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PubMed1995

[Results of a series of 104 consecutive bilateral bone marrow biopsy specimens in lymphoproliferative disorders].

PURPOSE: To establish the incidence of discordance in a series of bilateral bone marrow biopsies (b-BMB) in lymphoproliferative disorders and to determine whether this might lead to changes in the present treatment of each patient. MATERIAL AND METHODS: Between March/1988 and February/1995, 89 patients underwent bilateral bone marrow biopsy (104 b-BMB). Seventy-six underwent one b-BMB; 11 two b-BMB and 2 patients three b-BMB. Sixty-eight b-BMB were done at diagnosis of the disease and 36 for reassessment prior to ABMT. The distribution of the b-BMB by diagnosis was as follows: 54 non-Hodgkin's lymphoma (NHL) -23 low grade NHL and 31 intermediate/high grade NHL-, 44 Hodgkin's disease (HD), 4 multiple myeloma (MM), 1 splenic lymphoma with villous lymphocytes and 1 MM+HD. Specimens were obtained under local anaesthesia with a Jamshidi gauge 8 needle. The biopsies were fixed, decalcified, embedded in paraffin wax and the section cuts were stained (haematoxylin and eosin, Giemsa, Wilder--reticulin--and Masson--collagen--). RESULTS: There was discordance in 5 of the 104 b-BMB (4.8%), but only in four of them was this related to the presence of bone marrow disease, so that incidence falls to 3.8%. Three of them were obtained at diagnosis of the disease (low grade NHL, high grade NHL and HD) and one during reassessment before ABMT. On considering only the specimens that had bone marrow infiltration (19 cases: 14 at diagnosis and 5 in reassessment before ABMT), the absence of concordance in four of them implies that if only unilateral biopsy had been carried out, up to 21% of the cases might have been missed. In one of these patients (HD) this finding led us to replace autologous bone marrow transplantation by autologous peripheral stem cell transplantation. CONCLUSION: On the basis of these data, the use of bilateral bone marrow biopsy specimens may be justified in lymphoproliferative disorders, both at the time of diagnosis and in reassessment prior to ABMT--when the bone marrow was initially infiltrated.

Adult↗

PubMed1985

Study of platelet-associated-immunoglobulins in lymphoproliferative disorders.

In the development of thrombocytopenia in patients with lymphoproliferative disorders immunological factors may play the decisive role. Platelet-associated immunoglobulins were investigated by anti-human IgG and anti-human IgM-coated polyacrylamide beads ("Immunobeads") with light microscopy. Among the 65 patients studied 19 had thrombocytopenia and four of them had an increased number of platelet-immunobead rosettes. In four cases from the group of patients with normal platelet count this phenomenon was also demonstrated. The platelet-associated immunoglobulin was IgG except of one case in which it was IgM. Studying of platelet-associated immunoglobulins might have significance first of all in the choice of the most adequate therapy.

Blood Platelets↗

PubMed2006

Central nervous system lymphoproliferative disorder in pediatric kidney transplant recipients.

Post-transplant lymphoproliferative disorder (PTLD) is a complication of transplantation resulting from impaired immune surveillance because of pharmacologic immunosuppression. We present two cases of central nervous system (CNS) PTLD in children on calcineurin-inhibitor free immunosuppression with dramatically different presentations and outcomes. One patient had brain and spinal cord lymphoma with a rapid and fatal course. The other patient had brain and ocular PTLD that responded to multimodal therapy with reduction of immunosuppression, high-dose steroids, and rituximab given in a dose-escalation protocol. This protocol may have enhanced the penetration of rituximab into the CNS. We review the literature on CNS and ocular PTLD and elaborate on the treatments available for both diseases.

Adolescent↗

PubMed1998

Analysis of the t(2;5) (p23;q35) translocation in CD30+ primary cutaneous lymphoproliferative disorders and Hodgkin's disease.

