scholarly journals Multifocal Primary Central Nervous System (CNS) Diffuse Large B-Cell Lymphoma (DLBCL) in a Patient with Aquired Immunodeficiency Syndrome (AIDS)

2021 ◽  
Vol 156 (Supplement_1) ◽  
pp. S90-S90
Author(s):  
H Khokhar ◽  
K Wang ◽  
D Luis
Keyword(s):  
Basal Ganglia ◽  
B Cell ◽  
Tumor Cells ◽  
B Cell Lymphoma ◽  
Brain Parenchyma ◽  
Lymphoid Cells ◽  
Cerebellar Hemisphere ◽  
Temporal Region ◽  
Barr Virus ◽  
The Brain

Abstract Introduction/Objective Primary CNS DLBCL is a rare entity, with an incidence of less than 0.47 per 100,000, however, in immunocompromised patients, especially those with Human Immunodeficiency Virus (HIV-1) infection, the incidence increases dramatically to 2-6 percent. Here we present a case of multifocal DLBCL in a young 28-year-old homeless male with untreated AIDS and polysubstance abuse. Methods/Case Report He presented to the hospital with altered state of consciousness; a Computerized Tomography (CT) scan showed three ring-enhancing masses; one in the left fronto-temporal region, the largest in the left basal ganglia and the third in the cerebellum. The main lesion was biopsied and diagnosed as DLBCL. The patient developed aspiration pneumonia and demised from respiratory failure Results (if a Case Study enter NA) NA Conclusion Coronal sections of the brain revealed a large grey-tan, soft lesion of poorly defined, irregular borders located in the left basal ganglia that measured 5 x 4 x 4 cm, extended dorsally and laterally. A similar lesion was observed in the deep left cerebral hemisphere, affecting the temporal lobe and extending rostrally into the frontal lobe, but completely separate from the tumor in the basal ganglia. A third, much smaller lesion was found in the right cerebellar hemisphere. Histologically, the tumor was composed of sheets of atypical lymphoid cells with increased nuclear to cytoplasmic ratio, increased mitotic activity, and showed scattered areas of necrosis. In the peripheral areas, tumor cells were located in the Virchow Robin space, and in more central areas they have broken into the brain parenchyma. Tumor cells were positive for CD20 and CD79a, indicating their B-cell origin. Other markers positive by immunohistochemistry were PAX5, MUM1 and BCL6 and the Epstein-Barr Virus (EBV) latent membrane protein (LMP). Fluorescence In situ hybridization (FISH) corroborated the presence of Eptein-Barr encoded RNAs.

scholarly journals Primary Cranial Vault Lymphoma Extending between Subcutaneous Tissue and Brain Parenchyma without Skull Destruction after Mild Head Trauma: A Case Report and Literature Review

2021 ◽  
pp. 1118-1123
Author(s):  
Kengo Setta ◽  
Takaaki Beppu ◽  
Yuichi Sato ◽  
Hiroaki Saura ◽  
Junichi Nomura ◽  
...  
Keyword(s):  
Tumor Cells ◽  
Head Trauma ◽  
Dura Mater ◽  
Subcutaneous Tissue ◽  
Bone Destruction ◽  
B Cell Lymphoma ◽  
Brain Parenchyma ◽  
Skin Tumor ◽  
Cranial Vault ◽  
The Brain

Malignant lymphoma of the head rarely arises outside of the brain parenchyma as primary cranial vault lymphoma (PCVL). A case of PCVL that invaded from subcutaneous tissue into the brain, passing through the skull, and occurred after mild head trauma is reported along with a review of the literature. The patient was a 75-year-old man with decreased activity. One month before his visit to our hospital, he bruised the left frontal area of his head. Magnetic resonance imaging showed homogeneously enhanced tumors with contrast media in the subcutaneous tissue corresponding to the head impact area and the cerebral parenchyma, but no obvious abnormal findings in the skull. A biopsy with craniotomy was performed under general anesthesia. The pathological diagnosis was diffuse large B-cell lymphoma. On histological examination, tumor cells grew aggressively under the skin. Tumor cells invaded along the emissary vein into the external table without remarkable bone destruction and extended across the skull through the Haversian canals in the diploe. Tumor cells were found only at the perivascular areas in the dura mater and extended into the brain parenchyma. Considering the history of head trauma and the neuroimaging and histological findings, the PCVL in the present case arose primarily under the skin, passed though the skull and dura mater, and invaded along vessels and reached the brain.

scholarly journals The potential usefulness of sputum cytology in the conclusive diagnosis of methotrexate-associated lymphoproliferative disorders: A case report

