD) is a life-threatening complication of transplantation, which comprises a morphologically and clinically heterogeneous spectrum of B-lymphocyte diseases. Risk factors include primary or reactivated Epstein-Barr virus (EBV) infection, and the type and duration of immunosuppression. Interleukin-10 (IL-10) is a pleiotropic cytokine, produced primarily by T-helper 2 (Th2) lymphocytes in the later stages of T-cell activation, suggested to play a role in EBV-associated PTLD. We recently reported preliminary findings on IL-10 in relation to the development of PTLD in three kidney transplanted patients. The study now includes nine patients that could be followed before and/or after the occurrence of lymphoma. METHODS: Nine patients with lymphomas (eight PTLDs and one Hodgkin's disease) were diagnosed among 268 consecutive renal transplantations (1990-1997). All were treated with cyclosporine with an initial 10-day course of antilymphocyte globulin, supplemented from 1995 with mycophenolate mofetil. Serum antibodies against EBV were detected using recombinant antigens. A double sandwich enzyme-linked immunosorbent assay using rabbit antibodies to purified human recombinant IL-10 was employed; the assay is specific for human natural and viral IL-10. RESULTS: Three patients experienced primary EBV infection, five reactivated EBV infections, and one did not change EBV status. Three patients had a fulminant course and died with EBV-associated PTLD confirmed post mortem. The other six are alive and are apparently cured. Treatment was immediate discontinuation of immunosuppression (in all PTLDs) and long-term high-dose aciclovir in all but one. Two patients have maintained excellent graft function for 3 and 2 years, respectively, without immunosuppression and are now in a state of operational tolerance. In three of four cases with initial lymphoma, EBV infection (primary or reactivation) preceded the increase in IL-10. In all four cases, the IL-10 increase preceded the PTLD diagnosis. In six cases, IL-10 could be followed after treatment showing either immediate zero or a decrease to zero. CONCLUSION: IL-10 seems to play a role in EBV-associated PTLD. Moreover, IL-10 may have an important role in transplant tolerance by inducing long-lasting anergy to donor- and host-specific alloantigens, perhaps caused by down-regulation of Th1 cytokines in the graft. If substantiated, this may provide new insight into the pathogenesis of PTLD introducing new strategies for prevention and therapy of PTLD, and for the induction of tolerance in transplanted patients.

Acyclovir↗

PubMed1998

The morphologic and molecular genetic categories of posttransplantation lymphoproliferative disorders are clinically relevant.

BACKGROUND: Posttransplantation lymphoproliferative disorders (PT-LPDs) are a well-known complication of immunosuppression associated with solid organ transplantation. The clinical course of PT-LPDs is unpredictable; some patients experience regression of all lesions with a reduction in immunosuppression, whereas other patients, despite chemotherapy, radiation therapy, or surgery, rapidly die of their disease. In this study, the authors attempted to establish whether the previously described morphologic and molecular genetic categories of PT-LPD--plasmacytic hyperplasia (PH), polymorphic PT-LPD (polymorphic), and malignant lymphoma/multiple myeloma (ML/MM)--are clinically relevant and helpful in predicting the clinical outcome of patients who develop these lesions. METHODS: To determine the clinical significance of the morphologic and molecular genetic categories of PT-LPDs, the clinical characteristics of 32 solid organ transplant recipients (26 heart, 5 kidney, and 1 lung), including age, time from transplantation to development of PT-LPD, stage of disease, and clinical outcome, were compared with the morphologic and molecular genetic features of the 41 PT-LPDs that they developed (15 PH in 12 patients, 19 polymorphic in 16 patients, and 7 ML/MM in 6 patients). Clinical outcome was defined by the following categories: 1) regression (after a reduction in immunosuppression) and surgical resolution (by surgical excision, with or without a reduction in immunosuppression); 2) medical resolution (by chemotherapy and/or radiation therapy); and 3) no response. RESULTS: Although there was no difference in the time from transplantation to PT-LPD development among patients belonging to the three morphologic and molecular genetic categories, there was a significant difference in patient age at the time of PT-LPD development (P < 0.0098). Younger patients developed PH (mean age of 19 years), whereas older patients developed polymorphic PT-LPD (mean age of 35 years) and ML/MM (mean age of 56 years). Patients with PH presented with lower stages of disease (Stages I-II) than patients with ML/MM (P < 0.0004). Furthermore, there was a statistically significant trend between morphologic and molecular genetic category and clinical outcome, with decreased likelihood that lesions categorized as PH, polymorphic, or ML/MM would regress with a reduction in immunosuppression or be resolved by surgery, whereas those classified as ML/MM were more likely to exhibit no response to aggressive clinical intervention (P < 0.00006). Furthermore, no patients with PH died, whereas 20% with polymorphic PT-LPD and 67% with ML/MM died as a direct result of their PT-LPDs. CONCLUSIONS: This study strongly suggests that classification of PT-LPDs into the morphologic and molecular genetic categories PH, polymorphic, PT-LPD and ML/MM is clinically relevant.