The t(2;5) (p23;q35) chromosomal translocation is found in about 40% of lymph node-based CD30+ anaplastic large cell lymphomas of T-cell or null-cell lineage. This translocation results in the expression of a fusion protein containing the catalytic domain of anaplastic lymphoma kinase (ALK) under the control of the promoter for nucleophosmin (NPM), a nucleolar phosphoprotein. Expression of ALK activity, normally absent in lymphocytes, is postulated to be involved in the pathogenesis of lymphomas bearing the t(2;5) translocation. Certain primary cutaneous lymphoproliferative disorders and Hodgkin's disease are also known to contain CD30+ large lymphoid cells. In order to determine the role of the t(2;5) translocation in these diseases, several investigators have employed a variety of techniques including cytogenetics, genomic Southern blot analysis, RNA- and DNA-based PCR assays, various forms of in-situ hybridization, and immunostaining for the p80 fusion protein encoded by the chimeric t(2;5) transcripts. These studies included approximately 415 cases of Hodgkin's disease, 65 cases of CD30+ primary cutaneous large cell lymphoma, and 38 cases of lymphomatoid papulosis. The aggregate results of these studies indicate that the t(2;5) translocation or other somatic mutations resulting in inappropriate expression of ALK are involved rarely if at all in the pathogenesis of Hodgkin's disease, but may be present in about 10% of cases of lymphomatoid papulosis and 20% of cases of CD30+ primary cutaneous large cell lymphoma. However, the t(2;5) has not been detected yet in any case involving multiple or secondary CD30+ lymphoproliferative disorders, thereby providing no evidence for a role in tumor clone progression. Additional studies will be needed to determine if t(2;5) status has any clinical significance for patients with CD30+ primary cutaneous lymphoproliferative disorders.

Anaplastic Lymphoma Kinase↗

PubMed2000

Posttransplantation lymphoproliferative disorder in children: clinical, histopathologic, and imaging features.

Posttransplantation lymphoproliferative disorder (PTLD) is a condition in patients who receive transplants in which chronic immunosuppression leads to an unregulated expansion of lymphoid cells; the condition ranges from hyperplasia to malignant lymphoid proliferation. Risk factors affecting the incidence of PTLD include allograft type, Epstein-Barr virus infection, and immunosuppression. In this article, we review the clinical, histopathologic, and imaging features of PTLD in children. Because PTLD can affect nearly any organ system, a wide variety of clinical manifestations is possible. The heterogeneous nature of the disease is also reflected on imaging studies. The goals of imaging in patients with PTLD are to detect disease, guide biopsy, and direct appropriate follow-up imaging rather than to establish a specific diagnosis. Because the clinical and imaging manifestations of PTLD are nonspecific and are not reliably predictive of histopathologic subtype, tissue biopsy is necessary for final diagnosis.

Biopsy↗

PubMed1997

Bcl-6 and lymphoproliferative disorders.

We report a series of 37 cases of lymphoproliferative disorders with 3q27 structural chromosomal abnormalities. Breakpoints at 3q27, the site of the bcl-6 gene, appear in a broad range of B cell lymphoma histologies but are most frequently detected in follicular lymphomas lacking a t(14;18) and diffuse large cell lymphomas. The majority of 3q27 rearrangements result from translocations involving the immunoglobulin heavy or light chain genes, however, involvement of other partner chromosomes is also observed. Molecular rearrangement of bcl-6 is demonstrable in a subset of cases. Bcl-6 is a recently identified gene encoding a zinc-finger protein. It is normally expressed in germinal center B cells where it is believed to have a developmental or differentiation function. Transcriptional deregulation of bcl-6 through translocations, submicroscopic molecular rearrangements or point mutations may be responsible for this gene's putative lymphomagenic potential.

Adolescent↗

PubMed2006

Review of Epstein-Barr virus and post-transplant lymphoproliferative disorder post-solid organ transplantation.

Post-transplant lymphoproliferative disorder (PTLD) following solid organ transplantation is an important form of post-transplant malignancy. PTLD is typically associated with Epstein-Barr virus (EBV) and occurs in the setting of profound immunosuppression resulting in a deficiency of EBV-specific cytotoxic T lymphocytes (CTL). Predisposing factors include EBV mismatch between donor and recipient, use of immunosuppression especially T-cell depletive therapies and genetic predisposition of recipients. The standard approach has been to reduce immunosuppression but is often insufficient to induce tumour regression. Further understanding of the immunobiology of PTLD has resulted in improved monitoring techniques (including EBV viral load determined by polymerase chain reaction) and newer treatment options. Recent work has highlighted a potential role for dendritic cells in both the pathogenesis and treatment of PTLD. Current treatment modalities include adoptive immunotherapy using ex vivo generated autologous EBV-specific CTL or allogeneic CTL, cytokine therapies, antiviral agents, and more recently, rituximab and dendritic-cell based therapies. This review focuses on the developments and progress in the pathogenesis, diagnosis and treatment of PTLD.

