Two for One: B-Cell Lymphomas with Features of Marginal and Follicular Lymphomas

2018 ◽  
Vol 139 (2) ◽  
pp. 84-88 ◽  
Author(s):  
Alexey Glazyrin ◽  
Chirag Patel ◽  
Lara Kujtan ◽  
Sheshadri Madhusudhana
Keyword(s):  
Bone Marrow ◽  
Follicular Lymphoma ◽  
Tumor Cells ◽  
Marginal Zone ◽  
Lymph Node Biopsy ◽  
Low Grade ◽  
Circulating Cells ◽  
Diagnosis And Classification ◽  
Follicular Lymphomas ◽  
Normal Architecture

Low-grade follicular lymphomas are genetically characterized by the translocation t(14; 18)(q32;q21) with BCL2 gene rearrangements. Marginal zone lymphomas are often associated with translocations or transcriptional deregulations of the MALT gene. We report 2 cases of lymphomas which harbor both the t(14;18)(q32;q21) translocation and MALT gene upregulation. Patients presented with numerous circulating atypical lymphocytes. Lymph node biopsy in both cases on HE staining demonstrated vague nodularity readily highlighted by CD10, CD23, or BCL6. Staining with CD20 and BCL2 demonstrated monotonous diffuse effacement of normal architecture with tumor cells without obvious follicular structures. Morphologically, tumor cells were consistent with centrocytes. Bone marrow biopsy demonstrated a combined peritrabecular and interstitial distribution of the tumor cells. These cases present substantial difficulties for diagnosis and classification. Clinical and morphological features were mostly consistent with follicular lymphoma, with a few features more often seen in marginal zone lymphomas (leukemic presentation, no CD10 in circulating cells, interstitial location of tumor cells in bone marrow); therefore, these cases were finally classified as follicular lymphoma grade I. Both patients were treated with standard chemotherapy regimens for follicular and nongastric MALT lymphomas with a good response to date.

scholarly journals Differential Expression of Matrix Metalloproteinase-2 Expression in Disseminated Tumor Cells and Micrometastasis in Bone Marrow of Patients with Nonmetastatic and Metastatic Prostate Cancer: Theoretical Considerations and Clinical Implications—An Immunocytochemical Study

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Nigel P. Murray ◽  
Eduardo Reyes ◽  
Pablo Tapia ◽  
Leonardo Badínez ◽  
Nelson Orellana
Keyword(s):  
Prostate Cancer ◽  
Bone Marrow ◽  
Matrix Metalloproteinase ◽  
Tumor Cells ◽  
Gleason Score ◽  
Stromal Cells ◽  
Disseminated Tumor Cells ◽  
Matrix Metalloproteinase 2 ◽  
Low Grade ◽  
Immunocytochemical Study

Matrix metalloproteinase-2 (MMP-2) is important in the dissemination and invasion of tumor cells and activates angiogenesis. We present an immunocytochemical study of MMP-2 expression in circulating prostate cells (CPCs), disseminated tumor cells (DTCs), and micrometastasis (mM) in bone marrow of men with prostate cancer. Methods and Patients. Tumor cells were identified with anti-PSA immunocytochemistry. Positive samples underwent processing with anti-MMP-2, its expression was compared with Gleason score, concordance of expression, and metastatic and nonmetastatic disease. Results. 215 men participated, CPCs were detected in 62.7%, DTCs in 62.2%, and mM in 71.4% in nonmetastatic cancer; in metastatic cancer all had CPCs, DTCs, and mM detected. All CPCs and DTCs expressed MMP-2; in mM MMP-2 expression was positively associated with increasing Gleason score. MMP-2 expression in CPCs and DTCs showed concordance. In low grade tumors, mM and surrounding stromal cells were MMP-2 negative, with variable expression in high grade tumors; in metastatic disease, both mM and stromal cells were MMP-2 positive. Conclusions. CPCs and DTCs are different from mM, with inhibition of MMP-2 expression in mM of low grade tumors. With disease progression, MMP-2 expression increases in both mM and surrounding stromal cells, with implications for the use of bisphosphonates or MMP-2 inhibitors.

scholarly journals MYC rearrangements in histologically progressed follicular lymphomas

