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G Frizzera

Publications and source records attributed to G Frizzera.

At least 73 records · Page 4Linked to original sources

Immunophenotyping of hematopoietic malignancies in paraffin sections.

Immunophenotyping of hematopoietic malignancies is usually accomplished in frozen sections or cell suspensions. To determine whether this procedure was also feasible in paraffin sections, we performed a double-blind immunoperoxidase study of 65 hematopoietic tumors whose phenotypes had been determined previously in fresh tissue. A selected antibody panel was used, including anti-LN2, UCHL-1, anti-cathepsin B, anti-Leu M1, anti-MB2, and anti-MT1. A correct phenotype was obtained on paraffin sections in 95% of cases. All 31 B-cell malignancies were properly classified, showing reactivity for LN2 and MB2. In 14 of 15 T-cell hematopoietic malignancies, all cells reacted with anti-MT1 and/or UCHL-1; the 1 case negative for these antigens was misdiagnosed as a B-cell tumor because of misinterpreted LN2 reactivity in benign histiocytes. Four of 5 true histiocytic neoplasms were positive for cathepsin B and LN2 but lacked other antigens; the fifth case was wrongly considered a B-cell proliferation because only bland histiocytes displayed cathepsin B. Only 1 of 7 Hodgkin's lymphomas was misdiagnosed (as a T-cell tumor); in the other 6 cases, Reed-Sternberg cells were reactive for LN2 and LEU M1. Five of 6 extramedullary myeloid leukemias also stained for LN2, MT1, and LEU M1. One showed LN2, MB2, and MT1; this case was classified as a B-cell neoplasm and indeed represented a pre-B-cell transformation of chronic myelogenous leukemia. These results show that the specified panel of antibodies may be useful for immunophenotyping of hematopoietic neoplasms when only paraffin sections are available for analysis. However, it cannot supplant traditional cell-marker studies of hematopoietic tumors because of its lesser accuracy.

Antibodies, Monoclonal↗

Inflammatory pseudotumor of lymph nodes. A distinctive pattern of nodal reaction.

We report seven cases of a previously undescribed, distinctive pattern of nodal reaction resembling inflammatory pseudotumor (IPT) of the lung and other organs. The four men and three women in the series ranged in age from 16 to 62 years (median, 33). All patients presented with prominent lymphadenopathy. Constitutional symptoms were present in five patients, and laboratory abnormalities (especially elevated erythrocyte sedimentation rate, anemia, or hypergammaglobulinemia) in four. All patients recovered (two without treatment) and are alive and well 7-40 months (median, 23) after presentation. Histologically, the process mainly involved the connective tissue framework of the node (hilum, trabeculae, capsule), secondarily spreading into the lymphoid tissue proper and the perinodal soft tissue. It was characterized by a storiform growth pattern, marked vascularity with associated vascular lesions, and a polymorphous reactive cellular infiltrate in a collagen-rich stroma. The differential diagnosis included other reactive processes (Castleman's disease, drug lymphadenopathies), malignant lymphoma (Hodgkin's, peripheral T-cell), histiocytic or reticulum cell lymphomas, and malignant fibrous histiocytoma. Some features of this process appear to be the result of an "acute phase" response; others might be accounted for by a specific target of the initial insult or alterations in the regulation of the inflammatory response to it, rather than by any specific etiologic agent.

Diagnosis, Differential↗

Cytogenetic abnormalities predict clinical outcome in non-Hodgkin lymphoma.

Tumor cytogenetic analysis was done for 68 patients with newly diagnosed non-Hodgkin lymphoma, and recurring cytogenetic abnormalities were correlated with achievement of complete remission, duration of complete remission, and survival. Among all patients, the presence of normal metaphases in tumor material was associated with a higher complete remission rate and longer survival. However, the duration of complete remission did not correlate with the presence or absence of chromosomal changes. Among patients with follicular lymphomas, the presence of normal metaphases in the tumor material was again associated with a higher rate of complete remission and with longer survival. Patients with structural abnormalities of chromosome 17 had a shorter survival than patients without these abnormalities. Among the patients with diffuse large-cell and immunoblastic lymphomas, those with breaks in the short arm of chromosome 2 had a longer survival than those without these breaks. We conclude that chromosomal abnormalities are predictive of clinical outcome in malignant lymphoma.