Adult↗

PubMed2002

Incidence of phenotypic aberrations in a series of 467 patients with B chronic lymphoproliferative disorders: basis for the design of specific four-color stainings to be used for minimal residual disease investigation.

Multiparameter immunophenotypic analysis of neoplastic cells has proven to be of great help for the investigation of minimal residual disease in acute leukemias; however, its utility has not been systematically explored in B cell chronic lymphoproliferative disorders. The aim of the present study was to investigate the incidence of phenotypic aberrations in a series of 467 consecutive leukemic B cell chronic lymphoproliferative disorders through the comparison of the phenotypic characteristics of tumor vs normal peripheral blood (n = 10) and bone marrow (n = 10) B cells, in order to explore the applicability of this strategy for minimal residual disease monitoring. An additional goal of our study was to evaluate the sensitivity of multiparameter flow cytometry for the detection of minimal residual disease in leukemic B cell chronic lymphoproliferative disorders through dilutional experiments (n = 19). From the patients analyzed 382 corresponded to B cell chronic lymphocytic leukemia/small lymphocytic lymphoma (353 typical and 29 atypical); five to prolymphocytic leukemia; 13 to hairy cell leukemias; 12 to lymphoplasmacytic lymphomas; 14 to splenic marginal zone lymphomas; 22 were follicular lymphomas; and 19 mantle cell lymphomas. The following triple stainings were systematically applied to both normal and leukemic samples: FMC7/CD5/CD19, CD22/CD23/CD19, CD103/CD25/CD19, CD10/CD11c/CD19 and sIg/sIg(lambda)/CD19. Overall, 98% of the leukemic B cell chronic lymphoproliferative disorders cases displayed aberrant phenotypes at diagnosis with no significant differences being found between cases analyzed in peripheral blood vs bone marrow samples. The most common types of aberrant criteria detected included asynchronous antigen expression (92%) and antigen over-expression (54%); abnormally light scatter characteristics were found in 17% of the cases. Most of the cases studied (90%) displayed four or more phenotypic aberrations. Once patients were divided according to the different diagnostic subgroups, the overall incidence of aberrant phenotypes ranged from 79 to 80% among atypical B cell chronic lymphocytic leukemia/small lymphocytic lymphoma and prolymphocytic leukemia to 97% of follicular lymphoma and 100% of typical B cell chronic lymphocytic leukemia/small lymphocytic lymphoma, hairy cell leukemia, lymphoplasmacytic lymphomas, splenic marginal zone lymphomas and mantle cell lymphomas. Based on the aberrant phenotypes detected unique four-color stainings could be built for the specific identification of aberrant phenotypes. These include CD22/CD23/CD19/CD5 and sIg(kappa)/sIg(lambda)/CD19/CD5 for lymphocytic leukemia/small lymphocytic lymphoma and prolymphocytic leukemia, CD103/CD25 or CD22/CD19/CD11c for hairy cell leukemia, FMC7/CD22/CD19/CD103 and sIg(kappa)/sIg(lambda)/CD22/CD19 for splenic marginal zone lymphomas, CD22/CD23/CD19/CD10 for follicular lymphomas and CD10/CD22/CD19/CD5 for mantle cell lymphomas. Serial dilutional experiments showed that the sensitivity level of immunophenotyping ranges between 10(-4) and 10(-5). In summary, the present study shows that immunophenotypic analysis allows the identification of aberrant phenotypes in 98% of leukemic B cell chronic lymphoproliferative disorders and these phenotypes can be used for minimal residual disease monitoring with a sensitivity limit of 10(-4)-10(-5).

