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Biomedical subjects

F Dallenbach

Publications and source records attributed to F Dallenbach.

32 records · Page 2Linked to original sources
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↗
PubMedDate not supplied

Growth fractions in malignant non-Hodgkin's lymphomas (NHL) as determined in situ with the monoclonal antibody Ki-67.

The proportion of proliferating cells in malignant non-Hodgkin's lymphomas (NHL) was determined in situ by immunostaining with the monoclonal antibody Ki-67, which reacts with a nuclear antigen that is present only in proliferating cells. A highly significant correlation could be demonstrated between the proportion of Ki-67 positive cells and the classification into high and low-grade NHL according to the Kiel classification. 93.8 per cent of high-grade and 88.5 per cent of low-grade malignancies were correctly allocated to these groups using the percentage of Ki-67 positive cells as discriminant parameter. On the basis of the medians, the degree of proliferation also paralleled the succession of entities within the Kiel classification. Within most of these different entities, however, the ranges of Ki-67 positive cells varied considerably, indicating that the growth fractions within these groups are rather heterogeneous. Thus it might be useful to determine the growth fraction of each individual case of NHL, because this might be of prognostic value.

Antibodies, Monoclonal↗