Blood ◽  
1992 ◽  
Vol 80 (3) ◽  
pp. 758-767 ◽  
Author(s):  
T Yano ◽  
ES Jaffe ◽  
DL Longo ◽  
M Raffeld
Keyword(s):  
Follicular Lymphoma ◽  
Molecular Organization ◽  
Aggressive Lymphoma ◽  
Chain Gene ◽  
Low Grade ◽  
Immunoglobulin Gene ◽  
High Grade ◽  
Light Chain Gene ◽  
Myc Gene ◽  
Follicular Lymphomas

Abstract Histologic transformation of low-grade follicular lymphoma to an aggressive-grade lymphoma occurs in 60% to 80% of patients during their clinical course. The events that drive the transformation process are poorly understood. Deregulation of the MYC gene has been implicated in a small number of cases. This observation led us to examine the molecular organization of the MYC oncogene in 38 cases of histologically transformed lymphomas that arose from follicular lymphomas, and in 18 of the initial pretransformation follicular lymphomas. In addition, we examined 58 “control” low-grade follicular lymphomas that had not yet shown evidence of histologic progression. Immunoglobulin heavy chain and light chain gene rearrangements were detected in all biopsies and rearrangements of the BCL-2 locus were seen in 36 of 38 of the transformed lymphomas (consistent with their origin from follicular lymphomas), in 18 of 18 of the pretransformation follicular lymphomas, and in 51 of 58 of the control follicular lymphomas. All 18 pretransformation follicular lymphoma specimens displayed at least one immunoglobulin gene and BCL-2 rearrangement in common with the corresponding histologically progressed lymphoma, indicating a clonal relationship between the original follicular lymphoma and the histologically transformed lymphoma. MYC rearrangements were detected in 3 of 38 (8%) transformed lymphomas and in 1 of 58 (2%) control follicular lymphomas. The latter MYC rearranged follicular lymphoma was clinically aggressive and transformed to a high- grade lymphoma that led to the death of the patient within 20 months. None of the 18 pretransformation follicular lymphomas showed MYC rearrangement, including two from patients who later demonstrated MYC rearrangement in the progressed aggressive lymphoma. PvuII mutational analysis failed to identify additional MYC gene abnormalities in the progressed lymphomas. Because the Epstein-Barr virus (EBV) is associated with a fraction of high-grade lymphomas and is known to upregulate BCL-2, we looked for a potential role for this agent in our progressed lymphomas. We did not detect viral sequences in any case indicating that EBV does not play a major role in progression. The presence of MYC rearrangements in a small fraction of progressed aggressive lymphomas, and not in the corresponding antecedent follicular lymphomas, suggests that acquisition of a MYC rearrangement is in some cases associated with the transformation event.

CD5+ Extranodal Marginal Zone B-Cell (MALT) Lymphoma:A Low Grade Neoplasm With a Propensity for Bone Marrow Involvement and Relapse

1996 ◽  
Vol 105 (1) ◽  
pp. 31-37 ◽  
Author(s):  
Judith A. Ferry ◽  
Woo-Ick Yang ◽  
Lawrence R. Zukerberg ◽  
Andrew C. Wotherspoon ◽  
Andrew Arnold ◽  
...  
Keyword(s):  
Bone Marrow ◽  
B Cell ◽  
Marginal Zone ◽  
Bone Marrow Involvement ◽  
Low Grade

scholarly journals p53 mutation is associated with progression in follicular lymphomas

Blood ◽  
1993 ◽  
Vol 82 (7) ◽  
pp. 1994-2004 ◽  
Author(s):  
CA Sander ◽  
T Yano ◽  
HM Clark ◽  
C Harris ◽  
DL Longo ◽  
...  
Keyword(s):  
Complete Remission ◽  
Follicular Lymphoma ◽  
Molecular Mechanisms ◽  
Single Strand Conformation Polymorphism ◽  
Suppressor Gene ◽  
Neoplastic Cell ◽  
P53 Mutation ◽  
Polymorphism Analysis ◽  
Low Grade ◽  
Follicular Lymphomas