Antibodies, Monoclonal↗

PubMed2004

Diagnosis by polymerase chain reaction of ocular posttransplant lymphoproliferative disorder after pediatric renal transplantation.

PURPOSE: To report diagnosis by polymerase chain reaction of intraocular posttransplant lymphoproliferative disorder in a pediatric renal transplant patient. DESIGN: Observational case report. METHODS: Retrospective review. RESULTS: An 11-year-old girl developed infectious mononucleosis 15 months after renal transplantation for focal segmental sclerosis. Papillitis and hypopyon uveitis developed 8 months later, followed by iris nodules. Diagnosis of intraocular posttransplant lymphoproliferative disorder was made by polymerase chain reaction of aqueous humor for Epstein-Barr virus and confirmed by histopathology of an iris biopsy specimen. Infiltrating iris lymphocytes in the biopsy specimen were positive for Epstein-Barr DNA. Polymerase chain reaction also revealed gene rearrangement of the variable region of the heavy immunoglobulin chain, consistent with a monoclonal B-lymphocyte population. Iris nodules resolved with reduction in immunosuppressive medication. CONCLUSION: Polymerase chain reaction for Epstein-Barr virus may be helpful in diagnosis of intraocular posttransplant lymphoproliferative disorder.

Aqueous Humor↗

PubMed1995

Epstein-Barr virus-related localized hepatic lymphoproliferative disorders after liver transplantation.

BACKGROUND: Localized hepatic post-transplant lymphoproliferative disease is uncommon. In such cases, lymphocyte Epstein-Barr virus (EBV) infection may promote an intrahepatic B-lymphocyte monoclonal expansion. METHODS: From 1990 to 1991, 149 patients underwent liver transplantation for various liver failures. Immunosuppressive therapy was azathioprine, cyclosporine-A, and methylprednisolone. Rejection episodes were treated by methylprednisolone bolus injection with or without OKT3 therapy. Three patients (2%), aged 38, 50, and 47 years, developed lymphoproliferative disease localized in the transplanted livers within 5 months of liver transplantation (a patient had been immunosuppressed for 3 years before the lymphoproliferative disease occurred within the third allografted liver). Diagnoses were obtained by fine needle aspiration. In situ hybridizations were performed with the kappa/lambda mRNA-kit FITC DAKO (DAKO Corporation, Carpenteria, CA) and the early mRNA-EBER oligonucleotide FITC DAKO: RESULTS: Lymphoproliferative diseases were all classified as diffuse polymorphic large cell lymphomas in the working formulation and considered as lymphoproliferative disorders with polymorphic large cells in the Frizzera classification. All large cells were CD20-positive, CD45-positive and CD45RO-negative. In situ mRNA light chain hybridization demonstrated monoclonality in two cases. In all three cases, EBV mRNA was detected in large cells by early mRNA-EBV (EBER) in situ hybridization. Patients were treated with doxorubicin, cyclophosphamide, vincristine, and VM26. Two patients maintained a complete remission 3 years after six cycles of chemotherapy, whereas one died of an early opportunistic infection. CONCLUSION: Epstein-Barr virus may play a special role in the pathogenesis of lymphoproliferative disorders that develop in patients who have undergone liver transplantation.

Adult↗

PubMedDate not supplied

The low-grade lymphoproliferative disorders.

Rapid advances in our understanding of the biology and pathology of lymphoproliferative disorders, permitted mainly by new diagnostic tools, constantly change our approach to this heterogenous group of disorders. In this review of the more indolent subgroup of lymphoproliferative disorders, some of the recent advances are highlighted, and treatment options discussed.

Humans↗

PubMed1989

Detection of fos oncogene products by monoclonal antibody FO-120 in lymphoproliferative disorders.

