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F Dallenbach

Publications and source records attributed to F Dallenbach.

At least 19 recordsLinked to original sources
PubMed1992

Heterogeneous Epstein-Barr virus infection patterns in peripheral T-cell lymphoma of angioimmunoblastic lymphadenopathy type.

In this study, 32 cases of T-cell lymphoma of angioimmunoblastic lymphadenopathy type (AILD-TCL) were investigated for their association with Epstein-Barr virus (EBV). For this purpose, three different approaches were applied: polymerase chain reaction (PCR) for the presence of EBV-DNA, in situ hybridization (ISH) for EBV-encoded small nuclear RNAs (EBER), and immunohistology for EBV-encoded latent membrane protein (LMP). PCR and EBER-ISH produced almost identical results, showing that all but one case of AILD-TCL contained EBV genomes. Three distinctive patterns of EBV infection were observed after immunophenotypical characterization of EBER-positive cells: (1) in 26% of the cases, B and T cells were infected, the majority of which were B cells of immunoblastic morphology located in the remnants of lymphoid follicles; (2) in 42% of the cases, the vast majority of infected cells were neoplastic T cells diffusely distributed in the lymph nodes, but infected B cells were also present; and (3) in 32% of the cases, there were only a few infected small lymphoid cells. Detectable LMP was frequent in cases exhibiting patterns 1 and 2. These findings suggest that in AILD-TCL patients, B cells and especially T cells are highly susceptible to a persistent EBV infection, which often leads to a growth advantage of the infected cells. Thus EBV, in conjunction with genetic abnormalities and selective defects of the immune system, might be involved in the pathogenesis of AILD-TCL.

Base Sequence↗
PubMed1992

EBV infection patterns in Hodgkin's disease and normal lymphoid tissue: expression and cellular localization of EBV gene products.

The present study was performed to clarify the reported inconsistencies regarding the frequency of the association of Epstein-Barr virus (EBV) and Hodgkin's disease (HD). Biopsies from 102 patients with HD were screened for the presence of EBV-encoded small nuclear RNA (EBER) and latent membrane protein (LMP) by using a non-isotopic in situ hybridization (ISH) and immunohistology (IH), respectively. The results were additionally compared with those obtained by polymerase chain reaction (PCR) for EBV-DNA detection. EBV was detected by EBER-ISH in 67% of the HD cases and in 25% of the control group cases consisting of normal lymph nodes. The results of PCR performed on cases with amplifiable DNA were overall congruent with those obtained by EBER-ISH. With respect to the cellular localization of EBV, four categories of HD could be established: (a) cases with EBV-infected tumour cells (42/102), (b) cases with additional infection of bystander cells (4/102); (c) cases with EBV infection restricted to non-malignant bystander cells (23/102); and (d) cases with neither EBV-infected tumour cells nor bystander cells (33/102). LMP expression was detectable only in the neoplastic cell population of those cases with EBER-positive tumour cells, suggesting a frequent involvement of EBV in the pathogenesis of HD.

Antigens, Viral↗
PubMed1992

[Granulocyte colony stimulating factor (G-CSF) in treatment of patients with HIV-associated mucocutaneous Kaposi sarcoma. Successful use in virus and drug-induced leukopenia].

Three patients with HIV-associated Kaposi sarcoma were treated with human recombinant granulocyte colony stimulating factor (G-CSF). They had all developed leucopenia during treatment with recombinant interferon-alpha-2a, in two cases combined with vincristine. In all three patients, there was an obvious rapid stimulation after s.c. injection of 300 or 150 micrograms G-CSF per day; the white blood count reached normal values within only a few days and partial transformation to leucocytosis took place. After discontinuation of G-CSF, leucocyte counts regressed rapidly to pretreatment levels. A dose of 150 micrograms of G-CSF twice to three times per week proved to be sufficient to keep the white blood cell count in the normal range allowing the treatment necessary for Kaposi sarcoma. G-CSF therapy had no serious side effects. One of the patients developed a tumour-like infiltration in his left upper jaw, which histologically simulated Burkitt's lymphoma and which regressed spontaneously after discontinuation of the G-CSF therapy. G-CSF plays an important role in the treatment of patients with HIV-associated Kaposi sarcoma and enables combined treatment with zidovudine, interferon, and cytostatic drugs.