2019 ◽  
Vol 7 ◽  
pp. 2050313X1983601 ◽  
Author(s):  
Seiya Mizuguchi ◽  
Kenichi Mizutani ◽  
Manabu Yamashita ◽  
Hiroshi Minato ◽  
Sohsuke Yamada
Keyword(s):  
B Cell ◽  
Lymphoproliferative Disorder ◽  
Epstein Barr Virus ◽  
B Cell Lymphoma ◽  
Lymphoid Cells ◽  
Sputum Cytology ◽  
Barr Virus ◽  
Large B Cell Lymphoma ◽  
Epstein Barr ◽  
Conclusive Diagnosis

Background: Methotrexate has been used as an anchor drug for the treatment of rheumatoid arthritis and is considered to be a cause of methotrexate-associated lymphoproliferative disorder. Spontaneous regression can occur after withdrawal of methotrexate and may be associated with Epstein–Barr virus positivity and non-diffuse large B cell lymphoma histological type. Methotrexate-associated lymphoproliferative disorders are often diagnosed pathologically by lung biopsy. To the best of our knowledge, there have been no studies on the cytological diagnosis of methotrexate-associated lymphoproliferative disorder using sputum smears. Case: A 70-year-old man, who was diagnosed with rheumatoid arthritis 13 years previously and who had been treated with methotrexate, presented shortness of breath and productive cough. Methotrexate-associated lymphoproliferative disorder was suspected as the sputum cytology showed many atypical lymphoid cells with hyperchromatic enlarged nuclei, foamy cytoplasm and distinct nucleoli. Chest computed tomography revealed multiple nodular shadows with interstitial pneumonia in the bilateral lower lung field. A lung biopsy specimen contained atypical lymphoid cells that were immunohistochemically positive for CD20 and MUM-1, and weakly positive for bcl-6, but negative for CD3 and CD10. There were no Epstein–Barr virus-infectious lymphoid cells by ISH-EBER. He was finally diagnosed with methotrexate-associated lymphoproliferative disorder (non-germinal center B-cell-like diffuse large B cell lymphoma histological type). Most of the nodules disappeared spontaneously following the withdrawal of methotrexate. Discussion and conclusion: A cytologically conclusive diagnosis of methotrexate-associated lymphoproliferative disorder may be reached using sputum smears and clinical information.

Detection of Epstein-Barr virus DNA and expression of CD30 antigen in primary anaplastic diffuse large B-cell lymphoma of the brain

2001 ◽  
Vol 18 (2) ◽  
pp. 161-165 ◽  
Author(s):  
T. Shimura ◽  
Y. Sugisaki ◽  
K. Fukino ◽  
Y. Node ◽  
A. Teramoto ◽  
...  
Keyword(s):  
B Cell ◽  
Epstein Barr Virus ◽  
Cell Lymphoma ◽  
B Cell Lymphoma ◽  
Barr Virus ◽  
Large B Cell Lymphoma ◽  
Epstein Barr ◽  
The Brain ◽  
Cd30 Antigen ◽  
Large B Cell

scholarly journals Prognostic Value of Epstein-Barr Virus (EBV)-Induced Gene 3 (EBI3) in Diffuse Large B Cell Lymphoma

Blood ◽  
2018 ◽  
Vol 132 (Supplement 1) ◽  
pp. 5411-5411
Author(s):  
Hong Zheng ◽  
Juan Huang
Keyword(s):  
Tumor Microenvironment ◽  
B Cell ◽  
Tumor Cells ◽  
Epstein Barr Virus ◽  
Cell Lymphoma ◽  
B Cell Lymphoma ◽  
Barr Virus ◽  
Large B Cell Lymphoma ◽  
Epstein Barr ◽  
Large B Cell

