scholarly journals Absence of the t(2;5) in Hodgkin's disease [see comments]

Blood ◽  
1995 ◽  
Vol 85 (10) ◽  
pp. 2845-2847 ◽  
Author(s):  
LM Weiss ◽  
JR Lopategui ◽  
LH Sun ◽  
OW Kamel ◽  
CH Koo ◽  
...  
Keyword(s):  
Polymerase Chain Reaction ◽  
Hodgkin's Disease ◽  
Hodgkin’S Disease ◽  
Blot Hybridization ◽  
Southern Blot Hybridization ◽  
Large Cell ◽  
Common Finding ◽  
Chain Reaction ◽  
Polymerase Chain ◽  
Hodgkin's Lymphomas

The cytogenetics of Hodgkin's disease (HD) is poorly understood. However, a t(2;5) is a common finding in CD30+ anaplastic large cell lymphoma (ALCL), a neoplasm thought by some to be closely related to HD. Recently, the t(2;5) has been cloned and found to represent fusion of the NPM gene with the ALK gene. Using Southern blot hybridization, one group has reported finding rearrangements of NPM in a proportion of cases of both ALCL and HD. In the current study, we used a highly sensitive reverse transcriptase-polymerase chain reaction methodology to analyze 34 cases of HD for the t(2;5). We were unable to find polymerase chain reaction evidence for the t(2;5) in any of the cases of HD, a result significantly different from our previous study of CD30+ non-Hodgkin's lymphomas (P < .02) including ALCL (P < .04), using identical methods. Our results do not support the hypothesis that the t(2;5) represents a common chromosomal abnormality for both HD and ALCL.

scholarly journals Nodular lymphocyte-predominant Hodgkin's disease associated with large- cell lymphoma: analysis of Ig gene rearrangements by V-J polymerase chain reaction

Blood ◽  
1996 ◽  
Vol 88 (2) ◽  
pp. 657-666 ◽  
Author(s):  
TC Greiner ◽  
RD Gascoyne ◽  
ME Anderson ◽  
DW Kingma ◽  
SA Adomat ◽  
...  
Keyword(s):  
Polymerase Chain Reaction ◽  
B Cell ◽  
Hodgkin's Disease ◽  
Hodgkin’S Disease ◽  
Large Cell ◽  
Single Step ◽  
Chain Gene ◽  
Gene Rearrangements ◽  
Chain Reaction ◽  
Polymerase Chain

The clonality of nodular lymphocyte-predominant Hodgkin's disease (NLPHD) and the relationship to composite or sequential large-cell lymphomas (LCLs) is poorly understood. Clonal Ig heavy-chain gene rearrangements (lgHGR) have infrequently been observed in NLPHD by Southern hybridization. The goals of this study were (1) to determine if IgHGR could be identified by polymerase chain reaction (PCR) techniques in the LCL associated with NLPHD; (2) to determine if the lgHGR identified in the LCL could also be found in the associated NLPHD; and (3) to determine if Epstein-Barr virus (EBV) played a role a role in histologic progression to LCL. Using consensus primers to conserved regions in the lgH variable (V) and joining (J) region genes, we analyzed formalin-fixed paraffin-embedded sections from the biopsies of 25 patients referred to the National Cancer Institute (NCI) registry for NLPHD and LCL using both single-step and seminested V-J PCR. The histologically aggressive component was further subclassified as frank LCL or as L&H-cell-rich, but not fulfilling criteria for LCL. Matched samples representing both NLPHD and aggressive components were available in 13 cases. In 12 cases, only one component was available (aggressive, n = 8; NLPHD, n = 4). In addition, we also amplified, with 32P labeling, 12 cases of NLPHD without associated LCL. Two clonal IgHGR were identified in 29 cases (7%) of typical NLPHD, both of which were associated with LCL containing a similar sized band by PCR. The clonal identity of the bands in the NLPHD and associated LCL was confirmed by sequencing the products in these two cases. Eight of 10 cases (80%) of LCL associated with NLPHD contained a clonal band by this technique. By contrast, none of the cases classified as L&H-cell- rich contained an IgHGR. The single-step and seminested PCR methods produced identical results. All clonal LCLs were studied for EBV sequences by in situ hybridization using the EBER1 probe, and were negative. We conclude that the LCLs associated with NLPHD are clonal B- cell malignancies. However, by these methods, the same clone can be identified in only a minority of cases of NLPHD and LCL. EBV does not appear to play a role in histologic progression. Moreover, our results suggest that many cases suspected of being LCL may actually represent NLPHD with increased numbers of L&H cells. In histologically equivocal cases, the diagnosis of LCL should be reserved for those cases in which a clonal B-cell neoplasm can be demonstrated.

scholarly journals Analysis of the t(2;5)(p23;q35) translocation by reverse transcription- polymerase chain reaction in CD30+ anaplastic large-cell lymphomas, in other non-Hodgkin's lymphomas of T-cell phenotype, and in Hodgkin's disease

