Primary Macroglobulinemia with t(11;18)(q21;q21)

Hirase, Nobuhisa; Yufu, Yuji; Abe, Yasunobu; Muta, Koichiro; Shiokawa, Satoshi; Nawata, Hajime; Nishimura, Junji

doi:10.1016/s0165-4608(99)00156-9

Cited by 22 publications

(14 citation statements)

References 28 publications

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“…8,11 MALT lymphoma with Waldenströ m's macroglobulinemia is usually at an advanced stage, typically showing bone marrow and peripheral blood involvement. 4,12 Thus, it is most likely that the incidence of these translocations in MALT lymphoma with Waldenströ m's macroglobulinemia is high. In this regard, it is noteworthy that t(11;18)(q21;q21) has been observed in several MALT lymphomas with Waldenströ m's macroglobulinemia.…”

Section: Discussionmentioning

confidence: 99%

“…In this regard, it is noteworthy that t(11;18)(q21;q21) has been observed in several MALT lymphomas with Waldenströ m's macroglobulinemia. 4,13 Thus, detection of these translocations will play a significant role in the differential diagnosis between lymphoplasmacytic lymphoma and MALT lymphoma.…”

Section: Discussionmentioning

confidence: 99%

“…3 Occasionally, MALT lymphoma involves bone marrow and spleen, and clinically presents with macroglobulinemia. 4 Thus, MALT lymphoma can mimic lymphoplasmacytic lymphoma in both histological and clinical presentations. Genetically, MALT lymphomas are specifically associated with t(11;18)(q21;q21), 5 t(1;14)(p22;q32)/ IgH-BCL10 6 and t(14;18)(q32;q21)/IgH-MALT1.…”

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confidence: 99%

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t(1;14) and t(11;18) in the differential diagnosis of Waldenström's macroglobulinemia

Chuang

Doğan

et al. 2004

Modern Pathology

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Waldenströ m's macroglobulinemia is caused by several B-cell proliferative disorders including lymphoplasmacytic lymphoma, marginal zone B-cell lymphoma, B-cell chronic lymphocytic leukemia and multiple myeloma. Differential diagnosis between lymphoplasmacytic lymphoma and extranodal marginal zone lymphoma of mucosa-associated lymphoid tissue is particularly difficult as there is a considerable overlap in histological presentation. We report a case of Waldenströ m's macroglobulinemia with involvement of the peripheral blood, bone marrow and stomach. Serum chemistry revealed an IgM of 5.4 g/dl, but Bence-Jones protein in urine was negative. Abnormal lymphoid cells were detected in both blood and the bone marrow. Flow cytometry of the bone marrow aspirate showed that majority of cells were CD20 þ , CD38 þ , expressing immunoglobulin lambda light chain, but CD5 À and CD10 À . Gastric biopsies revealed infiltration of the gastric mucosa by small lymphoid cells showing plasmacytoid differentiation and occasional Dutcher bodies. Lymphoepithelial lesions and Helicobacter pylori were not seen. Thus, the differential diagnosis between lymphoplasmacytic lymphoma and mucosa-associated lymphoid tissue lymphoma was raised. To resolve this, we performed BCL10 immunohistochemistry and reverse transcriptional polymerase chain reaction (RT-PCR) for the API2-MALT1 fusion transcript of t(11;18)(q21;q21). Both bone marrow and gastric biopsies showed strong BCL10 nuclear staining, similar to that seen in t(1;14)(p22;q32) positive mucosa-associated lymphoid tissue lymphoma, but absence of the API2-MALT1 fusion transcript. To further ascertain whether the detection of t(1;14)(p22;q32) and t(11;18)(q21;q21) can be reliably used for the differential diagnosis between lymphoplasmacytic lymphoma and mucosa-associated lymphoid tissue lymphoma, we screened for these translocations by BCL10 immunohistochemistry in 58 lymphoplasmacytic lymphomas and RT-PCR for t(11;18)(q21;q21) in 40 lymphoplasmacytic lymphomas, respectively. None of the lymphoplasmacytic lymphomas studied harbored these translocations. Thus, detection of t(1;14)(p22;q32) and t(11;18)(q21;q21) is useful in the differential diagnosis between lymphoplasmacytic lymphoma and mucosa-associated lymphoid tissue lymphoma.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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confidence: 99%