Abstract Background: Epstein-Barr virus (EBV)-induced gene 3 (EBI3) as a subunit for heterodimeric cytokines IL-27 and IL-35, plays important roles both in regulation of T cell proliferation and Th1,Th2 and Th17 cells differentiation. EBI3 was closely related with tumor prognosis. Diffuse large B-cell lymphoma (DLBCL) is the most common lymphoid malignancy in adults with cure-rates of 40-60%. However, Relapse and refractory rate remain in 40% or so. In the present study, we aimed to detect the expression of EBI3 in DLBCL and to analyze its relationship with prognosis. Methods: We retrospective reviewed medical records of 51 newly diagnosed DLBCL patients in Sichuan People's Hospital between January 2010 and December 2016. Immunohistochemical (IHC) assay was used to detect the expression of EBI3 and PD-1 in DLBCL. The expression of CD5, CD30, Bcl-2, Bcl-6, C-myc and Epstein-Barr virus (EBV)-encoded RNAs (EBERs) in tumor specimens from 53 patients was also detected by IHC. The Kaplan-Meier method with log-rank test was used for univariate analysis. Cox proportional hazards model was used for multivariate analysis. Results: Of the 51 patients, 40 (78.4%) were EBI3-positive in tumor specimens. And PD-1 expression (39/40) was almost in parallel with EBI3 in tumor specimens. EBI3 expression was common in the non-germinal center B-cell-like (GCB) subtype than in the GCB subtype. Patients with EBI3 expression in tumor were more likely to be resistant to first-line chemotherapy when compared with the patients without EBI3 expression in tumor microenvironment (P <0.05). EBI3 expression in tumor microenvironment was correlated with PD-1 expression (r = − 0.20, P = 0.04). Only one patient with EBI3 expression was no PD-1 expression. No correlations were detected between EBI3 expression and the expression of EBER as well as other markers: ALK, CD5, c-Myc and CD30. The complete remission (CR) rates were 7.5% (3/40) and 71.4% in patients with and without EBI3 expression in tumor cells (P = 0.02). EBI3 expression in tumor cells was an independent risk predictor for ORR (P < 0.05). Conclusions: Our results indicate that EBI3 associated with poor prognosis and EBI3 may be a potential therapeutic target and prognosis marker. Disclosures No relevant conflicts of interest to declare.

scholarly journals Frequent traces of EBV infection in Hodgkin and non-Hodgkin lymphomas classified as EBV-negative by routine methods: expanding the landscape of EBV-related lymphomas

2020 ◽  
Vol 33 (12) ◽  
pp. 2407-2421 ◽  
Author(s):  
Lucia Mundo ◽  
Leonardo Del Porro ◽  
Massimo Granai ◽  
Maria Chiara Siciliano ◽  
Virginia Mancini ◽  
...  
Keyword(s):  
B Cell ◽  
Tumor Cells ◽  
Cell Lines ◽  
High Sensitivity ◽  
B Cell Lymphoma ◽  
Rare Tumor ◽  
Barr Virus ◽  
Ebv Infection ◽  
Epstein Barr ◽  
Higher Sensitivity

AbstractThe Epstein–Barr virus (EBV) is linked to various B-cell lymphomas, including Burkitt lymphoma (BL), classical Hodgkin lymphoma (cHL) and diffuse large B-cell lymphoma (DLBCL) at frequencies ranging, by routine techniques, from 5 to 10% of cases in DLBCL to >95% in endemic BL. Using higher-sensitivity methods, we recently detected EBV traces in a few EBV-negative BL cases, possibly suggesting a “hit-and-run” mechanism. Here, we used routine and higher-sensitivity methods (qPCR and ddPCR for conserved EBV genomic regions and miRNAs on microdissected tumor cells; EBNA1 mRNA In situ detection by RNAscope) to assess EBV infection in a larger lymphoma cohort [19 BL, 34 DLBCL, 44 cHL, 50 follicular lymphomas (FL), 10 T-lymphoblastic lymphomas (T-LL), 20 hairy cell leukemias (HCL), 10 mantle cell lymphomas (MCL)], as well as in several lymphoma cell lines (9 cHL and 6 BL). qPCR, ddPCR, and RNAscope consistently documented the presence of multiple EBV nucleic acids in rare tumor cells of several cases EBV-negative by conventional methods that all belonged to lymphoma entities clearly related to EBV (BL, 6/9 cases; cHL, 16/32 cases; DLBCL, 11/30 cases), in contrast to fewer cases (3/47 cases) of FL (where the role of EBV is more elusive) and no cases (0/40) of control lymphomas unrelated to EBV (HCL, T-LL, MCL). Similarly, we revealed traces of EBV infection in 4/5 BL and 6/7 HL cell lines otherwise conventionally classified as EBV negative. Interestingly, additional EBV-positive cases (1 DLBCL, 2 cHL) relapsed as EBV-negative by routine methods while showing EBNA1 expression in rare tumor cells by RNAscope. The relapse specimens were clonally identical to their onset biopsies, indicating that the lymphoma clone can largely loose the EBV genome over time but traces of EBV infection are still detectable by high-sensitivity methods. We suggest EBV may contribute to lymphoma pathogenesis more widely than currently acknowledged.