Dendritic Cells↗

PubMed2000

[T-cell lymphoproliferative disorder involving the central nervous system in two cases].

Lymphoproliferative disorder (LPD) sometimes occurs in immunosuppressive patients. B-cell proliferation is predominantly seen in patients with LPD and T-cell proliferation is rare. We here report two patients with T-cell LPD involving the central nervous system (CNS). A 7-year-old boy developed increased intracranial pressure and computed tomography showed a ring-enhanced mass lesion in the right frontal lobe. A 10-year-old boy developed gait disturbance and magnetic resonance imaging showed a non-enhanced lesion in the left parietal lobe. Radiological findings could not differentiate CNS-LPD from other intracranial diseases. Only histologic examination could diagnose LPD in both cases, and Epstein-Barr virus associated RNA was found in the infiltrated T-cell of the latter case. Although chemotherapy with antitumor agents was effective for remission of LPD in both cases, both patients died 3 years after their operations. As CNS-LPD shows rapid progression and frequently results in fatality, this disease requires immediate histologic diagnosis followed by extensive chemotherapy.

Central Nervous System↗

PubMed1997

Donor or recipient origin of post-transplantation lymphoproliferative disorders: evaluation by in situ hybridization.

Post-transplantation lymphoproliferative disorders (PTLDs) have been reported after bone marrow and solid-organ transplantation. It might be of interest to know the origin of PTLDs, because it has been suggested that a donor origin could be related to a better prognosis. We studied five cases of PTLD in sex-mismatched allografted recipients by in situ hybridization technique for chromosome Y on isolated cells as well as on frozen and on routinely fixed and paraffin-embedded material. Two proved to be of donor origin, including the only case of PTLD arising in the graft, and three of recipient origin. The best results were obtained on isolated cells, but it must be emphasized that hybridization on tissue sections from frozen material or from material fixed in formalin or in formalin-acetic acid-alcohol and then paraffin embedded also gave good results. Hybridization after fixation in Bouin's liquid was not reliable. These results suggest that evaluation of the origin of PTLDs can easily be performed on routinely processed cytologic and histologic material.

Adult↗

PubMed1996

Lack of the t(2;5) or other mutations resulting in expression of anaplastic lymphoma kinase catalytic domain in CD30+ primary cutaneous lymphoproliferative disorders and Hodgkin's disease.

The t(2;5) (p23;q35) chromosomal translocation has been found in a high proportion of lymph node-based CD30+ large cell lymphomas of T-cell lineage. This translocation is believed to result in the expression of a fusion protein containing the catalytic domain of anaplastic lymphoma kinase (ALK) under the control of the promoter for nucleophosmin, a nucleolar phosphoprotein. Expression of ALK activity, which does not normally occur in lymphocytes, is postulated to be involved in the pathogenesis of lymphomas bearing the t(2;5) translocation. Several primary cutaneous lymphoproliferative disorders and Hodgkin's disease are also known to contain CD30+ large lymphoid cells. To determine the role of the t(2;5) translocation in these diseases, we developed a DNA-based polymerase chain reaction (PCR)/Southern blot assay to detect this translocation at the genomic level in lymphomatoid papulosis (14 cases), primary cutaneous CD30+ large cell lymphoma of T-lineage (10 cases) and Hodgkin's disease (13 cases). Two cases of pityriasis lichenoides were also studied. The t(2;5) translocation was not present in any of these specimens. To determine if some other somatic mutation might have resulted in inappropriate expression of ALK catalytic domain, we devised an RNA-based reverse transcriptase-PCR assay to detect transcripts encoded by this ALK region. None were found in the six additional cases of lymphomatoid papulosis that were studied. In aggregate, these results strongly suggest that inappropriate expression of ALK is not involved in the pathogenesis of these CD30+ lymphoproliferative disorders, and that lymph node-based CD30+ large cell lymphoma is a disease that is biologically distinct from skin-based CD30+ lymphoproliferative disorders and Hodgkin's disease. Using methods developed for this report, we also cloned and sequenced the t(2;5) genomic junctional sequences present in the SUP-M2 and SU-DHL-1 cell lines. These intron sequences will be useful for mapping t(2;5) breakpoint clusters.