The majority of low-grade follicular lymphomas will eventually transform to an aggressive intermediate, or high-grade lymphoma. The molecular mechanisms responsible for this transformation have not been determined. We studied serial biopsies from 34 patients with follicular lymphomas that underwent histologic transformation, for abnormalities of the p53 tumor suppressor gene by a combination of immunohistochemistry, single strand conformation polymorphism analysis (SSCP), and sequencing. We found overexpression of p53 in 10 of the 34 transformed aggressive lymphomas, 9 of which contained mutations identified by SSCP analysis and subsequent sequencing. Matched pretransformation low-grade follicular lymphoma biopsies were available for 7 of the 10 cases. None of six studied by immunohistochemistry showed overexpression of p53 and only 1 of 4 studied by SSCP/sequencing showed the presence of mutation in the pretransformation biopsy. Interestingly, an eighth p53 positive transformed lymphoma recurred with a clonally related, p53 negative low-grade lymphoma 5 years after the patient had achieved a complete remission. Immunohistochemistry also showed that several pretransformation biopsies from p53 positive transformed cases showed rare p53 positive cells and in one case we could document an increase in their number over time. Twenty-five additional low-grade follicular lymphoma biopsies were also examined. Three patients had lymphomas positive for p53 mutation. One of the three subsequently transformed within a year of the biopsy studied; the second patient had an earlier (unavailable) biopsy at a different site that showed transformed histology. The third patient was treated with ProMACE-MOPP combination chemotherapy and attained a complete remission. We conclude that (1) mutations of p53 are associated with histologic transformation in approximately 25% to 30% of follicular lymphomas and (2) p53 positive cells can be detected before histologic transformation, but do not comprise a significant percentage of the neoplastic cell population (identifiable by SSCP) until late in the disease, just before or after histologic progression. Finally, the data also suggest that p53 positive low-grade lymphomas are at risk for progression and that in this subset, aggressive therapy may be warranted.

scholarly journals MYC rearrangements in histologically progressed follicular lymphomas

Blood ◽  
1992 ◽  
Vol 80 (3) ◽  
pp. 758-767 ◽  
Author(s):  
T Yano ◽  
ES Jaffe ◽  
DL Longo ◽  
M Raffeld
Keyword(s):  
Follicular Lymphoma ◽  
Molecular Organization ◽  
Aggressive Lymphoma ◽  
Chain Gene ◽  
Low Grade ◽  
Immunoglobulin Gene ◽  
High Grade ◽  
Light Chain Gene ◽  
Myc Gene ◽  
Follicular Lymphomas

Histologic transformation of low-grade follicular lymphoma to an aggressive-grade lymphoma occurs in 60% to 80% of patients during their clinical course. The events that drive the transformation process are poorly understood. Deregulation of the MYC gene has been implicated in a small number of cases. This observation led us to examine the molecular organization of the MYC oncogene in 38 cases of histologically transformed lymphomas that arose from follicular lymphomas, and in 18 of the initial pretransformation follicular lymphomas. In addition, we examined 58 “control” low-grade follicular lymphomas that had not yet shown evidence of histologic progression. Immunoglobulin heavy chain and light chain gene rearrangements were detected in all biopsies and rearrangements of the BCL-2 locus were seen in 36 of 38 of the transformed lymphomas (consistent with their origin from follicular lymphomas), in 18 of 18 of the pretransformation follicular lymphomas, and in 51 of 58 of the control follicular lymphomas. All 18 pretransformation follicular lymphoma specimens displayed at least one immunoglobulin gene and BCL-2 rearrangement in common with the corresponding histologically progressed lymphoma, indicating a clonal relationship between the original follicular lymphoma and the histologically transformed lymphoma. MYC rearrangements were detected in 3 of 38 (8%) transformed lymphomas and in 1 of 58 (2%) control follicular lymphomas. The latter MYC rearranged follicular lymphoma was clinically aggressive and transformed to a high- grade lymphoma that led to the death of the patient within 20 months. None of the 18 pretransformation follicular lymphomas showed MYC rearrangement, including two from patients who later demonstrated MYC rearrangement in the progressed aggressive lymphoma. PvuII mutational analysis failed to identify additional MYC gene abnormalities in the progressed lymphomas. Because the Epstein-Barr virus (EBV) is associated with a fraction of high-grade lymphomas and is known to upregulate BCL-2, we looked for a potential role for this agent in our progressed lymphomas. We did not detect viral sequences in any case indicating that EBV does not play a major role in progression. The presence of MYC rearrangements in a small fraction of progressed aggressive lymphomas, and not in the corresponding antecedent follicular lymphomas, suggests that acquisition of a MYC rearrangement is in some cases associated with the transformation event.

scholarly journals Detection of clonal CD34+19+ progenitors in bone marrow of BCL2-IgH- positive follicular lymphoma patients