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t(1;14) and t(11;18) in the differential diagnosis of Waldenström's macroglobulinemia

Chuang

Doğan

et al. 2004

Modern Pathology

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“…There are several potential explanations for leukemogenesis via this unusual route. [1][2][3][4] Perhaps, the most plausible was predicted for cord blood before the recent series of case reports. 5,6 Systematic screening of a large series of unselected cord blood samples revealed that B1% harboured putative pre-leukaemic clones with TEL-AML1 fusion or B0.2% with AML-ETO.…”

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“…1,2 The translocation t(11;18)(q21;q21), a specific abnormality, observed in about 20% of extranodal marginal zone lymphomas has been reported in few cases of patients with WM. 3,4 However, this translocation was not detected in the tumor cells of 24 WM patients using well-validated probe for its detection. 1 Deletions of chromosome 13q14 are present in approximately 50% of patients with MM or B-cell chronic lymphocytic leukemia (B-CLL), but are rare in WM at the time of diagnosis (o5%) and with a low frequency in patients after treatment (15%).…”

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Trisomy 4, a new chromosomal abnormality in Waldenström's macroglobulinemia: a study of 39 cases

et al. 2006

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estimated, but it appears that this event may be substantially more frequent with a cord blood source of stem cells. There are several potential explanations for leukemogenesis via this unusual route. [1][2][3][4] Perhaps, the most plausible was predicted for cord blood before the recent series of case reports. 5,6 Systematic screening of a large series of unselected cord blood samples revealed that B1% harboured putative pre-leukaemic clones with TEL-AML1 fusion or B0.2% with AML-ETO. 5 The frequency of such cells in positive cord bloods was of the order of 10 À3 -10 À4 , indicative of a clone size of B10 6 cells in the new born. It was suggested that the clinical use of such 'preleukaemic' samples as a source of stem cells might involve a risk of leukaemia in association with the proliferative stress consequent to transplantation. 5 Several inferences can be drawn from the data. First, if results with these particular fusion genes are typical of prenatal leukemia initiation in general, 7 then something like 5% of cord bloods may contain pre-leukemic clones. Second, the risk of the cord blood donor with such clones developing leukaemia him or herself is very low and of the order of 1%.These conclusions have implications for how one should respond to the cases of donor 'relapse'. The priority must be to establish the mechanism of donor cell leukaemia. If the above mechanism is at play, then the clear prediction is that cells bearing at least one of the molecular abnormalities found in the 'relapse' leukaemic blasts (i.e. the initiating mutation) would be present and detectable in archived donor cells. This would need to be assessed by carefully controlled reverse transcriptasepolymerase chain reaction plus combined immunophenotypefluorescence in situ hybridization technologies as described. 5 If this turns out to be the case, then there are other issues to be addressed, including additional ethical concerns. 8 Given the B1% risk of leukaemia in the donor, one would not expect to see leukaemia emerging in that individual and one can argue that it would be unethical to inform the donor or the donor's parents. Screening all cord bloods for potential 'contamination' with pre-leukaemic clones might be desirable, but would not be very practical given the wide variety of chromosomal and mutational events that could initiate acute leukaemia. Cord blood transplantation has been a very considerable success 9 and it is unlikely that donor cell leukaemia would seriously compromise its continued use. Nevertheless, there is now some urgency to establish the frequency of donor cell leukaemia by more systematic screening of 'relapse' cases in the EUROCORD project and elsewhere and identifying whether or not this does indeed reflect transfer of pre-leukaemic clones. MF Greaves

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