Adult↗

PubMed1997

Iatrogenic lymphoproliferative disorders in nontransplantation settings.

Iatrogenic (IAT) immunosuppression-related lymphoproliferative disorders (LPDs) can occur outside the solid organ transplantation setting in patients who receive immunomodulatory therapy for a variety of underlying diseases. Most frequently, these patients suffer from rheumatologic diseases and are receiving one or more therapies during the time that LPDs develop. Specific therapies include methotrexate, azathiaprine, cyclosporine, prednisone, and others as well as combinations of therapies. In a significant subset of patients, these IAT LPDs spontaneously regress when therapy is discontinued, a finding that implicates immunomodulatory therapy, at least in part, in the development of these LPDs. The morphological spectrum of IAT LPDs includes atypical polymorphous LPDs, diffuse aggressive non-Hodgkin's lymphomas, Hodgkin's disease, and lymphoproliferations resembling Hodgkin's disease. The diagnosis requires a combined morphological and immunonphenotypic approach; in situ hybridization studies for Epstein-Barr virus (EBV) provide important information in the evaluation of these lesions. Withdrawal of immunosuppressive therapy and observation for a short period should be considered in the initial treatment of IAT LPDs, especially when they are EBV positive. This approach may obviate the need for unnecessary cytotoxic chemotherapy or radiation therapy in a significant subset of patients. However, some of these IAT LPDs behave in an aggressive manner; therefore, close clinical management is warranted.

Humans↗

PubMed2005

Post-transplant lymphoproliferative disorders (PTLD) after solid organ transplantation.

Post-transplant lymphoproliferative disorders (PTLD) are a well-recognised and potentially fatal complication after solid organ transplantation. They include a spectrum of disorders ranging from benign hyperplasia to invasive malignant lymphoma. The majority of cases are associated with Epstein Barr virus (EBV)-driven tumour formation in B cells and are a consequence of the detrimental effect of immunosuppressive agents on the immune-control of EBV. This review provides an update on the pathogenesis and clinical features of PTLD after solid organ transplantation and discusses recent progress in management. Reduction in immunosuppressive therapy remains a key component of therapy for EBV-positive PTLD and may lead to remission in early disease. Chemotherapy is used when reduced immunosuppression fails to control early disease and as initial therapy for many cases of late disease. Unfortunately, the mortality for PTLD that fails to respond to a reduction in immunosuppression remains high. Newer treatments include manipulation of the cytokine environment, B lymphocyte depleting antibodies and adoptive T cell immunotherapy using allogeneic or autologous EBV-specific cytotoxic T lymphocytes. Although early results appear promising, well-designed clinical trials are needed to assess the efficacy of these novel approaches. EBV vaccination may in the future prove an effective prophylaxis against EBV-driven PTLD but until then, avoiding excessive immunosuppressive therapy may help minimise the risk of PTLD.

Epstein-Barr Virus Infections↗

PubMed2004

Surveillance of Epstein-Barr virus infection as a risk factor for post-transplant lymphoproliferative disorder in pediatric renal transplant recipients.

Post-transplant lymphoproliferative disorder (PTLD) represents a heterogeneous group of abnormal lymphoid proliferations, generally of B-cells, that occur in the setting of ineffective T-cell function because of pharmacological immunosuppression after organ transplantation. The vast majority of PTLDs are associated with Epstein-Barr virus (EBV) infection, as manifested by the presence of EBV within the malignant tissue. Surveillance for the presence of primary or reactivated EBV infection may have the potential to prevent the development of PTLD by early intervention. However, there are, at present, no means of discriminating between innocent infectious mononucleosis syndromes and PTLD. Furthermore, standardization of measurement of EBV copies between centers is urgently required for the definition of "high" EBV viral load. Because of a lack of a close relationship between viral load and the occurrence of PTLD, other strategies such as the combined analysis of EBV viral load and EBV-specific T-lymphocytes may be better to assess the risk for the development of PTLD. Whereas the mainstay of therapy for overt PTLD is reduction of immunosuppression, such reduction based solely on a high EBV viral load without clinical evidence for PTLD is not based on scientific evidence. This strategy could result in the under-immunosuppression of many transplant recipients in the absence of a real risk for PTLD, with potentially harmful consequences such as an increased rate of acute rejection episodes.