Adult↗
PubMed1992

[Heterogeneous Epstein-Barr virus infection patterns in peripheral T cell lymphoma of the angioimmunoblastic lymphadenopathy type].

32 cases of T cell lymphoma of angioimmunoblastic lymphadenopathy type (AILD-TCL) were investigated for their association with Epstein-Barr virus (EBV). Polymerase chain reaction (PCR) for detection of EBV-DNA and in situ hybridization for EBV-encoded small nuclear RNAs (EBER) produced almost identical results, showing that all but one of AILD-TCL cases contained EBV genomes. Three distinctive patterns of EBV infection were observed after immunophenotypical characterization of EBER positive cells: 1. predominant infection of B-immunoblasts (26% of the cases), 2. predominant infection of neoplastic T cells (42% of the cases) and 3. infection of few small lymphocytes (32% of the cases). EBV-encoded latent membrane protein was frequently detectable in cases exhibiting patterns 1 and 2. These findings suggest that, in AILD-TCL patients B cells and especially T cells are highly susceptible to a persistent EBV infection which may lead to a growth advantage of infected cells.

DNA, Viral↗
PubMed1992

[Epstein-Barr virus associated lymphocyte proliferation].

In recent years, techniques, probes, and reagents became available to reliably visualize individual Epstein-Barr virus (EBV)-infected cells, to assess EBV gene expression, and to analyze the clonal composition of EBV genomes in human tissues. Application of these techniques to more than 1000 lymphoid tissue specimens revealed (1) characteristic cellular and compartmental distribution patterns of EBV-infected cells in normal lymph nodes, reflecting the interference of EBV with physiologic B cell differentiation pathways, (2) an association of EBV with various mono- and oligoclonal lymphoproliferations ranging from benign conditions to overtly malignant lymphomas, and (3) characteristic patterns of EBV gene expression among EBV-associated lymphoproliferations. In the context of the established immortalizing and transforming properties of EBV, the findings support the concept of an etiologic role of EBV for cases of certain lymphomas such as Burkitt's lymphoma, anaplastic large cell lymphoma, Hodgkin's disease, and lymphomas arising in immunocompromised individuals. In contrast, lymphomas harboring EBV in only proportions of the tumor cells (such as cases of peripheral T cell lymphoma and some B cell lymphoma types) argue against an etiologic role in the primary process of malignant transformation for the virus in these instances. Since in many of these cases a proportion of the EBV infected tumor cells express the EBV oncoprotein LMP (latent membrane protein) the virus may influence, however, the proliferative properties as well as the morphological and molecular phenotype of the neoplastic cells.

B-Lymphocytes↗
PubMed1991

Epstein-Barr virus DNA and latent gene products in Ki-1 (CD30)-positive anaplastic large cell lymphomas.

Epstein-Barr virus (EBV)-specific DNA sequences were detected by polymerase chain reaction analysis in 15 of 47 (32%) DNA extracts prepared from CD30-positive (Ki-1 antigen-positive) anaplastic large cell (ALC) lymphomas. EBV-encoded RNA (EBER) transcripts could be detected by in situ hybridization in the tumor cells of 9 of 11 EBV DNA-positive cases. Twenty-eight cases were examined by immunohistology on cryostat sections for the presence of the EBV-encoded latent membrane protein (LMP), the nuclear antigen 2 (EBNA2), the BZLF1 transactivator protein, and the late viral glycoprotein gp350/250. A distinct LMP-specific membrane and cytoplasmic staining was detected exclusively in lymphoma cells of five cases (18%); two of these cases additionally expressed EBNA2. BZLF1 protein and gp350/250 immunoreactivity was absent in all instances. All LMP-positive cases contained EBV DNA and EBER sequences. The pattern of EBV latent protein expression in ALC lymphomas showed heterogeneity with respect to EBNA2 expression: LMP-positive/EBNA2-negative cases displayed a pattern previously described for undifferentiated nasopharyngeal carcinomas and Hodgkin's disease, whereas LMP-positive and EBNA2-positive cases showed parallels to lymphoblastoid cell lines. Because the LMP gene has transforming potential, our findings support the concept of a pathoetiologic role for EBV in a proportion of CD30-positive ALC lymphomas.