Blood ◽  
1995 ◽  
Vol 86 (6) ◽  
pp. 2321-2328 ◽  
Author(s):  
A Wellmann ◽  
T Otsuki ◽  
M Vogelbruch ◽  
HM Clark ◽  
ES Jaffe ◽  
...  
Keyword(s):  
Polymerase Chain Reaction ◽  
T Cell ◽  
Reverse Transcription ◽  
Hodgkin’S Disease ◽  
Large Cell ◽  
Cell Phenotype ◽  
Chain Reaction ◽  
Fusion Transcripts ◽  
Polymerase Chain ◽  
Hodgkin's Lymphomas

The t(2;5)(p23;q35) translocation is associated with a high percentage of anaplastic large-cell lymphomas (ALCL) of T- or null-cell phenotype. This translocation was recently cloned and results in the fusion of the nucleophosmin gene (NPM) on chromosome 5q35 to a novel tyrosine kinase- encoding gene designated anaplastic lymphoma kinase (ALK) on chromosome 2p23. Using a sensitive and specific reverse transcription-polymerase chain reaction (RT-PCR) assay to detect the NPM/ALK fusion transcript, we assessed the involvement of NPM/ALK in a series of histologically and immunohistochemically confirmed ALCL, in non-ALCL aggressive non- Hodgkin's lymphomas of T-cell phenotype, and in Hodgkin's disease (HD) to better define the morphologic spectrum of disease associated with this translocation. Twenty-four cases of ALCL were selected on the basis of CD30 positivity and histologic features. Seventeen cases presented as classical nodal and extranodal disease, four cases presented as primary cutaneous disease, and three were associated with human immunodeficiency virus (HIV) infection. As ALCL may show overlapping histology with both HD and other aggressive non-Hodgkin's lymphomas, particularly of T-cell phenotype (T-NHL), we also studied 34 cases of HD and 19 of T-NHL. NPM/ALK chimeric transcripts of identical size were detected in 11 of the 24 (46%) cases of ALCL. NPM/ALK fusion transcripts were found in 11 of 17 (65%) classical ALCL cases but were not detected in the four primary cutaneous cases of ALCL or in the three HIV-related ALCL cases. In addition, NPM/ALK transcripts were not detected in any of the 34 cases of HD or in the 19 cases of T-NHL. These data indicate that NPM/ALK fusion transcripts occur in a high percentage of classical nodal ALCL (65%). In addition, these data strongly suggest that ALCL, as defined in this study, is not pathogenetically related to either HD disease or the majority of other types of aggressive T-NHL. This is a US government work. There are no restrictions on its use.

scholarly journals HTLV-I-induced lymphoma mimicking Hodgkin's disease. Diagnosis by polymerase chain reaction amplification of specific HTLV-I sequences in tumor DNA

Blood ◽  
1988 ◽  
Vol 71 (4) ◽  
pp. 1027-1032 ◽  
Author(s):  
DB Duggan ◽  
GD Ehrlich ◽  
FP Davey ◽  
S Kwok ◽  
J Sninsky ◽  
...  
Keyword(s):  
Polymerase Chain Reaction ◽  
Hodgkin's Disease ◽  
Polymerase Chain Reaction Amplification ◽  
Hodgkin’S Disease ◽  
Dna Amplification ◽  
Disease Diagnosis ◽  
Lymphoproliferative Disease ◽  
Enzyme Linked Immunosorbent Assay ◽  
Chain Reaction ◽  
Polymerase Chain

Abstract A patient with a localized HTLV-I-associated lymphoproliferative disease that was misdiagnosed as Hodgkin's disease is presented. The patient's serum was negative for HTLV-I antibodies by enzyme-linked immunosorbent assay (ELISA), Western blot, and radioimmunoprecipitation. Tumor tissue DNA was negative for HTLV-I by Southern blotting but was positive for distinct HTLV-I sequences when subjected to DNA amplification using the polymerase chain reaction. We conclude that the clinical and pathologic diagnosis of HTLV-I-related lymphoma can be difficult and can be confused with Hodgkin's disease. Extremely sensitive molecular biological techniques may be required to establish a diagnosis of HTLV-I-induced lymphoma.