Blood ◽  
1995 ◽  
Vol 86 (12) ◽  
pp. 4691-4698 ◽  
Author(s):  
EA Macintyre ◽  
C Belanger ◽  
C Debert ◽  
D Canioni ◽  
AG Turhan ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Follicular Lymphoma ◽  
B Cell ◽  
Tumor Cells ◽  
Cell Sorting ◽  
Chain Reaction ◽  
Selection Procedures ◽  
Polymerase Chain ◽  
B Cell Precursors ◽  
Selection Of

The frequent occurrence of BCL2-IgH rearrangements in follicular lymphoma (FL) makes detection of low numbers of tumor cells possible by polymerase chain reaction (PCR). The presence of BCL2-IgH in the bone marrow (BM) and peripheral blood of many FL patients at the time of autografting has led to the suggestion that selection of the CD34- enriched fraction may lead to reinfusion of lower numbers of tumor cells. To address this issue, we PCR-amplified BCL2-IgH from fluorescence-activated cell sorting (FACS)-purified BM CD34+ and CD34- fractions in seven FL patients showing a PCR-detectable translocation in the major breakpoint region of BCL2, five of which showed morphological BM involvement. The total CD34+ fraction showed diminished but residual positivity in the first two cases tested. Therefore, BM cells from the remaining five patients were sorted for the CD34+19- immature population, the CD34+19+ B-cell precursors, and the CD34–19+ mature B-cell fraction. The CD34+19- subpopulation was negative in four of five, despite evident BM infiltration in three cases. In contrast, the CD34+19+ fraction was positive in all three cases tested. These cells represented 0% to 50% (mean, 18%) of the total CD34+ population, suggesting that, if reinfusion of BCL2-IgH- positive cells plays a role in postautograft relapse in FL, therapeutic CD34 selection procedures should include additional purging of the CD34+19+ B-cell precursors or, at least, assessment of the proportion of CD19+ cells in the CD34+ fraction and its correlation with clinical outcome postreinfusion.

scholarly journals Immunohistochemical Expression of Lymphoid Enhancer Binding Factor 1 in CD5-Positive Marginal Zone, Lymphoplasmacytic, and Follicular Lymphomas

2020 ◽  
Vol 153 (5) ◽  
pp. 646-655
Author(s):  
Nisha Patel ◽  
Lisa Durkin ◽  
Juraj Bodo ◽  
Eric D Hsi
Keyword(s):  
Chronic Lymphocytic Leukemia ◽  
Tumor Cells ◽  
Lymphoid Tissue ◽  
Marginal Zone ◽  
Lymphocytic Leukemia ◽  
Immunohistochemical Expression ◽  
Small Lymphocytic Lymphoma ◽  
Binding Factor ◽  
Reliable Marker ◽  
Follicular Lymphomas

Abstract Objectives Lymphoid enhancer binding factor 1 (LEF1) is expressed in most cases of chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL) and has shown utility in distinguishing CLL/SLL from other small B-cell lymphomas. LEF1 expression has not been systematically studied in CD5-positive marginal zone lymphomas (MZLs), lymphoplasmacytic lymphomas (LPLs), and follicular lymphomas (FLs). We evaluated whether these cases lacked LEF1, helping to distinguish them from CLL/SLL. Methods MZLs, LPLs, and FLs expressing CD5 were retrospectively studied for expression of LEF1 by immunohistochemistry. Results LEF1 was absent in 17 of 18 CD5-positive lymphomas including 13 MZLs (2 nodal, 3 splenic, and 8 mucosa-associated lymphoid tissue lymphomas), 3 LPLs, and 1 of 2 FLs. One grade 3A CD5-positive FL expressed LEF1 in a majority of tumor cells. Conclusions LEF1 is not expressed in most CD5-positive MZLs and LPLs; therefore, it is a reliable marker for distinguishing them from CLL/SLL. LEF1 may be expressed in CD5-positive FLs.

