scholarly journals High-grade B-cell lymphoma/leukemia associated with t(14;18) and 8q24/MYC rearrangement: a neoplasm of germinal center immunophenotype with poor prognosis

Haematologica ◽  
2007 ◽  
Vol 92 (10) ◽  
pp. 1297-1301 ◽  
Author(s):  
P. Lin ◽  
L. J. Medeiros
Keyword(s):  
B Cell ◽  
Germinal Center ◽  
Poor Prognosis ◽  
Cell Lymphoma ◽  
B Cell Lymphoma ◽  
High Grade

scholarly journals Molecular High-Grade B-Cell Lymphoma: Defining a Poor-Risk Group That Requires Different Approaches to Therapy

2019 ◽  
Vol 37 (3) ◽  
pp. 202-212 ◽  
Author(s):  
Chulin Sha ◽  
Sharon Barrans ◽  
Francesco Cucco ◽  
Michael A. Bentley ◽  
Matthew A. Care ◽  
...  
Keyword(s):  
Gene Expression ◽  
B Cell ◽  
Germinal Center ◽  
Poor Prognosis ◽  
Cell Lymphoma ◽  
B Cell Lymphoma ◽  
High Grade ◽  
Data Set ◽  
Germinal Center B Cell ◽  
Double Hit

Purpose Biologic heterogeneity is a feature of diffuse large B-cell lymphoma (DLBCL), and the existence of a subgroup with poor prognosis and phenotypic proximity to Burkitt lymphoma is well known. Conventional cytogenetics identifies some patients with rearrangements of MYC and BCL2 and/or BCL6 (double-hit lymphomas) who are increasingly treated with more intensive chemotherapy, but a more biologically coherent and clinically useful definition of this group is required. Patients and Methods We defined a molecular high-grade (MHG) group by applying a gene expression–based classifier to 928 patients with DLBCL from a clinical trial that investigated the addition of bortezomib to standard rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) therapy. The prognostic significance of MHG was compared with existing biomarkers. We performed targeted sequencing of 70 genes in 400 patients and explored molecular pathology using gene expression signature databases. Findings were validated in an independent data set. Results The MHG group comprised 83 patients (9%), with 75 in the cell-of-origin germinal center B-cell-like group. MYC rearranged and double-hit groups were strongly over-represented in MHG but comprised only one half of the total. Gene expression analysis revealed a proliferative phenotype with a relationship to centroblasts. Progression-free survival rate at 36 months after R-CHOP in the MHG group was 37% (95% CI, 24% to 55%) compared with 72% (95% CI, 68% to 77%) for others, and an analysis of treatment effects suggested a possible positive effect of bortezomib. Double-hit lymphomas lacking the MHG signature showed no evidence of worse outcome than other germinal center B-cell-like cases. Conclusion MHG defines a biologically coherent high-grade B-cell lymphoma group with distinct molecular features and clinical outcomes that effectively doubles the size of the poor-prognosis, double-hit group. Patients with MHG may benefit from intensified chemotherapy or novel targeted therapies.

Lymphocytic infiltrations of the lung

2020 ◽  
pp. 4241-4244
Author(s):  
S. J. Bourke
Keyword(s):  
Connective Tissue ◽  
B Cell ◽  
Interstitial Pneumonia ◽  
Lymphoid Tissue ◽  
Poor Prognosis ◽  
Cell Lymphoma ◽  
Connective Tissue Diseases ◽  
B Cell Lymphoma ◽  
Low Grade ◽  
High Grade

Lymphocytic infiltrations of the lung arise from the proliferation of bronchus-associated lymphoid tissue, resulting in a spectrum of rare conditions ranging from benign polyclonal lymphoid interstitial pneumonia to monoclonal primary malignant lymphomas of the lung. Lymphoid interstitial pneumonia is most commonly seen in Sjögren’s syndrome or other connective tissue diseases, and in association with HIV infection, and is characterized by reticulonodular shadowing on CT imaging and (usually) a good response to corticosteroids. Primary pulmonary lymphomas fall into three categories: lymphomatoid granulomatosis, low-grade B-cell lymphoma, and high-grade B-cell lymphoma. The latter require treatment with cytotoxic drugs and have a poor prognosis.