Animals↗

PubMed2006

Reduced-intensity allogeneic haemopoietic stem cell transplantation induces durable responses in patients with chronic B-lymphoproliferative disorders.

Thirty-six patients with chronic B-lymphoproliferative disorders (B-LPD) underwent reduced-intensity allogeneic transplantation (RIT) from HLA-identical related donors. Diagnoses included follicular (n=17), mantle cell (n=9) and small lymphocytic lymphoma (n=2), and chronic lymphocytic leukaemia (n=8). Median age at transplant was 51 years (range, 30-66) and time from diagnosis was 3.4 years (range, 0.3-9.5). At transplant, 28% were in CR, 36% were in PR and 36% were chemorefractory. Conditioning therapy included fludarabine and either cyclophosphamide (n=27) or melphalan (n=9). Graft-versus-host disease (GVHD) prophylaxis consisted of cyclosporin (CsA)/methotrexate (n=21), CsA/mycophenolate mofetil (n=13) or CsA alone (n=2). Eight patients died owing to acute GVHD (n=3), infection in association with chronic GVHD (n=4) and intra-abdominal bleeding (n=1). Treatment-related mortality was 8% at day 100, and 17 and 20% at one and two years, respectively. The cumulative incidence of grade II-IV acute GVHD was 58%, whereas limited and extensive chronic GVHD occurred in 25 and 56%, respectively. No patient has relapsed or progressed. At a median follow-up of 48 months, overall survival probability is 80% (95% CI, 67-93%). We confirm that RIT in chronic B-LPD can result in high and durable CR rates but with significant incidences of acute and chronic GVHD.

Adolescent↗

PubMed2001

Posttransplant lymphoproliferative disorder after liver transplantation in miniature swine.

BACKGROUND: Posttransplant lymphoproliferative disorder (PTLD) is a well-known, life-threatening complication of immunosuppressive therapy, occurring in both adult and pediatric transplant recipients. METHODS: To study the effect of major histocompatibility complex on tolerance induction to primarily vascularized liver allograft, a semi-identical miniature swine model was developed to mimic the clinical situation of parent-into-infant liver transplantation. Long-term acceptance of semi-identical liver allograft was obtained by a transient course of FK506. In a subgroup of six animals, three developed a lethal PTLD. These animals were studied by histology and immunohistochemistry and the anti-donor cellular immune response was assessed. In addition, the possible viral origin of the proliferative process was evoked. RESULTS: Histology and immunohistochemistry revealed an abnormal B-cell proliferation in many organs of swine suffering from PTLD. Evidence of human Epstein-Barr virus, cytomegalovirus, and adenovirus was not evidenced, but a porcine virus responsible for a respiratory and reproductive syndrome (PRRS) was identified in the lymphoid tissue of these animals. In mixed lymphocyte reaction, a significant antiself immune response confirmed an infection by a virus. CONCLUSIONS: This is the first report suggesting that PRRS virus might provoke PTLD in immunosuppressed miniature swine after orthotopic liver transplantation. Whether PTLD could be induced by injection of the PRRS virus in immunosuppressed animals, a pig model of PTLD might be developed and would represent an interesting preclinical model for testing anti-PTLD therapies.

Animals↗

PubMed2002

Identification of prognostic factors in post-transplant lymphoproliferative disorders.

Organ transplantations can lead to post-transplant lymphoproliferative disorders (PT-LPDs) as a result of immunosuppressive therapy. PT-LPDs clearly differ from non-Hodgkin's lymphomas occurring in immunocompetent patients, in terms of clinical presentation, pathological findings and treatment response. Several studies have tried to establish some prognostic factors but the small number of patients hinders the analysis. We studied 61 patients from two transplant centers who developed a PT-LPD after kidney (34 patients), heart (19 patients), lung (4 patients) or liver (3 patients) transplantation. Treatment consisted of modification of the immunosuppressive regimen, chemotherapy and/or monoclonal antibody infusions. Analyzing potential prognostic factors, we found that factors predictive of failure to achieve a complete remission were, in univariate analysis, a performance status (PS) > or =2 and negativity of the tumor for the Epstein-Barr virus (EBV), and in multivariate analysis, only the PS. Factors predictive of lower survival were, in univariate analysis, a PS > or =2, number of sites > 1, primary central nervous system (CNS) location, T-cell phenotype, monoclonality of the tumor, tumor negativity for EBV and chemotherapy as a first treatment; in multivariate analysis, only PS and the number of sites were statistically significant. The International Prognostic Index (IPI) failed to identify a patient subgroup with a lower survival or treatment response, whereas a simple index using PS and number of sites clearly identified three different groups. The median survival has not yet been reached in the lower-risk group, whereas it is 34 months in the intermediate-risk patients and 1 month in the high-risk group. Studies on larger cohorts of patients need to be performed to confirm these data.