Splenic Marginal Zone Lymphoma (SMZL): Clinical Course after Splenectomy. A Single Institution Experience

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 3993-3993
Author(s):  
Susanna S Gaykazyan ◽  
Nalini Janakiraman ◽  
Philip Kuriakose ◽  
Koichi Maeda ◽  
Tareq Hammour
Keyword(s):  
Bone Marrow ◽  
B Cell ◽  
Systemic Therapy ◽  
Marginal Zone ◽  
Clinical Course ◽  
Bone Marrow Involvement ◽  
Marginal Zone Lymphoma ◽  
Low Grade ◽  
Splenic Marginal Zone Lymphoma ◽  
Symptomatic Disease

Abstract SMZL is an indolent B-cell malignancy accounting for 1–2% of chronic lymphoid leukemia found on bone marrow examination and up to 25% of low-grade B-cell neoplasms in splenectomy patients. Aggressive transformation of SMZL rarely occurs. It usually presents as an incidental finding or with symptoms of splenomegaly and anemia. There is still no reliable clinical or biological scoring system for prognostic stratification. We reviewed pathology reports of 41 splenectomized patients at HFHS from 1994 to 2007 and identified 14 patients with splenic marginal zone lymphoma (SMZL). The reasons for splenectomy were symptoms of splenomegaly in all 14 patients, anemia in 13 patients, thrombocytopenia in 12 patients, AIHA in 4 patients, splenic laceration in one patient. We report here the demographics, clinical course and pathology review of these patients. The median age of patients was 77.8 years. There were 7 male and 7 female patients. ECOG performance status was 0–1 in 12(86%), and 2 in 2(14%). Of the 14 patients, 8(57%) were at Ann Arbor stage IV, 1(7%) was at stage III, 4(29%) were at stage II, and 1(7%) at stage I. LDH was above normal in 9(64%) patients B-symptoms were observed in 1(7%). Bone marrow involvement was documented in 8(57%) of the patients. Anemia in 13(93%), thrombocytopenia in 12(86%), AIHA in 4(29%). IPI score was 1–2 in 5(36%), and score 3–4 in 9(64%) of the patients. Median weight of the spleen was 1235 gm. Bone marrow cytogenetics were abnormal in 4(29%) cases. Following splenectomy, cytopenias resolved completely or partially (CR/PR) in 13(93%) patients. Bacterial infections were observed in 4(29%) patients and 2(14%) died of infectious complications. Progressive disease requiring additional systemic therapy was documented in 5(36%) patients. Total of 5(36%) patients died. One secondary to NSLC, 1(7%) of urothelial carcinoma, 1(7%) secondary to hypercalcemia, 2(14%) due to bacterial sepsis. Patients were followed up to 139 months (with median follow-up time of 42 months). The estimated median overall survival (OS) for this group was 116.5 months (9.7 years), the median progression-free survival (PFS) was 91 months (7.6 years). The Kaplan Meier method was used to calculate these estimates. A simple median was calculated for the sample median. In summary, we report the course of 14 patients with SMZL who underwent splenectomy for symptomatic disease. Only 5(36%) required systemic therapy following splenectomy. No death was attributed to progressive SMZL. Overall course was indolent even after splenectomy. Estimated OS was 116.5 months (9.7 years), PFS - 91 month (7.6 years).

Safety and Efficacy of Fludarabine Plus Mitoxantrone (FM) Followed by Yttrium-90 (90Y) Ibritumomab Tiuxetan (Zevalin®) and Maintenance Rituximab in Intermediate- to High-Risk Newly Diagnosed and Relapsed Follicular Non-Hodgkin’s Lymphoma (NHL).

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 4789-4789 ◽  
Author(s):  
Stephanie A. Gregory ◽  
Parameswaran Venugopal ◽  
Jamile M. Shammo ◽  
Teresa M. O’Brien ◽  
Amjad Ali
Keyword(s):  
Bone Marrow ◽  
Follicular Lymphoma ◽  
Bone Marrow Involvement ◽  
Complete Response ◽  
Low Grade ◽  
Newly Diagnosed ◽  
Ibritumomab Tiuxetan ◽  
Safety And Efficacy ◽  
Grade 3 ◽  
Relapsed Disease