High-grade B cell lymphoma, unclassifiable, with blastoid features: an unusual morphological subgroup associated frequently withBCL2and/orMYCgene rearrangements and a poor prognosis

2012 ◽  
Vol 61 (5) ◽  
pp. 945-954 ◽  
Author(s):  
Rashmi Kanagal-Shamanna ◽  
L Jeffrey Medeiros ◽  
Gary Lu ◽  
Sa A Wang ◽  
John T Manning ◽  
...  
Keyword(s):  
B Cell ◽  
Poor Prognosis ◽  
Cell Lymphoma ◽  
B Cell Lymphoma ◽  
High Grade

Patients with "Single-Hit" but Not MYC -Amplified Non-Burkitt High-Grade B Cell Non-Hodgkin Lymphomas Experience Poor Survival Outcomes and May Benefit from Intensive Induction Therapy

Blood ◽  
2015 ◽  
Vol 126 (23) ◽  
pp. 2696-2696
Author(s):  
Daniel J. Landsburg ◽  
Marissa K. Falkiewicz ◽  
Jennifer J.D. Morrissette ◽  
April M. Schrank-Hacker ◽  
Sunita Dwivedy Nasta ◽  
...  
Keyword(s):  
B Cell ◽  
Induction Therapy ◽  
Research Funding ◽  
Poor Prognosis ◽  
Cell Lymphoma ◽  
B Cell Lymphoma ◽  
High Grade ◽  
Baseline Characteristics ◽  
Ecog Ps

