Gastric low-grade MALT lymphoma, high-grade MALT lymphoma and diffuse large B cell lymphoma show different frequencies of trisomy

Hoeve, Marieke A.; Gisbertz, I. A. M.; Schouten, Harry C.; Schuuring, Ed; Bot, Fredrik J.; Hermans, Jos; Hopman, Anton H. N.; Kluin, Philippus; Arends, Jan‐Willem; Krieken, J. Han van

doi:10.1038/sj.leu.2401404

Cited by 58 publications

(44 citation statements)

References 14 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…For the detection of trisomies (peri-)centromeric repetitive a-satellite DNA probes specific for chromosomes 1, 3 (D3Z1, Oncor Gaithersburg, MD, USA), 12 (pa12H8) and 18 (L1.84) were selected. 34 All probes were hybridized on metaphase spreads of lymphocytes to confirm chromosomal location and specificity.…”

Section: Fluorescence In Situ Hybridization (Fish) Analysismentioning

confidence: 99%

“…12 Four mutually exclusive and apparently sitespecific, chromosomal translocations have been implicated in the development and progression of extranodal marginal zone lymphoma of mucosaassociated lymphoid tissue. These extranodal marginal zone lymphoma-associated translocations, t(11;18)(q21;q21), 11,13-22 t(1;14)(p22;q32), 13,14,23 t(14;18) (q32;q21) 14,15,24,25 and t(3;14) 8,15,17,[27][28][29][30][31][32][33][34][35] One may wonder whether these extranodal marginal zone lymphoma-associated translocations and numerical aberrations occur in extranodal diffuse large B-cell lymphoma with marginal zone lymphoma components, which may belong to the extranodal marginal zone lymphoma spectrum.This study investigated for the presence of extranodal marginal zone lymphoma-associated translocations and numerical aberrations in diffuse large B-cell lymphoma with and without extranodal marginal zone lymphoma components and in extranodal marginal zone lymphoma of the breast, testis and thyroid, to test the hypothesis that also these lymphomas may belong to the spectrum of extranodal marginal zone lymphoma. …”

mentioning

confidence: 99%

“…Criteria for trisomy detection were described previously. 34 The cutoff levels determined for individual probe sets ranged from 2.1 to 2.7% for YAC and cosmid probes and between 5 and 7% for the various centromeric probes. …”

mentioning

confidence: 99%

“…In addition, several studies have reported the presence of various cytogenetic numerical aberrations, including trisomy 3, 7, 12 and 18, in extranodal marginal zone lymphoma at different extranodal sites. 8,15,17,[27][28][29][30][31][32][33][34][35] One may wonder whether these extranodal marginal zone lymphoma-associated translocations and numerical aberrations occur in extranodal diffuse large B-cell lymphoma with marginal zone lymphoma components, which may belong to the extranodal marginal zone lymphoma spectrum.…”

mentioning

confidence: 99%

See 3 more Smart Citations

T(14;18)(q32;q21) involving MALT1 and IGH genes occurs in extranodal diffuse large B-cell lymphomas of the breast and testis

et al. 2013

View full text Add to dashboard Cite

Primary B-cell lymphoma of the testis, breast and thyroid are rare and data concerning cytogenetic aberrations at these extranodal sites are scarce. We examined the presence of extranodal marginal zone lymphomaassociated translocations, t(11;18)(q21;q21), t(1;14)(p22;q32), t(14;18)(q32;q21), t(3;14)(p14.1;q32) and numerical aberrations of chromosomes 1, 3, 12 and 18 by fluorescence in situ hybridization in 6 extranodal marginal zone lymphomas and 24 diffuse large B-cell lymphomas with (n ¼ 9) or without (n ¼ 15) marginal zone lymphoma components, with primary localizations in the breast (n ¼ 15), testis (n ¼ 9) and thyroid (n ¼ 6). We found t(14;18)(q32;q21), with breakpoints in IGH and MALT1, in one testicular diffuse large B-cell lymphoma and in two diffuse large B-cell lymphomas of the breast. No other translocations, amplifications or deletions involving IGH, BCL-10, BCL-2, MALT1 and IAP2 were detected. Numerical aberrations occurred in 67% of the lymphomas, 67% of extranodal marginal zone lymphomas, 56% of diffuse large B-cell lymphomas with marginal zone lymphoma components and in 73% of 'de novo' diffuse large B-cell lymphomas. These included 78% of testis, 67% of thyroid and 60% of breast lymphomas, and included mainly trisomy 18 (n ¼ 16), trisomy 3 (n ¼ 8) and trisomy 1 (n ¼ 3). One testicular diffuse large B-cell lymphoma harbored both t(14;18)(q32;q21) and trisomy 3. Our results indicate that at least a few cases of diffuse large B-cell lymphoma of the testis and the breast belong to the spectrum of extranodal marginal zone lymphoma. Modern Pathology (2013) 26, 421-427; doi:10.1038/modpathol.2012; published online 28 September 2012Keywords: B-cell lymphoma; FISH; IGH; MALT1; numerical chromosomal aberrations; translocations Primary B-cell lymphoma of the testis, breast and thyroid are rare, each accounting for between 0.5 and 2.5% of all non-Hodgkin's lymphomas (NHLs). [1][2][3][4][5][6] Diffuse large B-cell lymphoma is the most common histological entity at these extranodal sites. Extranodal marginal zone lymphoma of mucosa-associated lymphoid tissue, commonly found in extranodal sites devoid of native lymphoid tissue, like the stomach, lung, salivary gland, thyroid and ocular adnexa, occur infrequently in the breast and testis. Although extranodal marginal zone lymphoma and diffuse large B-cell lymphoma are considered distinct clinicopathological entities in the World Health Organization (WHO) classification, 7 many extranodal diffuse large B-cell lymphomas have derived from a background of extranodal marginal zone lymphoma. [8][9][10][11] We found that a large subgroup of primary testicular diffuse large B-cell lymphoma has marginal zone lymphoma components, including small cell components and lymphoepithelial lesions. 12 Four mutually exclusive and apparently sitespecific, chromosomal translocations have been implicated in the development and progression of extranodal marginal zone lymphoma of mucosaassociated lymphoid tissue. These extranodal marginal zone lymphoma-associated translocations, t(11...