Abstract Background: The combination of fludarabine and mitoxantrone (FM) as a frontline therapy for advanced follicular lymphoma has been shown to result in higher complete response rates when compared with standard-dose CHOP. We assessed the safety and efficacy of FM followed by 90Y ibritumomab tiuxetan (IT) and maintenance rituximab in previously untreated or relapsed follicular NHL. Patients and methods: Patients with newly diagnosed stage II-IV low-grade NHL and an intermediate-high or high IPI, as well as those with relapsed low-grade or transformed disease, were initially eligible. The protocol was later amended to include patients with follicular NHL with an intermediate or high FLIPI. Adult patients were required to have an expected survival of at least 3 months, a performance status ≤2, and adequate bone marrow function (ANC 1500/mm3, platelets 100,000/mm3), liver, and renal function. Exclusion criteria included impaired bone marrow reserve, history of failed stem cell collection, and prior radioimmunotherapy. Initial treatment consisted of 4 cycles of FM (mitoxantrone 12 mg/m2 on day 1, fludarabine 25 mg/m2 on days 1–3 of each 28-day cycle). After restaging, complete and partial responders with ≤25% bone marrow involvement proceeded to the IT therapeutic regimen. Partial responders with >25% bone marrow involvement received 2 additional cycles of FN before IT. The 90Y IT dose (0.3 or 0.4 mCi/kg) was adjusted according to the patient’s platelet count. Maintenance rituximab (375 mg/m2 × 4) was scheduled for every 6 months over 2 years. Results: Twelve patients have been enrolled, including 5 with relapsed disease. The median age was 57 years (range, 38–67), and 5 were male. All patients presented with grade 1–3 follicular NHL; most had stage IV disease and lymphomatous bone marrow involvement (10/12). The median FLIPI score was 2 (range, 1–4). Patients with relapsed disease had received prior CVP (3/5) or FMR (2/5). In those with relapsed NHL, hematologic toxicities were grade 3 or 4 neutropenia (4/5), grade 3 thrombocytopenia (2/5), and grade 3 anemia (2/5) with FN. Four did not proceed to 90Y IT (1 had progressive disease, 1 had >25% bone marrow involvement, 1 had myelosuppression, and 1 went on to transplant). The patient, who later received 90Y IT, had a partial response but relapsed at 9 months. Four patients with newly diagnosed disease were assessable for safety and response. The incidence of grade 3 or 4 neutropenia, thrombocytopenia, and anemia with chemotherapy were 75%, 50%, and 50%, respectively, in these patients. All 4 patients went on to receive 90Y IT; platelet, ANC, and hemoglobin nadirs occurred at 5–8 weeks following 90Y IT, and were reversible. Partial responses were achieved after 4–6 cycles of FN in all cases. One patient converted to a complete response after 90Y IT; another 2 patients were PET-negative after radioimmunotherapy. As of yet, no patients have gone on to rituximab maintenance. The remaining patient relapsed at 6 months. Conclusions: This preliminary data suggests that FM followed by the 90Y ibritumomab tiuxetan therapeutic regimen is highly effective in patients with untreated follicular lymphoma. This combination, however, may be too toxic for patients with relapsed disease, especially if they have been treated with prior fludarabine.

Simultaneous Discordant B-Lymphoblastic Lymphoma and Follicular Lymphoma

2020 ◽  
Author(s):  
Ayumi Fujimoto ◽  
Fumiyoshi Ikejiri ◽  
Fumiko Arakawa ◽  
Shunsuke Ito ◽  
Yusuke Okada ◽  
...  
Keyword(s):  
Follicular Lymphoma ◽  
Tumor Cells ◽  
Gene Rearrangement ◽  
Lymphoblastic Lymphoma ◽  
Critical Event ◽  
Low Grade ◽  
Clonal Relationship ◽  
Myc Gene ◽  
Lymphoblastic Transformation ◽  
B Lymphoblastic Lymphoma

Abstract Objectives We report a rare case of B-lymphoblastic lymphoma (B-LBL) and low-grade follicular lymphoma (FL) identified concurrently in biopsies from different sites at the initial diagnosis in a 39-year-old man. The clonal relationship between the 2 histologic subtypes was investigated. Methods A diagnosis of FL grade 1/2 (low grade) was made by bone marrow (BM) biopsy. B-LBL was identified in biopsies from the testis and pancreas. Cytogenetic and molecular analyses were performed to investigate their clonal relationship. Results Interphase fluorescence in situ hybridization analyses and G-banding karyotype analyses identified the BCL2-IGH and MYC-IGH translocation in tumor cells from both the BM and testis. The tumor cells from the BM and testis shared the same IGH VDJ usage and a high degree of somatic mutations. These findings suggest that acquisition of MYC gene rearrangement is a critical event for lymphoblastic transformation of FL. Of note, the presence of intraclonal diversity in the B-LBL sample further suggests an earlier or concurrent event of MYC translocation than the somatic IGH mutation in the germinal center and the dedifferentiation of lymphoma cells to a precursor stage of B-cell development. Conclusions B-lymphoblastic transformation of FL can occur with MYC gene rearrangement.

Sign in / Sign up

Export Citation Format

Share Document