Abstract Introduction While patients (pts) with diffuse large B cell lymphoma (DLBCL) and B cell lymphoma unclassifiable with features intermediate between DLBCL and Burkitt lymphoma (BCLU) harboring rearrangement of MYC (MYC-R) face a poor prognosis as compared to DLBCL/BCLU pts without MYC-R, the prognosis of DLBCL/BLCU pts with MYC-R in the absence of rearrangements of BCL2 (BCL2-R) and BCL6 (BCL6-R) has not clearly been reported in the literature. Additionally, it is not well known whether amplification of MYC in the absence of MYC-R portends a poor prognosis for DLBCL/BCLU pts. Here, we analyze outcomes for these pts in comparison to DLBCL/BCLU pts without MYC-R or MYC amplification. Methods Pts diagnosed with DLBCL or BCLU treated at the University of Pennsylvania and Northwestern University from 3/2002-3/2015 whose diagnostic specimens underwent fluorescence in situ hybridization for MYC-R with8q24 breakapart and/or t(8;14)(q24;q32) fusion probes were included in this analysis. Pts with primary CNS and HIV-associated lymphoma were excluded. Cases with MYC-R but not BCL2-R and BCL6- R were defined as single hit (SH), cases with MYC-R as well as BCL2 -Rand/or BCL6-R as double hit (DH), cases with >4 copies of MYC as amplified (MYC amp) and cases without MYC-R and ≤4 copies of MYC as normal (MYC normal). Therapy was given at the discretion of the treating clinician. Progression free survival (PFS) was defined as time from diagnosis to radiographic progression, regimen change, death or last follow-up. Overall survival (OS) was defined as time from diagnosis to death or last follow-up. Data were censored on 7/1/15. Results 224 pts were included in the full analysis: 190 MYC normal, 19 SH and 15 MYC amp. An additional 46 DH pts were analyzed for PFS and OS only. No pts were both SH and MYC amp. Pts baseline characteristics were reported as follows: 52% female, 47% age >60 years (yrs), 66% LDH >normal, 62% stage ≥3, 15% lymphomatous involvement of bone marrow, 11% ECOG performance status (PS) >2, 66% extranodal disease, 29% B symptoms, 42% International Prognostic Index (IPI) score ≥3, 4% BCLU histology and 18% low-grade transformation. Only the presence of BCLU histology differed significantly between SH and MYC normal pts (26% vs. 1%, p=0.001) and between MYC amp and MYC normal pts (13% vs. 1%, p=0.028). PFS and OS are depicted in Figure 1. For all pts, the median length of follow-up was 15.4 months (mos) (range 0.1-156.1 mos), median PFS not yet reached and median OS not yet reached. Rates of PFS and OS at 2 yrs for MYC normal, SH and MYC amp pts were 72%, 52%, 62% and 81%, 65%, 74%, respectively. When compared to MYC normal pts, SH pts experienced significantly shorter rates of PFS (p=0.043) and OS (p=0.038) at 2 yrs; however, rates of PFS and OS at 2 yrs did not differ significantly between MYC amp and MYC normal pts (p=0.29 and p=0.67, respectively). For comparison, rates of PFS and OS at 2 yrs for DH pts were 32% and 37%, and did not differ significantly from those of SH pts (p=0.26 and p=0.18, respectively). For SH patients, rates of PFS and OS at 2 yrs for those receiving induction therapy with R-CHOP vs. intensive induction (II), defined as either R-EPOCH, R-hyperCVAD or R-CODOX-M/IVAC, were 25% vs. 76% (p=0.13) and 75% vs. 73% (p=0.94), respectively. Baseline characteristics significantly associated with progression on univariate analysis (UVA) were LDH > normal (HR 2.50, 95% CI 1.20-5.17, p=0.014), ECOG PS >2 (HR 2.17, 95% CI 1.05-4.70, p=0.036) and B symptoms (HR 2.49, 95% CI 1.48-4.19, p=0.001); however, only B symptoms remained statistically significant on multivariate analysis (MVA) (HR 2.66, 95% CI 1.41-5.01, p=0.003). Baseline characteristics significantly associated with death on UVA were LDH > normal (HR 3.99, 95% CI 1.19-13.4, p=0.025), ECOG PS >2 (HR 3.19, 95% CI 1.29-7.90, p=0.012), B symptoms (HR 2.70, 95% CI 1.31-5.57, p=0.007) and SH vs. MYC normal (HR 2.59, 95% CI 1.06-6.31, p=0.037); however, no factor remained statistically significant on MVA. Conclusions This analysis of the largest reported series of SH and MYC amp pts suggests inferior rates of PFS and OS at 2 yrs for SH pts, but not MYC amp pts, as compared to MYC normal pts. SH pts receiving II experienced similar rates of PFS and OS at 2 yrs as compared to MYC normal pts. Much like DH pts, SH pts should be considered a poor prognosis subgroup of non-Burkitt high-grade B cell non-Hodgkin lymphomas and identified as candidates for risk-adapted and/or targeted therapies. Figure 1. Figure 1. Disclosures Dwivedy Nasta: Millenium Takeda: Research Funding; BMS: Research Funding. Svoboda:Immunomedics: Research Funding; Celldex: Research Funding; Celgene: Research Funding; Seattle Genetics: Research Funding. Schuster:Genentech: Consultancy; Pharmacyclics: Consultancy, Research Funding; Celgene: Consultancy, Research Funding; Hoffman-LaRoche: Research Funding; Janssen: Research Funding; Gilead: Research Funding; Novartis: Research Funding; Nordic Nanovector: Membership on an entity's Board of Directors or advisory committees. Mato:Gilead: Consultancy, Research Funding; Celgene Corporation: Consultancy, Research Funding; Genentech: Consultancy; Pharmacyclics: Consultancy, Research Funding; AbbVie: Consultancy, Research Funding; Pronai Pharmaceuticals: Research Funding; TG Therapeutics: Research Funding. Petrich:Seattle Genetics: Consultancy, Honoraria, Research Funding.

Elevated Monoclonal Free Light Chains Are a Serum Marker of ABC Type Diffuse Large B-Cell Lymphoma

Blood ◽  
2011 ◽  
Vol 118 (21) ◽  
pp. 1591-1591
Author(s):  
Matthew J Maurer ◽  
James R Cerhan ◽  
Jerry A Katzmann ◽  
Ahmet Dogan ◽  
Mamta Gupta ◽  
...  
Keyword(s):  
B Cell ◽  
Germinal Center ◽  
Poor Prognosis ◽  
Cell Lymphoma ◽  
B Cell Lymphoma ◽  
Serum Marker ◽  
Light Chains ◽  
Free Light Chains ◽  
Large B Cell Lymphoma ◽  
Large B Cell