We investigated the expression of fos oncogene proteins in lymphoproliferative disorders, using a monoclonal antibody (FO-120) that was prepared against a synthetic oligopeptide of fos protein (amino acid sequence from 127 to 152). Although peripheral blood leukocytes were rarely positive for FO-120, they were transiently stained after lectin (PHA) stimulation. After culture with IL-2 for 1 or 2 weeks, less than 40% of the lymphocytes weakly reacted with FO-120, whereas strongly positive cells were detected in more than 70% of cells in half the T-cell lines established from preleukemic state of adult T-cell leukemia (pre-ATL) and all of ATL derived T-cell lines. All in vivo specimens of non-Hodgkin's malignant lymphomas, except for one case of T-cell lymphoma were also strongly positive. In addition, the extent of the antibody reactivity correlated with the histopathological grade of malignancy in B-cell lymphoma. The reactivity to most AILD-IBL lesions overlapped with that to T-lymphomas, and could be distinguished from that to reactive lesions. FO-120 appears to be a useful tool for detecting early neoplastic changes in lymphoproliferative disorders.

Antibodies, Monoclonal↗

PubMed1998

Anti-B-cell monoclonal antibody treatment of severe posttransplant B-lymphoproliferative disorder: prognostic factors and long-term outcome.

B-lymphoproliferative disorder (BLPD) is a rare but severe complication of organ and bone marrow transplantation (BMT). Profound cytotoxic T-cell deficiency is thought to allow the outgrowth of Epstein-Barr virus-transformed B cells. When possible, reduction of immunosuppressive treatment or surgery for localized disease may cure BLPD. Therapeutic approaches using chemotherapy or antiviral drugs have limited effects on survival. Adoptive immunotherapy with donor T-cell infusions has given promising results in BMT recipients. We previously reported that administration of two monoclonal anti-B-cell antibodies (anti-CD21 and anti-CD24) could contribute to the control of oligoclonal BLPD. Here we report the long-term results of treatment with these monoclonal anti-B-cell antibodies for cases of severe BLPD. In an open multicenter trial, 58 patients in whom aggressive B-cell lymphoproliferative disorder developed after BMT (n = 27) or organ (n = 31) transplantation received 0.2 mg/kg/d of specific anti-CD21 and anti-CD24 murine monoclonal antibodies (MoAbs) for 10 days. The treatment was well tolerated. Thirty-six of the 59 episodes of BLPD in the 58 patients presented complete remission (61%). The relapse rate was low (3 of 36, 8%). Multivariate analysis identified the following risk factors for partial or no response to anti-B-cell MoAb therapy: multivisceral disease (P </= .005), central nervous system involvement (P </= .05), and late onset of BLPD (P </= .005). The overall long-term survival was 46% (median follow-up, 61 months); it was lower among BMT patients (35%) than organ transplant patients (55%). None of the patients who had received BMT for hematological malignancy survived for 1 year. Eight of these 11 patients presented monoclonal BLPD. Tumor burden was the only other variable that contributed significantly to poor survival. Thus, as assessed from this long-term study, the use of anti-B-cell MoAbs therefore appears to be a safe and relatively effective therapy for severe posttransplant BLPD.

Adolescent↗

PubMed1986

Coexpression of T- and B-markers in a lymphoproliferative disorder.

An atypical case of lymphoproliferative disorder in which T- and B-cell antigens were coexpressed in the neoplastic cells is described. The disease was characterised by hepatosplenomegaly, lymphadenopathy, a low WBC (5 X 10(9)/l) and bone marrow infiltration. The predominant cell population (greater than 70%) comprised lymphoid cells with a range of nuclear irregularities and included some blast cells. 90% of the peripheral blood lymphocytes showed a mature T-helper phenotype (E+, T11+, T3+, T4+, T8-, T6-, TdT-) with coexpression of the specific B-markers B1 and FMC7, in 90% and 50% of cells, respectively. HLA-DR antigens were present in 55% of cells while surface and cytoplasmic immunoglobulins (Ig) were detected in less than 10% of cells. Molecular investigations with appropriate probes showed evidence of T-cell receptor gene rearrangement but no rearrangement for the genes of the Ig-heavy and -light chains. Cytogenetic studies revealed a translocation t(10;19) (p12; q13) in all the metaphases analyzed. This case demonstrates that the study of neoplastic cells with a battery of monoclonal antibodies may disclose the existence of a hitherto unrecognised lymphoid cell population with atypical expression of B- and T-cell antigens. On the other hand, the presence of T-cell receptor gene rearrangement indicates that this is a T-cell disorder with the aberrant co-expression of specific B-cell markers.