Adult↗
PubMed1991

Epstein-Barr virus latent membrane protein expression in Hodgkin and Reed-Sternberg cells.

Cryostat sections from lymph nodes of 47 Hodgkin disease patients were examined by immunohistology for the Epstein-Barr virus (EBV)-encoded latent membrane protein (LMP), nuclear antigen 2, and late viral glycoprotein gp350/250. A distinct LMP-specific membrane and cytoplasmic staining was detected exclusively in Hodgkin and Reed-Sternberg cells in 18 patients (38%); EBV nuclear antigen 2 and gp350/250 immunoreactivity was absent in all instances. Thirty-two of 47 (68%) cases contained EBV-specific DNA sequences as detected by PCR, all LMP-positive cases being in this category. Our results confirm previous studies establishing the presence of EBV genomes in Hodgkin and Reed-Sternberg cells by demonstrating expression of an EBV-encoded protein in the tumor-cell population. The finding of LMP expression in the absence of EBV nuclear antigen 2 suggests a pattern of EBV gene expression different from that of B-lymphoblastoid cell lines and Burkitt lymphoma, whereas this finding shows similarities with that seen in undifferentiated nasopharyngeal carcinoma. Because the LMP gene has transforming potential, our findings support the concept of a pathoetiological role of EBV in many cases of Hodgkin disease.

Adult↗
PubMed1991

Peripheral T-cell lymphomas.

The development of T cells from stem (progenitor) cells to effector cells results from a two-wave process of proliferation and differentiation. The cells of the first differentiation wave are the precursor T cells, and those of the second differentiation wave are peripheral T cells. In the first differentiation wave, resting/circulating naive antigen-reactive T lymphocytes are produced which differ from each other in their antigen receptor-specificity. In the second differentiation wave, those T lymphocytes multiply whose antigen receptors have found the corresponding antigen. Thus three major forms of differentiation can be distinguished in the peripheral T cells: (1) resting/circulating naive antigen-reactive T cells, (2) activated T cells, and (3) effector T cells and memory T cells. In addition, there are at least three major organ-restricted sublines of peripheral T cells, i.e., nodal T cells, mucosa-associated T cells, and skin-associated T cells. Thanks to the availability of markers for most of the above-mentioned T-cell sublines and differentiation forms, all these cellular forms can be associated with certain lymphoma types, i.e., lymphomas of T-cell type can be divided into categories of precursor T-cell lymphomas and peripheral T-cell lymphomas. The peripheral T-cell lymphomas can be subdivided into those derived from lymph nodal, mucosal, and cutaneous T cells. The gut mucosal T-cell lymphomas are associated with enteropathy. The lymph node, mucosal, and cutaneous T-cell lymphomas can be further subdivided into those in which all tumor cells are similar to recirculating resting (nonactivated) T cells, those in which some of the tumor cells resemble activated T cells, and those in which all tumor cells resemble activated T cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Biomarkers, Tumor↗
PubMed1991

The nature of Hodgkin and Reed-Sternberg cells, their association with EBV, and their relationship to anaplastic large-cell lymphoma.