Adolescent↗

Castleman's disease and related disorders.

Three disorders that bear the eponym of Castleman's disease (CD) are discussed. The localized CD of hyaline-vascular (HV) type features an architecturally abnormal, hypervascular lymphoid tissue with burned-out germinal centers, and presents as an asymptomatic, slowly growing mass. It may represent a lymphoid hyperplasia associated with excessive angiogenesis. The localized CD of plasma cell (PC) type, instead, features an architecturally recognizable lymph node with solid sheets of PCs and presents with systemic manifestations of inflammation and B cell hyperreactivity. It appears as a localized chronic reaction to unknown antigens. "Multicentric" CD indicates a clinicopathologic entity characterized by the histology of CD of "mixed" type, a predominantly lymphadenopathic presentation consistently involving peripheral nodes, manifestations of multisystem involvement, and an idiopathic nature. It is best considered as a systemic B cell lymphoproliferation, which probably arises in a setting of immunoregulatory deficit, and may result in the outgrowth of clonal B cell populations. An attempt is presented to place the latter two forms of CD in the larger perspective of idiopathic PC disorders, by taking into account both the nature of the diseases (hyperplastic, dysplastic, neoplastic) and the lymphocyte traffic system that is involved (bone marrow-bound, mucosa-associated or peripheral-node-bound). In such a scheme, localized CD, PC type, and multicentric CD appear as a hyperplastic and a dysplastic disorder, respectively, of peripheral-node-bound B cells, related to, and often associated with, primary nodal plasmacytoma and osteosclerotic myeloma (so-called POEMS, Takatsuki's or Crow-Fukase's syndrome).

Blood Vessels↗

Clonal rearrangement for immunoglobulin and T-cell receptor genes in systemic Castleman's disease. Association with Epstein-Barr virus.

Castleman's disease is a morphologically and clinically heterogeneous lymphoproliferative disorder. Both a localized benign variant and an aggressive form with systemic manifestations have been described. To investigate the differences between these variants of Castleman's disease, the authors analyzed lymph node DNA from 4 patients with the localized type and 4 with the systemic type of Castleman's disease for immunoglobulin and T-cell receptor gene rearrangements. The role of Epstein-Barr virus (EBV) and cytomegalovirus (CMV) was also studied by viral genomic DNA probes. They detected clonal rearrangements in 3 of the 4 patients with the systemic variant of Castleman's; no patients with localized disease had rearrangements. Copies of EBV genome were also detected in 2 of the 3 patients with clonal rearrangements. These results suggest that systemic Castleman's disease is a disorder distinct from the classical localized variant in that it may evolve into a clonal lymphoproliferation.

Adolescent↗

Epstein-Barr virus associated B cell lymphoproliferative disorders following bone marrow transplantation.

B cell lymphoproliferative disorders (BLPD) developed in eight patients following bone marrow transplantation (BMT) for leukemia (five patients) or immunodeficiency (three patients). Recipients of T depleted marrow from a mismatched donor were at particularly high risk of this complication. Six of 25 (24%) recipients of mismatched T depleted bone marrow developed BLPD. In contrast, none of 47 matched T depleted transplants, one of ten (10%) who received non-depleted marrow from an unrelated donor, and only one of 424 matched non-depleted transplants were associated with BLPD. Epstein-Barr virus (EBV) specific serology and DNA hybridization studies demonstrating five to 50 copies of EBV genome/cell in involved tissues implicate this virus as an associated etiologic agent. Restriction fragment length polymorphism (RFLP) and cytogenetic analysis of involved tissue demonstrated donor origin (five of seven) or host origin (two of seven). Histologic appearance was similar to EBV-induced polymorphic B cell proliferations described following solid organ transplantation, or which occur de novo in primary immunodeficiency. Six of seven patients with adequate tissue available for study were found to have monoclonal proliferations by: in situ immunofluorescence (six of seven), and/or immunoglobulin gene rearrangement, (four of six). Cytogenetic analysis of involved tissues from four patients showed a normal karyotype, whereas two had multiple clonal chromosomal abnormalities. Seven patients died despite aggressive attempts at therapy with combinations of antiviral, immunologic, and chemotherapeutic agents.