show abstract

Section: Fluorescence In Situ Hybridization (Fish) Analysismentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

See 2 more Smart Citations

T(14;18)(q32;q21) involving MALT1 and IGH genes occurs in extranodal diffuse large B-cell lymphomas of the breast and testis

et al. 2013

View full text Add to dashboard Cite

show abstract

“…1,2 MALT lymphoma is a distinct entity within the group of extra-nodal marginal zone B cell lymphomas 3 but is as yet not characterised by a distinct genetic aberration. Genetic aberrations reported in MALT lymphomas, especially of low-grade type, mainly involve cytogenetic analysis including trisomy [4][5][6] and the translations t (11;18) 7 and t(1;14). 8 Microsatellite instability (MSI), which is caused by errors during DNA replication and reflects defects in genes that are involved in the DNA mismatch repair pathway, has been reported in frequencies ranging from 14% to as high as 90%.…”

Section: Introductionmentioning

confidence: 99%

True

1999

Leukemia

View full text Add to dashboard Cite

Specific defects in DNA repair pathways are reflected by DNA microsatellite instability (MSI) and play an important role in carcinogenesis. Reported frequencies in gastric non-Hodgkin's lymphomas (NHL) vary from 14% to as high as 90%. Another form of genetic instability in tumours is allelic imbalance (AI) due to loss or gain of genetic material at a specific chromosomal region. This might point to the presence of a tumour suppressor gene or oncogene. We examined both MSI and AI in 26 gastric lymphomas (10 low-grade and 13 high-grade MALT lymphomas and three cases lacking MALT features and categorised as diffuse large B cell lymphoma (DLCL)). Tumour components and normal cells (epithelium, muscle) were microdissected from paraffin-embedded resection samples. Contrary to other studies we did not observe frequent MSI when investigating 18 different loci distributed over 12 chromosomes. Microsatellite instability of a single locus was found in 1/10 (10%) low-grade MALT lymphomas and 2/13 (15%) highgrade MALT lymphomas. These data indicate that DNA mismatch repair genes do not play a role in the pathogenesis of these lymphomas. Allelic imbalance was detected in 60% (6/10) of low-grade MALT lymphomas, in 62% (8/13) of high-grade MALT lymphoma and in 67% (2/3) of DLCL. In high-grade lymphomas more loci showed AI (one to seven loci, with a mean of 2.5 loci per case) than in the low-grade lymphomas (one to two loci, with a mean of 1.3 loci per case), possibly reflecting an increased genomic instability.

show abstract

Telomerase activity in B-cell non-Hodgkin lymphoma

Ely

Chadburn

Dayton

et al. 2000

Cancer

View full text Add to dashboard Cite

BACKGROUND Studies have shown telomerase activity to be present in some B‐cell non‐Hodgkin lymphomas (B‐NHLs). However, no large studies have assayed telomerase activity in a systematic and quantitative manner. Furthermore, the relation between telomerase and proliferation suggested by in vitro studies has not been adequately tested in B‐NHLs in vivo. This information is necessary to understand the relation between proliferation and telomerase and to predict the efficacy of antitelomerase drugs currently in development. METHODS Eighteen benign biopsies and 111 B‐NHLs of varying types were classified according to the revised European‐American classification of lymphoid neoplasms (REAL classification) and assayed for telomerase activity and proliferation index (PI). RESULTS All B‐NHLs contained telomerase activity except for low grade marginal zone B‐cell lymphomas (MZBCLs) (96 of 111, 86%) (χ2 95.90, P < 0.001). Telomerase activity correlated with PI (r = 0.7536, r2 = 0.5678, t = 10.51, P < 0.001) and showed a threshold whereby telomerase activity was not present below a PI of 9.2% (t = 4.875, P < 0.001). CONCLUSIONS The level of telomerase activity fell within characteristic ranges and generally correlated with the clinical aggressiveness of each B‐NHL category. Low grade MZBCLs of extranodal, nodal, and splenic types were unique among the categories of B‐NHL in lacking or containing very little telomerase activity. The association between telomerase activity and PI is evidence that telomerase is controlled in vivo along with the cell cycle and is not constitutively active in B‐NHL. These data provide evidence that antitelomerase drugs may be efficacious in most types of B‐NHL. Cancer 2000;89:445–52. © 2000 American Cancer Society.

show abstract

Gastric low-grade MALT lymphoma, high-grade MALT lymphoma and diffuse large B cell lymphoma show different frequencies of trisomy

Cited by 58 publications

References 14 publications

T(14;18)(q32;q21) involving MALT1 and IGH genes occurs in extranodal diffuse large B-cell lymphomas of the breast and testis

T(14;18)(q32;q21) involving MALT1 and IGH genes occurs in extranodal diffuse large B-cell lymphomas of the breast and testis

True

Telomerase activity in B-cell non-Hodgkin lymphoma

Contact Info

Product

Resources

About