Abstract Abstract 1591 Background: The serum free light chain (FLC) assay quantitates free kappa and free lambda immunoglobulin light chains. We previously showed elevated FLC are present in approximately 1 in 3 diffuse large B cell lymphoma (DLBCL) patients from both a phase II cooperative group clinical trial and a large clinic based epidemiology cohort. Approximately 10% of DLBCL patients had elevated FLC that was monoclonal in these series. Patients with monoclonal elevated FLC have very poor outcome with almost 50% of patients progressing in the first 15 months following initial treatment with immunochemotherapy. Unlike patients with polyclonal FLC elevation, where a variety of host effects may cause a rise in both kappa and lambda, it is likely the excess FLC in monoclonal patients is directly related to the tumor. DLBCL are a heterogenous group of tumors that can be classified into germinal center (GCB) or activated B cell (ABC) groupings using immunohistochemistry (IHC) staining algorithms. Here we examine the association of monoclonal free light chains with ABC vs. GCB DLBCL tumors. Methods: Newly diagnosed DLBCL patients were prospectively enrolled in the University of Iowa/Mayo Clinic SPORE Molecular Epidemiology Resource (MER) or NCCTG clinical trial N0489. Serum FLC was quantitated from enrollment research serum draws using the Freelite FLC assay (The Binding Site, Ltd., Birmingham, UK). Monoclonal elevated FLC was defined as an elevated kappa or lambda with a corresponding abnormal FLC ratio. Immunohistochemistry (IHC) staining was performed on paraffin tissue from research tissue microarrays (TMAs). Results: IHC tissue staining was available from 12 patients with monoclonal elevated FLC unrelated to renal failure. Germinal center markers were predominantly negative: 2 of 11 were LMO2 positive (18%), 1 of 12 was CD10 positive (8%), and zero cases out of 11 were GCET1 positive. FoxP1 was positive in 5 of 9 cases (56%) and MUM1 was positive in 4 of 12 cases (33%). By the Tally algorithm, 10 of 11 cases (91%) were ABC type DLBCL The percentage of ABC patients by the Tally algorithm in the corresponding DLBCL patients without monoclonal FLC was 45% (N=108, p=0.004). Conclusions: Approximately 10% of DLBCL patients have elevated monoclonal FLC and these patients have poor prognosis. Elevated monoclonal FLC may be a serum marker for ABC-type lymphoma, as the tumors from patients are predominantly negative for germinal center stains and ABC by the Tally algorithm. The secretion of light chains by the tumor suggests an activated B cell clone and the poor prognosis is characteristic of ABC type DLBCL and. Given the likelihood of the excess monoclonal FLC being tumor related, the potential exists for tracking of tumor response and progression via serum FLC in these patients. Replication of these findings in an additional cohort of DLBCL patients is planned. Disclosures: No relevant conflicts of interest to declare.

Ruxolitinib in Combination with Orally Etoposide and Corticosteroids (REC) Is Safe and Effective in Heavily Pretreated Hodgkin and Non-Hodgkin Lymphomas

Blood ◽  
2015 ◽  
Vol 126 (23) ◽  
pp. 3962-3962
Author(s):  
Anne Parcelier ◽  
Pierre Morel ◽  
Bruno Royer ◽  
Caroline Delette ◽  
Isabelle Leduc ◽  
...  
Keyword(s):  
B Cell ◽  
Stable Disease ◽  
Germinal Center ◽  
Poor Prognosis ◽  
Response Rate ◽  
Cell Lymphoma ◽  
B Cell Lymphoma ◽  
Large B Cell Lymphoma ◽  
Large B Cell ◽  
Stat Pathway