Antibodies, Viral↗

A novel translocation, t(9;17)(q34;q23), in aggressive childhood lymphoblastic lymphoma.

In a chromosome study of childhood lymphoblastic lymphoma, we found a novel translocation, t(9;17)(q34;q23), in three patients. They presented with mediastinal mass and no bone marrow involvement. Despite intensive chemotherapy, one patient had no response, the other two relapsed after a brief remission, and all progressed to death. The 9;17 translocation may have a clinical implication for lymphoblastic lymphoma patients in predicting a poor prognosis. Since, in addition to our cases, involvement of the 9q34 breakpoint, together with 2q33, 14q11, or 7q34, has been reported in the literature in four lymphoblastic lymphoma patients, a gene located in 9q34 and referred to as tcl-3 may participate in the genesis of the T cell malignancies carrying these translocations. Furthermore, as is the case in other lymphomas, the reciprocal breakpoint, 17q23, might be the site of a yet unidentified T cell function gene.

Adolescent↗

Characteristic karyotypic pattern in T-cell lymphoproliferative disorders with reactive "angioimmunoblastic lymphadenopathy with dysproteinemia-type" features.

We report the clinical, histological, immunophenotypic, and cytogenetic findings in ten patients with T-cell lymphoproliferative disorders demonstrating reactive "angioimmunoblastic lymphadenopathy with dysproteinemia (AILD)-type" features. Fifteen available specimens were diagnosed as atypical hyperplasias (four) or malignant lymphomas (11). The latter were classified as AILD-type (five), T-zone (four), lymphoepithelioid (one), and low-grade, unclassified lymphoma (one). Despite the histologic differences, all these lesions shared minor nuclear atypicalities and reactive AILD-type features such as prominent vascularity, plasma cells, eosinophils, macrophages, and residual germinal centers. All lesions were immunophenotyped as predominantly T cell. The chromosome pattern was characterized by the frequent presence of karyotypically unrelated abnormal clones and/or cells with nonclonal chromosome abnormalities, a large population of normal mitotic cells, and a high incidence of trisomies 3 and 5. Sequential cytogenetic and histologic studies in five patients revealed that atypical hyperplasia and lymphoma with AILD-type features shared the same cytogenetic characteristics, ie, an unstable coexistence of normal mitotic cells and small-clonal and/or nonclonal abnormal cells, and that histologic transformation from low-grade lymphoma to immunoblastic lymphoma was accompanied by a selective proliferation of abnormal clonal cells. The AILD-type histology and the characteristic karyotypic pattern may be the expression of a specific pathogenesis and may warrant the separation of these neoplasias from other peripheral T-cell lymphomas.

Adult↗

Agreement rates and American-Japanese pathologists' comparability of a modified Working Formulation for non-Hodgkin's lymphomas. An analysis of the cases collected for the Fifth International Workshop on Chromosomes in Leukemia-Lymphoma.

Histopathologic slides of 368 cases collected from 16 institutions around the world for the Fifth International Chromosome Workshop were independently reviewed by a group of five hematopathologists consisting of two Americans and three Japanese. Agreement rates of their diagnoses using the Working Formulation (WF) for non-Hodgkin's lymphomas were studied. A modified classification scheme of the WF was used in order to define cytologic subtypes more specifically, enabling 65 possible diagnostic choices. Data analyses by computer revealed that at least four out of five diagnostic agreements were observed in 290 cases (78.9%). Similar agreements were observed in more than 80% of the cases for most of the categories of the WF, excepting diffuse small cleaved (73.3%), diffuse mixed (64.2%), diffuse large cell (76.5%), and immunoblastic lymphoma (70.2%). Agreement rates between American and Japanese pathologists did not demonstrate statistically significant differences against expected values. It was concluded that the WF was a reliable and useful classification system for multi-institutional as well as international projects, although refinements may be necessary in some categories for better diagnostic agreement.

Humans↗

Multiple recurrent genomic defects in follicular lymphoma. A possible model for cancer.