Study of the HLA-DPβ1 Locus by the Polymerase Chain Reaction Technique in Patients with Hodgkin's Disease

1993 ◽  
Vol 79 (2) ◽  
pp. 133-136 ◽  
Author(s):  
Guseppe Pellegris ◽  
Claudia Lombardo ◽  
Annelisa Cantoni ◽  
Liliana Devizzi ◽  
Monica Balzarotti
Keyword(s):  
Polymerase Chain Reaction ◽  
Hodgkin's Disease ◽  
Hodgkin’S Disease ◽  
Polymerase Chain Reaction Method ◽  
Healthy Controls ◽  
Chain Reaction ◽  
Reaction Method ◽  
Significant Difference ◽  
Polymerase Chain

Background A number of reports have studied associations between Hodgkin's disease and HLA. Some of them established correlation between several antigens and Hodgkin's disease, and others found no correlations. Methods The HLA DP locus was determined by the polymerase chain reaction method in 31 Hodgkin's disease patients and 58 healthy controls. Results No significant difference between patients and controls was noted. Conclusions Further investigations are needed to confirm the hypothesis of a possible role of the HLA complex as one of the factors involved in Hodgkin's disease.

Pitfalls in the epidemiologic classification of human papillomavirus types associated with cervical cancer using polymerase chain reaction: driver and passenger

2008 ◽  
Vol 18 (5) ◽  
pp. 1042-1050 ◽  
Author(s):  
T. Matsukura ◽  
M. Sugase
Keyword(s):  
Cervical Cancer ◽  
Polymerase Chain Reaction ◽  
Human Papillomavirus ◽  
Large Scale ◽  
Blot Hybridization ◽  
Southern Blot Hybridization ◽  
Cervical Lesions ◽  
Chain Reaction ◽  
Polymerase Chain

Cervical cancer is a common malignancy in women worldwide, and it has now been established that the human papillomavirus (HPV) is both necessary and causal for these lesions. HPV itself is both ubiquitous and markedly heterogeneous but can nevertheless be classified as either a high-risk type or a low-risk type based upon its frequency of detection in cervical cancer. Given that the association between HPV and cervical cancer is causal, the classification of this virus has been strengthened by large-scale epidemiologic studies and is widely accepted across many disciplines. It is evident, however, that cervical cancer is frequently associated with multiple HPV types. Therefore, it is crucial to distinguish causal types of HPV (drivers) from noncausal types (passengers) in cervical lesions. In this review, we highlight the current pitfalls of using polymerase chain reaction methods instead of Southern blot hybridization for detecting HPV and discuss the distinction between driver and passenger HPVs with regard to the viral type, the length of the viral genome, and the levels of viral DNA associated with cervical cancer. Finally, we newly propose three categories of HPV instead of two risk groups, based on similarities between viral genes

scholarly journals High incidence of the t(2;5)(p23;q35) translocation in anaplastic large cell lymphoma and its lack of detection in Hodgkin's disease. Comparison of cytogenetic analysis, reverse transcriptase-polymerase chain reaction, and P-80 immunostaining

Blood ◽  
1996 ◽  
Vol 87 (1) ◽  
pp. 284-291 ◽  
Author(s):  
L Lamant ◽  
F Meggetto ◽  
T al Saati ◽  
L Brugieres ◽  
BB de Paillerets ◽  
...  
Keyword(s):  
Hodgkin's Disease ◽  
Cytogenetic Analysis ◽  
Cell Lymphoma ◽  
Hodgkin’S Disease ◽  
Large Cell ◽  
Rt Pcr ◽  
Chain Reaction ◽  
Polymerase Chain ◽  
Large Cell Lymphoma ◽  
Alk Protein

Abstract Fifty-six cases of anaplastic large cell lymphoma (ALCL), 23 cases of Hodgkin's disease, and 16 cases of diffuse large cell lymphoma were investigated for the t(2;5)(p23;q35) translocation. The translocation was detected by using cytogenetic analysis, reverse transcriptase-polymerase chain reaction (RT-PCR) and immunohistochemistry with P80 antibody directed against the kinase domain of anaplastic lymphoma kinase (ALK) of the chimeric NPM/ALK protein. In all but three cases of ALCL, we found an agreement between cytogenetic analysis, RT-PCR, and P80 staining. However, in one case, the t(2;5) translocation was detected with cytogenetic analysis, but RT-PCR and P80 staining were found to be negative. Conversely, in another case the karyotype was normal, but the hybrid mRNA and P80 staining were found to be positive. In one case, malignant cells showed a translocation involving chromosomes 1q25 and 2p23 and were strongly positive for P80 staining. Such a result could be expected because P80 antibody detects the kinase domaine of the ALK protein encoded by chromosome 2p23. Overall 73.2% (41 of 56) of cases were found to be positive. However, the highest percentage (23 of 26 cases; 88.5%) of P80 positive cases was found in children compared with 60% (18 of 30 cases) in adult ALCL (P < .05). In Hodgkin's disease, Reed-Sternberg cells were found to be clearly negative by RT-PCR and with P80 antibody. The latter results suggest that Hodgkin's disease and t(2;5)-positive ALCL are distinct biological entities and that the demonstration of the t(2;5) translocation is of diagnostic importance in differentiating these two entities. The results of the present study indicate that immunohistochemistry with P80 antibody is a reliable method for detecting NPM/ALK chimeric protein.

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