Aged↗

PubMedDate not supplied

Posttransplant lymphoproliferative disorder of the nasopharynx.

Posttransplant lymphoproliferative disorder (PTLD) is a serious complication of organ transplantation. Although the precise etiology is unknown, the Epstein-Barr virus and immunosuppressive agents appear to he risk factors. The presentation PTLD is diverse, including many patients with symptoms of the head and neck, which may make diagnosis difficult. We present a patient who had undergone renal transplantation referred for recurrent sinusitis. She was found to have PTLD of the nasopharynx. Three cases of head and neck PTLD treated at our institution are described. Although PTLD is uncommon in the general community, the incidence has continued to increase as more patients undergo transplants and clinical presentations of PTLD should be familiar to the otolaryngologist.

Acyclovir↗

PubMed2002

Posttransplantation lymphoproliferative disorder presenting as a unilateral leg mass 10 years after kidney transplantation.

Epstein-Barr virus (EBV)-associated lymphoproliferative disorder is a well-known complication of solid organ transplantation. The risk factors include type and degree of immunosuppression and EBV status of the donor and recipient before transplantation. The manifestations of posttransplantation lymphoproliferative disorders are myriad, from subtle findings such as tonsillar hypertrophy to fulminant manifestations such as hepatocellular failure and death. Here we report an unusual presentation of posttransplantation lymphoproliferative disorder as unilateral leg swelling in a 68-year-old man 10 years after kidney transplantation. The patient had detectable EBV-DNA by polymerase chain reaction in the peripheral blood and EBV messenger RNA by in situ hybridization in biopsy tissue. The patient's tumor did not respond to reductions in immunosuppressive medication, intravenous immunoglobulin, ganciclovir, and rituximab. Eventually the patient responded to CHOP (cyclophosphamide, Oncovin [vincristine, Eli Lilly, Indianapolis, IN], prednisone, and doxorubicin) therapy. He is currently 2 years posttreatment, with a serum creatinine of 0.8 mg/dL, on no immunosuppression.

Aged↗

PubMed2001

Posttransplantation lymphoproliferative disorder initially seen as iris mass and uveitis.

Primary ocular posttransplantation lymphoproliferative disorder is rare. Epstein-Barr virus is implicated as the cause as a result of systemic immunosuppression after transplant surgery. We studied a patient who developed ocular posttransplantation lymphoproliferative disorder after orthotopic liver transplantation. Slitlamp and light microscopic photographs confirmed the diagnosis.

Female↗

PubMed1998

Lymphoproliferative disorders: CT findings in immunocompromised children.

OBJECTIVE: The objective was to evaluate the CT imaging appearance, distribution of disease, type of immunocompromised state, and outcome of children with Epstein-Barr virus-induced lymphoproliferative disorders. MATERIALS AND METHODS: Medical records and imaging studies (from four tertiary children's medical centers) were reviewed for pathologically proven cases of lymphoproliferative disorders in patients less than 20 years old. Trends between the CT imaging appearance, distribution, and type of immunocompromised state and prognosis were noted and analyzed with Fisher's exact test. RESULTS: Twenty-seven cases were identified (mean age, 7 years 8 months). Eighteen children had undergone solid organ transplantation (heart, n = 9; liver, n = 7; kidney, n = 2), and four had undergone bone marrow transplantation. Five patients had primary immunodeficiencies. The CT appearance of lymphoproliferative disorders varied and included lymphadenopathy, focal mass or masses, and diffuse infiltration and enlargement of organs without focal mass. The distribution of disease included abdomen (n = 17), chest (n = 10), neck (n = 8), and brain (n = 1). In eight of nine heart transplant recipients, the disease predominantly involved the chest and neck, whereas in all seven liver transplant recipients, the disease was isolated to the abdomen (p = .001). The overall mortality rate of 44% was less related to anatomic extent (multiorgan, 46%; localized, 43%) than to type of immune dysfunction (p = .001): bone marrow transplantation (100%), primary immunodeficiency (80%), heart transplantation (55%), liver transplantation (0%), and kidney transplantation (0%). CONCLUSION: Lymphoproliferative disorders in children had a variable distribution, imaging appearance, and outcome. However, in recipients of solid organ transplants, the disease tended to occur in the anatomic region of the transplant. Mortality rates were more closely related to the type of underlying immune dysfunction than to distribution of disease.