Several steps in the clinical evolution of human neoplasia are associated with a variety of recurrent chromosomal defects that could prove essential to the understanding of cancer. We found 15 types of nonrandom chromosomal abnormalities in a study of 71 patients with follicular lymphoma; 10 of the types appeared to influence the histopathological findings, clinical course, or response to treatment. A translocation, t(14;18), observed in 85 percent of all patients appeared to be the main determinant of a follicular pattern. Ten patients with a t(14;18) as a single defect had the histologic features of follicular small cleaved-cell lymphoma. Most did not require treatment for one to four years, because their tumors had an initial indolent course. In contrast, patients with follicular small cleaved-cell lymphoma with t(14;18) and deletion 13q32 acquired the hematologic features of leukemia and had an acceleration of the disease. A deletion 6q together with a complete or partial trisomy 7 or trisomy 12 (or both) was associated with the clinically more aggressive follicular mixed small- and large-cell or large-cell histologic type, which often evolves from follicular small-cell lymphoma. A complete or partial trisomy 3, 18, or 21 correlated almost exclusively with follicular large-cell lymphoma. In all follicular stages, a trisomy 2 or duplication 2p often accompanied an accelerated clinical course and a poor response to treatment. This study suggests that several discrete genomic defects may govern the evolution of a patient's malignant disease.

Adult↗

Three immunostaining techniques for the localization of leukocyte common antigen in formalin-fixed, paraffin-embedded dermatological biopsy specimens.

Although leukocyte common antigen is a valuable discriminant between lymphoreticular proliferations and other histologically similar neoplasms, several publications have described difficulties in adequately labeling this determinant in formalin-fixed, paraffin-embedded tissues. We studied 662 paraffinized cutaneous and noncutaneous neoplasms for the presence of leukocyte common antigen, using an extended avidin-biotin-peroxidase complex (ABC) method, a combined ABC-peroxidase-antiperoxidase technique, and a biotin-strept-avidin procedure. Each of the three immunohistochemical techniques produced effective results in the detection of leukocyte common antigen in all malignant lymphomas, but none of them produced false-positive staining in nonhematopoietic lesions. These results suggest that antibodies to leukocyte common antigen are highly specific and that the methods employed in this study allow for excellent diagnostic sensitivity in the recognition of cutaneous lymphomas.

Biopsy↗

The Immunodeficiency Cancer Registry. A research resource.

The Immunodeficiency Cancer Registry (ICR) contains nearly 500 case records regarding patients with primary immunodeficiencies who have developed malignancies. There is a proportional excess of lymphomas (50.7%) among the ICR cases and more than one-half of these cases were diagnosed at less than 10 years of age. Information in the ICR database is accessible to investigators conducting research on the biology or epidemiology of cancers associated with immunodeficiency.

Child↗

Hodgkin's disease in pediatric patients with naturally occurring immunodeficiency.

A case/control study of pediatric patients with Hodgkin's disease (HD) was undertaken to compare clinical characteristics in patients with known underlying immunodeficiency (20 Immunodeficiency Cancer Registry cases) and without known immunodeficiency (100 Late Effects Study Group cases). Immunodeficiency Cancer Registry cases demonstrated a younger mean age at diagnosis (p = 0.03), and a significantly higher rate of failure to achieve remission (p = 0.001) than did the Late Effects Study Group controls. Also, Immunodeficiency Cancer Registry cases showed a proportional excess of unfavorable histologies when compared with large published pediatric series. These discrepancies are consistent with a common etiology of HD relating to underlying immune defect in Immunodeficiency Cancer Registry HD patients as well as HD patients (or a select subgroup) without known immunodeficiency disorders.

Adolescent↗

Immunostaining for leukocyte common antigen using an amplified avidin-biotin-peroxidase complex method and paraffin sections. A study of 735 hematopoietic and nonhematopoietic human neoplasms.

Antibodies to leukocyte common antigen (LCA) are valuable in surgical pathology in the diagnostic separation of malignant lymphomas from poorly differentiated neoplasms of other types. However, several publications have reported difficulty in obtaining adequate LCA labeling in paraffin-embedded specimens. To assess this problem further, we applied an amplified version of the avidin-biotin-peroxidase complex procedure to 315 formaldehyde-fixed hematopoietic malignancies, and 420 nonhematopoietic tumors that had been similarly processed. All non-Hodgkin's lymphomas were LCA-reactive with this method, whereas none of the nonhematopoietic neoplasms were stained. Twelve of 25 cases of Hodgkin's disease displayed LCA-positivity in Reed-Sternberg cells, but all contained reactive, benign inflammatory cells. Hence, the specificity of the amplified anti-LCA/avidin-biotin-peroxidase technique was 100%, and its sensitivity was 96%. This procedure should allow surgical pathologists to obtain reliable, reproducible staining of hematopoietic neoplasms in paraffin-embedded tissues.