This review focuses on the cellular origin of Hodgkin and Reed-Sternberg (HRS) cells, their association with the Epstein-Barr virus (EBV), and their relation to Ki-1+ anaplastic large-cell (ALC) lymphoma. The tingibility of HRS cells in paraffin sections for polyclonal immunoglobulin represents a staining artifact and thus can no longer serve as an argument for the histiocytic nature of HRS cells. Immunolabeling studies do not support the putative relationship of HRS cells to cell types such as macrophages or interdigitating reticulum cells, but instead suggest: a) that lymphocyte-predominant (LP) Hodgkin's disease (HD) represents a B-cell neoplasm which is distinct from non-LP HD, and b) that non-LP HD constitutes a syndrome rather than a disease entity, with the existence of T-cell types and B-cell types. HRS cells (and the tumor cells in ALC lymphomas) frequently display an immature genotype in association with late activation markers, leading to the assumption that the tumor cells in many cases of HD (and some cases of ALC lymphoma) may be derived from immature lymphoid cells that are infected by a virus that superimposes characteristics of mature activated lymphocytes on these cells. Southern blotting, in situ hybridization, and polymerase chain reaction (PCR) experiments revealed an association of EBV with HRS cells in a significant proportion of HD cases, suggesting that EBV may be responsible for the dissociation between genotype and phenotype in HRS cells, because EBV is a strong inducer of the activation antigens CD30 and CDw70.(ABSTRACT TRUNCATED AT 250 WORDS)

Herpesvirus 4, Human↗
PubMed1991

[Expression of latent membrane proteins (LMP) of Epstein-Barr virus in malignant lymphomas].

The presence of Epstein-Barr virus (EBV) DNA and antigens was assessed by polymerase chain reaction and immunohistology, respectively, in a total of 92 cases of Hodgkin's disease, angioimmunoblastic lymphadenopathy, CD30-positive anaplastic large cell (ALC) lymphomas, and AIDS-associated atypical lymphoproliferations (ALP). Proportions of the EBV DNA-positive lesions showed latent membrane protein (LMP) expression; some of the LMP-positive ALC lymphomas and ALP cases also displayed EBNA2 immunostaining. BZLF1-protein and gp250/350 immunoreactivity were absent in all instances indicating latent EBV infection. Since the LMP gene has transforming potential, our findings support the concept of a pathoetiological role for EBV in these lymphoproliferative lesions.

Acquired Immunodeficiency Syndrome↗
PubMed1991

Diffuse lymphocyte-predominant Hodgkin's disease (diffuse paragranuloma). A variant of the B-cell-derived nodular type.

Lymph node sections from 10 cases of mixed nodular/diffuse and 10 cases of completely diffuse lymphocyte-predominant Hodgkin's disease (LPHD) were immunophenotyped. The results obtained were compared with those of nodular LPHD (nodular paragranuloma). In conventional stains, nodular/diffuse LPHD differed from diffuse LPHD in the presence of nodularity, which can be best demonstrated with silver impregnation. Immunohistologic analysis showed a correlation of the difference in nodularity with the presence or absence and pattern of follicular dendritic cell (FDC) meshwork, ie, a relatively sharply defined and large spherical meshwork was present in nodular areas of nodular/diffuse LPHD, whereas FDCs were either absent or present in a diffuse, ill-defined meshwork, usually of small size, in the diffuse zones of nodular/diffuse LPHD and in diffuse LPHD. The amount of FDC meshwork corresponded roughly to the number of reactive B cells and T cells, meaning that in diffuse areas significantly fewer B cells and more T cells were observed than in nodular areas. The immunohistologic analysis also showed that the antigen profile (positivity with the monoclonal B-cell marker L26 in the majority [14/20] of cases and negativity for CD15 in all but one of 20 cases) of the tumor cells in both nodular/diffuse LPHD and diffuse LPHD were comparable while it was different from the antigen profile (L26- and CD15+) in most cases of nodular sclerosis and mixed cellularity types of HD. This suggests that the considered subtypes of LPHD differ mainly in FDC pattern, but not in origin and nature of the tumor cells. This further justifies assignment of the above-mentioned LPHD subtypes to the category paragranuloma (LPHD).

B-Lymphocytes↗
PubMed1990

Variable expression of leucocyte-common (CD45) antigen in CD30 (Ki1)-positive anaplastic large-cell lymphoma: implications for the differential diagnosis between lymphoid and nonlymphoid malignancies.

