High frequency of t(14;18) translocation in salivary gland lymphomas from Sjögren's syndrome patients.

Pisa, Eva K.; Pisa, Pavel; Kang, Hoil; Fox, Robert I.

doi:10.1084/jem.174.5.1245

Cited by 91 publications

(37 citation statements)

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“…In two previous studies of lymphomas in patients with SS, t(14;18)(q32;q21) was detected by PCR (28,29). In these patients, however, BCL2 and not MALT1 was juxtaposed to IGH.…”

Section: Discussionmentioning

confidence: 99%

“…This patient suffered from a pulmonary MALT lymphoma, which showed rapid transformation into a diffuse large B-cell lymphoma with consecutive nodal involvement, which also harbored t(14;18)(q32;q21). In the other study (29), BCL2 translocations were detected in 5 of 7 SS-associated B-cell lymphomas involving the salivary glands. However, the exact histological classification of these lymphomas was not provided.…”

Section: Discussionmentioning

confidence: 99%

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Frequency of Chromosomal Aberrations Involving MALT1 in Mucosa-Associated Lymphoid Tissue Lymphoma in Patients with Sjögren’s Syndrome

Streubel¹,

Hüber²,

Wöhrer

et al. 2004

Clinical Cancer Research

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Purpose: Mucosa-associated lymphoid tissue (MALT) lymphoma develops in the context of longstanding antigenic stimulation such as infection with Helicobacter pylori or autoimmune disease, including Sjögren's syndrome (SS). Recently, two chromosomal aberrations involving the MALT1 gene, i.e., t(11;18)(q21;q21) and t(14;18)(q32;q21) have been reported as genetic events specific for MALT lymphoma. In view of the association between SS and the development of MALT lymphoma, we have analyzed the frequency of t(11;18)(q21;q21) and t(14;18)(q32;q21) in patients with MALT lymphomas arising in the background of SS.Experimental Design: A retrospective analysis of patients diagnosed with MALT lymphoma and SS was performed. The t(11;18)(q21;q21) was analyzed using reverse transcriptase-PCR, whereas t(14;18)(q32;q21) was assessed by two-color interphase fluorescence in situ hybridization.Results: Twenty-six patients (20 female and 6 male) with MALT lymphoma and SS could be identified. The lymphoma was located in the parotid (n ‫؍‬ 14), orbit (n ‫؍‬ 2), and submandibular gland (n ‫؍‬ 1), whereas 9 patients had gastric MALT lymphoma. Seven of 26 patients (27%) harbored t(11;18)(q21;q21). Interestingly, only 1 of 17 patients (6%) with extragastrointestinal lymphoma was positive, as opposed to 6 of 9 patients (67%) with gastric MALT lymphoma. Four of 26 patients were positive for t(14;18)(q32; q21): 3 of 17 extragastrointestinal (18%) and 1 of 9 gastric lymphomas (11%).Conclusions: The overall frequency of MALT1 rearrangement appears to be low in patients with extragastrointestinal MALT lymphoma associated with SS. By contrast, MALT1 rearrangement was demonstrated in 7 of 9 patients (78%) with gastric MALT lymphoma and SS. This finding may explain at least in part why gastric MALT lymphomas in patients with SS are refractory to H. pylori eradication therapy.

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“…In two previous studies of lymphomas in patients with SS, t(14;18)(q32;q21) was detected by PCR (28,29). In these patients, however, BCL2 and not MALT1 was juxtaposed to IGH.…”

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Frequency of Chromosomal Aberrations Involving MALT1 in Mucosa-Associated Lymphoid Tissue Lymphoma in Patients with Sjögren’s Syndrome

Streubel¹,

Hüber²,

Wöhrer

et al. 2004

Clinical Cancer Research

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“…19 Interestingly, 1 patient with HCV/MC developed a monoclonal, multistep lymphoproliferative disorder that, in the initial phase of the disease, was associated with t(14;18). 8 In addition, a high frequency of t(14;18) has been observed in salivary gland lymphomas from patients with Sjö gren' s syndrome, 20 another disease recently associated with HCV infection. 21 Bcl-2 recombination is interpreted as an error during the VDJ-gene-rearrangement process in Ig genes 22 and may take place as a consequence of particularly strong antigenic stimulation.…”