Antibodies, Monoclonal↗

Use of the working formulation for non-Hodgkin's lymphoma in epidemiologic studies: agreement between reported diagnoses and a panel of experienced pathologists.

Independent review of slides of 668 cases of non-Hodgkin's lymphoma (NHL) by a panel of 4 experienced pathologists using the Working Formulation (WF) allowed determination of the agreement between reported diagnoses and panel review of slides. The panel agreed with the reported diagnosis of NHL in 93% of cases, but with the NHL subtype in only 55% of cases overall. The ability of the panelists to agree among themselves, however, was only slightly better than the panelists' agreement with the reported diagnosis (60% vs. 54%, respectively). Agreement of the panel with the reported subtype diagnosis varied from 14% to over 90%. The best agreement was with small lymphocytic lymphoma and follicular subtypes. Conclusions from this study are: 1) The WF functions well as common language for translation and comparison of diagnoses of subtypes of NHL. 2) Relative to time and cost involved, panel review using only light microscopy may not be useful in epidemiologic studies of NHL. 3) Small lymphocytic and follicular subtypes of NHL can be used more confidently in epidemiologic studies than can other subtypes whether the subtyping is done from abstracted reports or by panel review.

Humans↗

Neoplastic plasma cells in follicular lymphomas. Clinical and pathologic findings in six cases.

Six cases of follicular lymphoma contained an abundant plasma cell component. With immunoperoxidase techniques, this was found to demonstrate monotypic cytoplasmic marking for either K or L Ig light chain in five cases, and for IgA heavy chain only in one case. A histogenetic relationship between follicular center cells and plasma cells was suggested by cell forms morphologically intermediate between these two types and by monotypic plasma cells in the neoplastic follicles. The progressive differentiation of follicular center cells into Ig-secreting cells in these cases is likely to be the result of an alteration of the immunoregulatory mechanisms that usually block the differentiation of follicular lymphomas. Four of our patients presented with disseminated disease, three had extranodal presentation and four manifested serum paraproteins. Their median survival was 40 months; two of them died of disease. The published data and our own suggest that follicular lymphoma with plasmacytic differentiation is a malignancy of intermediate grade, with survival and clinical features closer to lymphoplasmacytic/lymphoplasmacytoid lymphoma (LP immunocytoma) than to follicular lymphoma.

Aged↗

The coexistence of Langerhans' cell granulomatosis and malignant lymphoma may take different forms: report of seven cases with a review of the literature.

Several reports in the literature have documented an association of Langerhans' cell granulomatosis (LCG) with malignant lymphoma (ML). Seven additional patients are described, and different aspects of such an association are demonstrated. The diagnosis of LCG, made on the basis of routinely stained biopsy material, was supported by S-100 protein immunoperoxidase reactivity and/or the presence of Birbeck granules on electron microscopy. In six patients (cases 1 to 6) the LCG consisted of localized foci in nodes involved by ML. However, in one of these patients (case 1) focal LCG was again associated with ML in a later lymph node biopsy specimen from a different site, and in another patient (case 6) LCG subsequently developed in the skin and lungs. In the remaining case (case 7) pulmonary LCG developed one year after the diagnosis of Hodgkin's disease. Localized LCG in a lymph node involved by ML could represent an immune response to ML (cases 1 to 6 in the present study and 16 literature cases). The findings in case 6 indicate that such a response has the potential to become disseminated. Cases in which LCG and ML are found at different sites (case 7 in the present study and five literature cases) probably represent the coincidental association of two unrelated disorders. Finally, it has been postulated that, in rare instances, the development of Hodgkin's disease or malignant histiocytosis in a patient with LCG might represent malignant evolution of this hyperplastic process.

Adult↗