Monoclonal antibodies (mAbs) directed against the leucocyte common (CD45) antigen have been proposed as a useful tool for the differential diagnosis between malignant lymphomas (CD45+) and poorly differentiated nonhemopoietic tumors (CD45-). Thanks to the availability of mAbs directed against fixative-resistant epitopes of the CD45 molecule, this distinction can now easily be made even in routinely processed tissues. However, a small percentage of morphologically poorly defined neoplasms are difficult to diagnose even with the help of immunohistochemistry. The investigators report that 63 out of 165 anaplastic large-cell (ALC) lymphomas did not show any reactivity for the CD45 antigen in paraffin sections. In routine biopsies, the lymphomatous nature of these cases, most of which had been sent for consultation, could be always unequivocally established by demonstrating negativity for cytokeratins (mAb KL1) and clear dot-like and/or surface reactivity with the Ber-H2 mAb, which is directed against a fixative-resistant epitope of the lymphoid cell activation antigen CD30. Strikingly, 54% of the CD45-cases reacted with mAbs directed against fixative-resistant epitopes of the T cell-restricted CD45RO antigen (mAb UCHL1) or the B-restricted molecules CD45RA (mAb 4KB5) and L26 (unclustered). In order to avoid confusion of ALC lymphomas with anaplastic nonlymphoid tumors, pathologists must be aware of the existence of CD30+/CD45- ALC lymphomas, as they can mimic the above-mentioned malignancies both morphologically (due to the sinusoidal growth pattern) and phenotypically (due to the expression of EMA). The investigators conclude that the combined use of mAbs directed against fixative-resistant epitopes of the CD30, CD45RO, CD45RA, and L26 antigens and cytokeratins is essential for the correct diagnosis and treatment of these equivocal cases.

Antibodies, Monoclonal↗
PubMed1990

Serum levels of soluble CD30 molecule (Ki-1 antigen) in Hodgkin's disease: relationship with disease activity and clinical stage.

In all cases of Hodgkin's disease (HD) Reed-Sternberg (RS) cells express the CD30 antigen. It has been recently demonstrated that this molecule can be released from the cell membrane of CD30+ neoplastic cells in a soluble form (sCD30), detectable in culture supernatants and body fluids. In this paper we investigated by an immunoassay the serum levels of sCD30 in 58 patients with HD, in order to define the possible relationship of this molecule to the clinical and pathological findings. sCD30 molecule was found at detectable levels in 24 out of 50 patients (48%) with active disease, whereas it was always absent in control sera and in cases in complete remission. Among the patients with active HD, the incidence and mean values of detectable levels (+/- SEM) of sCD30 were higher in cases with progressive or relapsing disease (61.5%, mean 458 +/- 190 U/ml) as compared to those at presentation (43.2%, mean 116 +/- 33 U/ml). Among the cases at presentation, detectable levels were observed more often in patients with advanced stages (III + IV: 61%) and constitutional symptoms ('B': 61.5%) than in early stages (I + II: 26%) and without symptoms ('A': 33.3%). In addition, higher mean values were found in stages III + IV (182 +/- 60 U/ml) and in 'B' cases (208 +/- 73 U/ml) than in stages I + II (65 +/- 30 U/ml) or 'A' patients (64 +/- 26 U/ml). The above findings suggest a possible role for the sCD30 as a tumour marker in HD.

Adolescent↗
PubMed1989

Paraffin section markers for Reed-Sternberg cells. A comparative study of peanut agglutinin, Leu-M1, LN-2, and Ber-H2.

Hodgkin's disease (HD) is sometimes difficult to distinguish from non-Hodgkin's lymphomas, and a reliable marker for Reed-Sternberg and related (R-S) cells in paraffin sections would be useful. Ninety-one cases of HD with PNA, anti-Leu M1, and LN-2, and 90 cases with Ber-H2 were studied. The staining results were evaluated independently. R-S cells stained positively with one or more of the reagents in all cases. PNA staining was positive in 78 cases (85.7%); Leu M1, 63 (69.2%); LN-2, 71 (78.0%); and Ber-H2, 80 cases (88.9%). Positively stained cells were readily recognized in 71 cases (91.0%) of PNA+, 51 (80.9%) of Leu M1+, and 51 (71.8%) of LN-2+ and 71 (88.7%) of Ber-H2+ cases; the cells were found only after careful search in the remaining cases. Sixteen cases of peripheral T-cell lymphoma (large cell type, ten; mixed, five; unclassifiable, one) were also stained. Tumor cells did not stain with PNA or anti-Leu M1 in any of the 16 cases but did stain positively with LN-2 in four and with Ber-H2 in five. Thus, the detection rate of R-S cells was the highest with Ber-H2, closely followed by PNA. PNA, however, stained the largest number of R-S cells per case, and the results were least affected by the type of fixative employed. Staining of peripheral T-cell lymphoma appeared to be nil or extremely rare with PNA and Leu M1, whereas it was not uncommon with Ber-H2 and LN-2. In conclusion, to facilitate the detection of R-S cells in paraffin sections, the application of a panel of three markers, PNA, Leu M1, and Ber-H2, appears to be necessary at this point in time.