Adolescent↗

PubMed2000

Expression of p16/INK4a in posttransplantation lymphoproliferative disorders.

It was recently demonstrated that classification of posttransplantation lymphoproliferative disorders (PT-LPDs) into morphological and molecular categories is clinically relevant. It was also reported that PT-LPD not associated with Epstein-Barr virus (EBV) had a more aggressive course than most lesions associated with EBV. Because the cyclin-dependent kinase inhibitor p16/INK4a has been reported to be frequently inactivated in high-grade lymphomas, we evaluated 17 PT-LPD to determine whether p16/INK4a expression could be correlated to morphology, EBV detection, and a Ki-67 labeling index. We demonstrated that tumors with no p16/INK4a expression (n = 8) had a predominantly monomorphic appearance, and most were EBV negative (respectively, 7/8 and 5/8), whereas lesions with p16/INK4a expression (n = 9) were mostly polymorphic PT-LPD (6/9) (P = 0.049) and associated with EBV (9/9) (P = 0.015). In particular, strong p16/INK4a expression was observed in atypical immunoblasts and Reed-Sternberg-like cells. Furthermore, the proliferation index was significantly higher in tumors lacking p16/INK4a expression than in other lesions (P = 0.0008). In conclusion, down-regulation of p16/INK4a was mostly observed in PT-LPD lesions known to follow more aggressive courses: monomorphic tumors and EBV-negative PT-neoplasms. Conversely, overexpression of p16/INK4a was associated with EBV-positive PT-LPD. While p16/INK4a might play a role in the proliferative rate of LP-LPD, further investigations are needed to assess the clinical relevance of p16/INK4a expression in predicting the evolution of tumors and to explain how EBV could favor p16/INK4a protein accumulation in lesions.

Adult↗

PubMed1998

BCL-6 gene mutations in posttransplantation lymphoproliferative disorders predict response to therapy and clinical outcome.

Posttransplantation lymphoproliferative disorders (PT-LPDs) represent a heterogeneous group of Epstein-Barr virus-associated lymphoid proliferations that arise in immunosuppressed transplant recipients. Some of these lesions regress after a reduction in immunosuppressive therapy, whereas some progress despite aggressive therapy. Morphological, immunophenotypic, and immunogenotypic criteria have not been useful in predicting clinical outcome. Although structural alterations in oncogenes and/or tumor suppressor genes identified in some PT-LPDs correlate with a poor clinical outcome, the presence of these alterations has not been a consistently useful predictor of lesion regression after reduction of immunosuppression. We examined 57 PT-LPD lesions obtained from 36 solid organ transplant recipients for the presence of mutations in the BCL-6 proto-oncogene using single-strand conformation polymorphism and sequence analysis, followed by correlation with histopathologic classification and clinical outcome, which was known in 33 patients. BCL-6 gene mutations were identified in 44% of the specimens and in 44% of the patients; none were identified in the cases classified as plasmacytic hyperplasia. However, mutations were present in 43% of the polymorphic lesions and 90% of the PT-LPDs diagnosed as non-Hodgkin's lymphoma or multiple myeloma. BCL-6 gene mutations predicted shorter survival and refractoriness to reduced immunosuppression and/or surgical excision. Our results suggest that the BCL-6 gene structure is a reliable indicator for the division of PT-LPDs into the biological categories of hyperplasia and malignant lymphoma, of which only the former can regress on immune reconstitution. The presence of BCL-6 gene mutations may be a useful clinical marker to determine whether reduction in immunosuppression should be attempted or more aggressive therapy should be instituted.

Cell Transformation, Neoplastic↗