Section: Discussionmentioning

confidence: 99%

T(14;18) translocation in chronic hepatitis C virus infection

et al. 2000

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Pathogenic mechanisms of B-cell lymphoproliferative disorders in chronic hepatitis C virus (HCV) infection are unclear. We studied t(14;18) translocation by polymerase chain reaction in peripheral blood mononuclear cells from 50 patients with HCV-related liver disease (group A), 7 with mixed cryoglobulinemia syndrome (group B), 55 with HCV-negative liver disease (group C), and 30 with HCVnegative chronic rheumatic disorders or chronic infection by nonhepatotropic agents (group D). T(14;18) was significantly more frequent in group A (13/50 patients ‫؍‬ 26 %) and group B (5/7 ‫؍‬ 71.4%) patients than in group C (1/55 ‫؍‬ 3.6%) and group D (1/30 ‫؍‬ 3.3%) ones. Immunoblot analysis showed bcl-2 over-expression in all t(14;18)-positive samples. In group A, 10/13 (77%) patients with t(14;18) and 13/37 (35%) without t(14;18) had serum cryoglobulins in the absence of mixed cryoglobulinemia symptoms (P F .05). These data indicate that t(14;18) and bcl-2 over-expression in lymphoid cells are frequent in chronic HCV infection and suggest that this event may contribute to the pathogenesis of HCV-related lymphoproliferative disorders. (HEPATOLOGY 2000;31:474-479.)Hepatitis C virus (HCV) infection has been associated with a series of B-cell lymphoproliferative disorders (LPDs), including essential mixed cryoglobulinemia (MC), B-cell non-Hodgkin' s lymphoma (NHL), and monoclonal gammopathies. [1][2][3][4] The mechanisms involved in LPDs, either virusrelated or virus-independent, are complex and still poorly defined. MC, the LPD most strictly associated with HCV infection, is a borderline (benign/malignant) disorder in that it frequently coexists with bone-marrow aspects of NHL and evolves, in about 5% to 8% of cases, into a clinically frank B-cell malignancy. 5,6 In addition, clonal expansion of IgMproducing B cells has been detected in patients with HCVpositive MC (HCV/MC). 7 Recently, 1 patient with HCV/MC has been shown to develop a monoclonal multistep lymphoproliferative disorder associated with t(14;18) translocation in the benign phase of the disease and additional genetic alterations in the accelerated one. 8 Over-expression of bcl-2 oncoprotein has been shown by immunohistochemistry in liver lymphocyte aggregates not only in the majority of HCV-positive MC, but also in about 45% of patients with chronic HCV-related hepatitis without MC. 9 The recombination of anti-apoptotic bcl-2 proto-oncogene [t(14;18)] has been widely investigated in the field of lymphomagenetic studies. Following t(14;18), the bcl-2 locus, normally located in chromosome 18, is juxtaposed with the immunoglobulin heavy chain locus (IgH), leading to bcl-2 activation. This genetic aberration, which occurs during early B-cell development, appears to be 1 step toward the progression of a normal cell to a cancer cell 10 ; in particular, its importance in regards to cooperative activities with different oncogenes, such as c-myc, has been experimentally shown. T(14;18) characterizes most follicular B-cell lymphomas as well as some diffuse ones. Recent data...

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“…High-risk situations should be unequivocally defined to avoid unnecessary chemo-or radiotherapeutic approaches and related complications. Definition of the oncogenic events involved in lymphoma progression (36)(37)(38) will also be crucial in the future, and definite markers of malignancy might be identified. Yet, only the concomitant definition of the role of local biologic networks (4,22) and (auto)antigenic triggering (4,31) would allow a fuller comprehension of B cell lymphomagenesis in SS, and would consistently improve the diagnostic and therapeutic approaches to this disease.…”

Section: Discussionmentioning

confidence: 99%

Characterization of prelymphomatous stages of B cell lymphoproliferation in Sjögren's syndrome

Vita

Boiocchi

Sorrentino

et al. 1997

Arthritis & Rheumatism

104

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Objective. To determine whether the prelymphomatous stages of B cell lymphoproliferation in Sjögren's syndrome (SS) may be better characterized by the integration of clinical, pathologic, and molecular data, the latter focusing on the expansion, persistence, and dissemination of clonal B cells in the course of the disease. Methods. Multiple tissue lesions (synchronous from different tissues and metachronous from the same tissue) were evaluated in biopsy specimens obtained from 6 consecutive patients with SS who had an associated lymphoproliferative disorder. Fully benign gastric lesions were evaluated in tissue from an additional 11 patients with SS who had no associated lymphoproliferative disorder. Multiple and complementary molecular analyses of B cell clonality were used: Southern blot, polymerase chain reaction, single‐strand conformation polymorphism, DNA sequencing, and hybridization with clonospecific oligoprobes. All the patients were then strictly followed up for the appearance of lymphoma. Results. Different scenarios of SS‐associated B cell lymphoproliferation were identified: 1) the ongoing expansion of the same dominant clone, localized or disseminated, in tissue from 2 patients, 1 of whom later developed an overt B cell lymphoma; 2) different dominant clones in different synchronous or metachronous tissues from the remaining 4 patients with an associated lymphoproliferative disorder; and 3) small oligoclonal expansions in 7 of the 11 benign gastric lymphoid infiltrates. Conclusion. Prelymphomatous B cell lymphoproliferation in SS was better characterized following integration of the findings. The different types of B cell clonal expansion (oligoclonal or monoclonal, smaller or larger in size, fluctuating or established, localized or disseminated) may imply a different risk of lymphoma progression. An accurate clinical, histopathologic, and molecular characterization may therefore be crucial in future studies aimed at clarifying the pathobiology of SS‐associated lymphoproliferation.

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High frequency of t(14;18) translocation in salivary gland lymphomas from Sjögren's syndrome patients.

Cited by 91 publications

References 35 publications

Frequency of Chromosomal Aberrations Involving MALT1 in Mucosa-Associated Lymphoid Tissue Lymphoma in Patients with Sjögren’s Syndrome

Frequency of Chromosomal Aberrations Involving MALT1 in Mucosa-Associated Lymphoid Tissue Lymphoma in Patients with Sjögren’s Syndrome

T(14;18) translocation in chronic hepatitis C virus infection

Characterization of prelymphomatous stages of B cell lymphoproliferation in Sjögren's syndrome

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