Antigens, Differentiation↗
PubMed1989

Primary and secondary cutaneous Ki-1+ (CD30+) anaplastic large cell lymphomas. Morphologic, immunohistologic, and clinical-characteristics.

Skin biopsies were collected from 15 patients with cutaneous tumors morphologically similar to Ki-1+ anaplastic large cell (ALC) lymphoma of the lymph nodes, including Ki-1+ ALC lymphoma of childhood. The histology and immunophenotype of these cutaneous tumors are reported and follow-up data on the patients are given. The tumorous infiltrates were composed of large, sometimes very bizarre cells with one nucleolus or multiple nucleoli. All tumor cells expressed the lymphoid cell activation antigen Ki-1 (CD30) in conjunction with CD25 and the beta-chain of the T cell receptor. In 11 patients, Ki-1+ cutaneous tumors developed primarily in the skin. In nine patients, these were restricted to the skin in follow-up periods ranging from 3 months to 6 years. Two patients developed lymph node involvement after 2 months and 2 years, indicating the spreading potential of these cutaneous tumors. Morphologic and immunophenotypical identity of the atypical cells found in primary cutaneous ALC lymphoma, in regressing atypical histiocytosis (RAH), and in lymphomatoid papulosis (LyP) of type A, together with the protracted clinical course in all three conditions, suggests that primary cutaneous ALC lymphoma, RAH, and LyP of type A represent clinical variants of the same lymphoma entity. Secondary development of Ki-1+ ALC skin tumors was observed in two patients with cutaneous T cell lymphomas of mycosis fungoides type. These secondary Ki-1+ ALC lymphomas of the skin showed rapid systemic progression similar to the primary lymphonodal Ki-1+ ALC lymphomas. Concomitant or subsequent occurrence of Ki-1+ ALC tumors in cutaneous T cell lymphomas thus may be a bad prognostic sign.

Adult↗
PubMed1988

Clonal gene rearrangement patterns correlate with immunophenotype and clinical parameters in patients with angioimmunoblastic lymphadenopathy.

T cell receptor beta (TcR beta) chain gene rearrangements have been reported in cases of angioimmunoblastic lymphadenopathy (AILD) and provided evidence for the presence of clonal T cell proliferations in this disorder. Twenty-three cases of AILD and two cases of hyperimmune reaction (HR) were investigated. In the two HR cases, essentially the same histologic pattern was present as in AILD but lymph node follicles were hyperplastic. Both HR cases showed germline configuration for the TcR and immunoglobulin heavy chain (IgH) genes. All other patients diagnosed with AILD had clonal rearrangements for TcR gamma and beta chain genes. In addition, seven out of these cases had clonally rearranged their IgH genes. These two different rearrangement patterns (TcR with or without Ig gene rearrangement) correlated to immunohistochemical and clinical data. Cases with TcR but without Ig gene rearrangements (group I) exclusively showed CD4+ proliferating T cells, whereas those cases with TcR and Ig gene rearrangements had significantly elevated numbers of CD8+ proliferating cells (group II). Group II patients significantly more often presented with hemolytic anemia and went into transient remission spontaneously or under steroid treatment. Group I patients, however, had a higher response to chemotherapy and a longer survival time. These data show that, based on different rearrangement patterns, it is possible to divide AILD into two different groups with distinct immunophenotypic properties and differences in clinical parameters. Immunogenotyping in AILD thus will have prognostic and therapeutic implications.

Adult↗