Abstract Purpose The JAK/STAT pathway is deregulated in Hodgkin lymphoma (HL) and primary mediastinal large B-cell lymphoma (PMBL) (Scott et al, 2015; Younes et al, 2014; Shipp et al, 2010). In Diffuse large B cell lymphoma (DLBCL), especially in ABC subtype, the LP265 mutation of the MYD88 gene enhances IL6 and IL10 secretion by the microenvironment permitting the activation of the JAK/STAT pathway. (Gandhi et al, 2015). The overexpression of JAK2 stimulates the phosphorylation of STAT3 in DLBCL and STAT6 in PMBL with a subsequent activation of target genes of the NFKB signaling pathway. Therapeutic inhibition of JAK2 decreases the growth of lymphoid tumors in vitro and in murine xenograft models. (Hao et al, 2014). Although Younes et al reported response in 3 of 15 patients with refractory or relapsed (R/R) follicular or mantle cell lymphoma who received pacritinib alone, no data are available on the effect of ruxolitinib (Jakavi®), the first approved JAK1/JAK2 inhibitor, in lymphoma patients. Here we report the effect and safety of the oral combination of continuous Ruxolitinib, Etoposide and Corticosteroids in patients with R/R lymphoma. Patients and Methods Since December 2014, patients with multirefractory/relapsed DLBCL, HL or plasmablastic lymphoma received Ruxolitinib 10mg X 2 or 5mg X 2 daily (in case of neutropenia < 1000/mm3) and oral Etoposide 50mg/m2 with prednisone 0,5 mg/kg daily. Retrospective immunostaining (IS) of phosphostat3 (pSTAT3) and phosphostat5 (pSTAT5) was performed on diagnostic samples. In these patients the response rate (including stable disease) was estimated ≤ 0,10 (null hypothesis). In order to identify a potentially relevant clinical activity in these patients with very poor prognosis, the alternative hypothesis was defined by a response rate ≥ 0,500. According to an optimal 2-Stage Designs for Phase II Clinical Trials, a total of 9 patients have to be enrolled in case of response (or stable disease) in at least 1 of the 3 first patients. All patients gave informed consent. Results Six patients (DLBCL: 4, HL: 1, plasmablastic lymphoma: 1) were treated between December 2014 and May 2015. All patients had a progressive disease before starting REC. Median age was 57,5 years (range 30-87). DLBCL Phenotype was non Germinal Center (non-GC) in 2 patients and Germinal Center (GC) in 1 patient. One patient had received autologous stem cell transplantation (ASCT) and one allogenic (HSCT); 3 months later he developed a severe macrophagic activation syndrome (MAS). Median prior treatment was 5 (range 1-12). Four of six patients had a response: 1 partial response (PR) and 3 stable disease (SD) (including control of MAS for 3 months). Two patients had a disease progression (PD). Progression-free survival (PFS) was 82.5 days (range 30-129). There were no side effects reported and only one day hospitalization for transfusion (Table 1). Immunostaining showed expression of pSTAT3 and pSTAT5 on tumoral cells but not in the microenvironment. There was a higher level of pSTAT3 expression (range 0-70%) compared with expression of pSTAT5 (range 0-50%); both were not predictive of the treatment response. (Table 1) Conclusion REC is the first orally combination with Ruxolitinib reported to our knowledge in R/R lymphoma patients. Stable disease or PR has been achieved without toxicity in the first 6 patients with poor prognosis lymphoma. These preliminary results of this ongoing trial suggest that Ruxolitinib chemotherapy combination may be a promising approach for R/R HL or DLBCL lymphoma patients. Biological analysis of the JAK/STAT "signature" including expression of pSTAT3 and pSTAT5 and mutations of activating genes like MYD 88 and SOCS-1 will be presented at the ASH meeting. Table 1. Characteristics of the 6 patients. (RT: radiotherapy) Patient Age Lymphoma subtype IPI score pSTAT3 IS(%) pSTAT5 IS(%) N° of prior therapies RuxolitinibDose Response PFS(day) Toxicity 1 34 DLBCL GC 3 0 0 6 (RCHOP, DHAP, IVAM, HSCT,VP16, Holoxan) 10mg X 2/d SD 82 0 2 48 Plasmablastic 2 30 1 7(RACVBP/ HoloxanVP16, CYVE,PAD, Gemcitabine,Vidaza,Revlimid,RT) 5mg X 2/d SD 83 0 3 87 DLBCL 2 20 10 1 (RminiCHVP) 5mgx 2/d PR 129 Anemia Grade 2 4 35 HL 50 50 12 (RCHOP, BEACOPP, ESHAP,RT, BEAM ASCT, SGN35, Bendamustine,methotrexate/L-asparaginase, Caelyx, everolimus, Navelbine, Revlimid) 10mg X2/d SD 102 0 5 67 DLBCL non-GC 3 30 1 4 (Fludarabine, Endoxan, RCHOP, DHAP) 5mgX2/jour PD 30 0 6 74 DLBCL non-GC 2 70 1 3 (MBVP, ARA-C, RT) 5mgx 2/d PD 75 0 Disclosures No relevant conflicts of interest to declare.

scholarly journals High-Grade B-Cell Lymphoma Not Otherwise Specified (HGBL, NOS) in the Maxillary Sinus Mimicking Periapical Inflammation: Case Report and Review of the Literature