Bone Marrow Transplantation↗

PubMedDate not supplied

Canine lymphoproliferative disorders. An ultrastructural study of 18 cases.

The ultrastructural features of lymphoproliferative disorders from 18 dogs are described and compared with those recorded in the veterinary literature. A spectrum of diseases was selected for study to demonstrate the structural heterogeneity of these disorders. The most extreme variations were noted in nuclear contour, where bizarre cerebriform-appearing nuclei were characteristic of neoplasms of T-cell lineage, or single deep nuclear clefts suggested B-cell lineage. The lesions surveyed included acute and chronic lymphocytic leukemias, plasma cell neoplasms, cutaneous and multicentric malignant lymphomas, and cutaneous lymphoproliferative disorders with histologic similarities to human mycosis fungoides.

Animals↗

PubMed2006

Lymphoproliferative disorders and chemokines.

Chemokines are low molecular weight cytokines specialized in leukocyte recruitment. Recent studies have shown that tumor cells of hematopoietic and non hematopoietic origin express different chemokine receptors that may be involved in neoplastic cell growth, metastasis and angiogenesis. Human lymphoproliferative disorders arise from the malignant transformation of normal lymphoid cells frozen at discrete maturational stages. Studies performed with acute or chronic lymphoproliferative disorders have shown that CXCR4, the unique receptor for CXCL12, is up-regulated in many B and T cells malignancies and may be involved in metastatic localization of the neoplastic elements. Additional chemokine receptors are expressed in the individual lymphoproliferative disorders, but some of these are often non functional. Here we shall review the state of the art on chemokine receptor expression and function in human lymphoproliferative disorders, stressing the potential value of chemokines receptors as novel therapeutic targets. In this respect, small antagonistic peptides are being produced by pharmaceutical companies and hold great promise for clinical application.

Animals↗

PubMed1997

Posttransplant lymphoproliferative disorders: summary of Society for Hematopathology Workshop.

Twenty cases of posttransplant lymphoproliferative disorders arising in solid organ allograft recipients (18 patients) or bone marrow allograft recipients (2 patients: 1 autologous; 1 allogeneic) were selected for presentation at the Society for Hematopathology Workshop. In the course of the Workshop discussions, based both on the submitted cases and the combined experience of the participants, it was possible to agree on several distinctive categories of PTLD. These include (1) early lesions, (2) polymorphic posttransplant lymphoproliferative disorders (PTLDs), (3) monomorphic PTLDs (B- and T-cell lymphomas), (4) plasmacytoma-like lesions, and (5) T-cell-rich large B-cell lymphoma/Hodgkin's disease-like lesions. Monomorphic lesions should be classified according to a recognized classification of non-Hodgkin's lymphoma, although specified in the report as PTLD. Polymorphic lesions should be carefully evaluated for clonality; by immunophenotyping; and, if necessary, analysis of antigen-receptor and Epstein-Barr virus (EBV) genomes. Minimal pathological evaluation should include routine morphology, immunophenotyping on fresh tissue (flow cytometry or frozen section), and preservation of tissue for molecular genetic analysis. Analysis of the presence of EBV can be useful in establishing whether early or equivocal lesions represent PTLD (EBV+) or unrelated processes, but is not required in most cases. The pathologist can make an important contribution to the management of patients with PTLD by providing a complete diagnostic evaluation of the biopsy specimens (this is the least expensive part of the care of a transplant patients, not a place to try to cut costs) and making sure the attending physicians understand the special issues in management of PTLD.

Bone Marrow Transplantation↗