2021 ◽  
Vol 11 (19) ◽  
pp. 8803
Author(s):  
Andrea Brody ◽  
Csaba Dobo-Nagy ◽  
Karoly Mensch ◽  
Zsuzsanna Oltyan ◽  
Judit Csomor ◽  
...  
Keyword(s):  
B Cell ◽  
Maxillary Sinus ◽  
Poor Prognosis ◽  
Cell Lymphoma ◽  
B Cell Lymphoma ◽  
High Grade ◽  
B Cell Lymphomas ◽  
Not Otherwise Specified ◽  
Systemic Spread ◽  
Periapical Inflammation

High-grade B-cell lymphoma not otherwise specified is listed as a new group in the WHO 2017 statement as a subtype of aggressive, mature B-cell lymphomas with a poor prognosis. To our knowledge, no description of this genetic type of maxillary lymphoma has appeared in the literature until now; thus, our case provides valuable data on its symptoms, clinical behavior, response to treatment and survival rate. The present report describes the early diagnosis and treatment of an extremely rare histological subtype of B-cell lymphoma, a case of high-grade B-cell lymphoma not otherwise specified, localized in the maxillary sinus and mimicking signs and symptoms of periapical inflammation. After chemotherapy, the presented patient showed complete remission without relapse and systemic spread. As far as we know, this is the first reported case of this rare type of lymphoma associated with the maxillary sinus. Considering that high-grade B-cell lymphomas are aggressive tumors with rapid growth and poor prognosis, which are often misdiagnosed in the early stages as inflammatory disease, it is relevant to highlight the importance of a detailed evaluation of clinical signs and radiological findings during diagnosis, especially if they contradict each other.

Metody cytogenetyki molekularnej w różnicowaniu agresywnych B-NHL

2019 ◽  
Vol 50 (3) ◽  
pp. 109-115
Author(s):  
Beata Grygalewicz
Keyword(s):  
B Cell ◽  
Cell Lymphoma ◽  
B Cell Lymphoma ◽  
World Health ◽  
High Grade ◽  
Non Hodgkin Lymphoma ◽  
Large B Cell Lymphoma ◽  
Health Organization ◽  
Large B Cell

StreszczenieB-komórkowe agresywne chłoniaki nieziarnicze (B-cell non-Hodgkin lymphoma – B-NHL) to heterogenna grupa nowotworów układu chłonnego, wywodząca się z obwodowych limfocytów B. Aberracje cytogenetyczne towarzyszące B-NHL to najczęściej translokacje onkogenów takich jak MYC, BCL2, BCL6 w okolice genowych loci dla łańcuchów ciężkich lub lekkich immunoglobulin. W niektórych przypadkach dochodzi do wystąpienia kilku wymienionych aberracji jednocześnie, tak jak w przypadkach przebiegających z równoczesną translokacją genów MYC i BCL2 (double hit), niekiedy także z obecnością rearanżacji BCL6 (triple hit). Takie chłoniaki cechuje szczególnie agresywny przebieg kliniczny. Obecnie molekularna diagnostyka cytogenetyczna przy użyciu techniki fluorescencyjnej hybrydyzacji in situ (FISH) oraz, w niektórych przypadkach, aCGH jest niezbędnym narzędziem rozpoznawania, klasyfikowania i oceny stopnia zaawansowania agresywnych, nieziarniczych chłoniaków B-komórkowych. Technika mikromacierzy CGH (aCGH) była kluczowym elementem wyróżnienia prowizorycznej grupy chłoniaków Burkitt-like z aberracją chromosomu 11q (Burkitt-like lymphoma with 11q aberration – BLL, 11q) w najnowszej klasyfikacji nowotworów układu chłonnego Światowej Organizacji Zdrowia (World Health Organization – WHO) z 2016 r. Omówione zostaną sposoby różnicowania na poziomie cytogenetycznym takich chłoniaków jak: chłoniak Burkitta (Burkitt lymphoma – BL), chłoniak rozlany z dużych komórek B (diffuse large B-cell lymphoma – DLBCL) oraz 2 nowych jednostek klasyfikacji WHO 2016, czyli chłoniaka z komórek B wysokiego stopnia złośliwości z obecnością translokacji MYC i BCL2 i/lub BCL6 (high-grade B-cell lymphoma HGBL, with MYC and BCL2 and/or BCL6 translocations) oraz chłoniaka BLL, 11q.

Sign in / Sign up

Export Citation Format

Share Document