T cell-rich B cell lymphoma bearing Epstein-Barr virus in tumor cells: A case of IBL-T-like lesion following Lennert's lesion

1995 ◽  
Vol 45 (6) ◽  
pp. 457-462 ◽  
Author(s):  
Susumu Wakatsuki ◽  
Norio Yumoto ◽  
Toshiyuki Takagi ◽  
Katsusi Kurosu ◽  
Chikara Sakai ◽  
...  
Keyword(s):  
T Cell ◽  
B Cell ◽  
Tumor Cells ◽  
Epstein Barr Virus ◽  
Cell Lymphoma ◽  
B Cell Lymphoma ◽  
Barr Virus ◽  
Epstein Barr

Utility of Chimerism Analysis to Determine Tissue of Origin in Post Transplant Lymphoproliferative Disorder (PTLD).

Blood ◽  
2009 ◽  
Vol 114 (22) ◽  
pp. 4305-4305
Author(s):  
Hailing Zhang ◽  
Qing Wang ◽  
Xiao Yan Yang ◽  
Michele L. Donato ◽  
Tao Hong ◽  
...  
Keyword(s):  
B Cell ◽  
Lymphoproliferative Disorder ◽  
B Cell Lymphoma ◽  
Lymphoid Cells ◽  
Unrelated Donor ◽  
Post Transplant ◽  
Barr Virus ◽  
Large B Cell Lymphoma ◽  
Chimerism Analysis ◽  
Tumor Dna

Abstract Abstract 4305 Post-transplant lymphoproliferative disorder (PTLD) is one of the major complications of organ transplantation. Most PTLDs are associated with Epstein-Barr virus (EBV) infection of B-lineage lymphocytes. Central nervous system (CNS) involvement is rare. Although most PTLDs following solid organ transplants is of recipient origin, PTLDs following bone marrow or stem cell transplant are mostly of donor cell origin. Origin of the tumor cells are of crucial importance in deciding treatment and predicting prognosis. Here we report a case of PTLD of diffuse large B cell Lymphoma of donor tissue origin determined by chimerism analysis. The patient was a 52-year-old woman with myelofibrosis (Myeloproliferative disorder) who received unrelated donor peripheral blood stem cell transplantation. The donor was an ABO compatible, HLA matched unrelated donor. Post transplant immunosuppression therapy was administered. The post transplant history was complicated by multiple viral infections, including BK, CMV and EB virus. Four months after transplantation, the patient developed fever and mental status changes, MRI of brain showed multiple enhancing lesions. Brain biopsy revealed brain tissue with dense infiltration of large atypical lymphoid cells predominantly perivascular in location. Immunohistochemical stains reveal that the large atypical lymphoid cells are of B-cell origin and these cells are 100% positive for Ebstein Barr virus by EBV encoded RNA by in-situ hybridization. The flowcytometry study revealed a monoclonal population of B cells with Kappa light chain restriction. These findings support the diagnosis of post transplant lymphoproliferative disorder (PTLD) of diffuse large B-cell lymphoma type. To determine the origin of tumor cells, chimerism analysis of the host DNA (buccal) and tumor DNA were performed. Short tandem repeat (STR) multiplex PCR assay were performed using the AmpFlSTR Identifiler PCR amplification kit (Applied Biosystems, Foster City, CA). After amplification, samples were analyzed on an ABI 310 DNA Sequencer (Applied Biosystems). The allele distribution was significantly different between the recipient DNA (from buccal swab) compared to tumor DNA indicating donor origin of the tumor (PTLD). The patient was then placed on high dose methotrexate and dexamethasome, however her condition deteriorated dramatically and the patient expired shortly following the diagnosis. It is known that the major pathogenetic defect of PTLD is the insufficient EBV-specific cytotoxic T-cell control of EBV-driven B-cell proliferations. Despite this understanding, determining the right therapy for any given patient with PTLD remains a major clinical issue. It is important to identify patients who will benefit from reduction of immunosuppression, who will benefit from Rituximab. It is also important to develop more effective, less toxic chemotherapies for resistant or aggressive disease. The chimerism analysis performed on our patient to identify tumor cell origin is an unique and reliable method to help directing clinical management of PTLD. Disclosures: No relevant conflicts of interest to declare.

Epstein-Barr Virus-associated Diffuse Large B-cell Lymphoma Arising on Cardiac Prostheses

2010 ◽  
Vol 34 (3) ◽  
pp. 377-384 ◽  
Author(s):  
Dylan V. Miller ◽  
Dennis J. Firchau ◽  
Rebecca F. McClure ◽  
Paul J. Kurtin ◽  
Andrew L. Feldman
Keyword(s):  
B Cell ◽  
Epstein Barr Virus ◽  
Cell Lymphoma ◽  
B Cell Lymphoma ◽  
Barr Virus ◽  
Large B Cell Lymphoma ◽  
Epstein Barr ◽  
Large B Cell

scholarly journals Macrophages and microglia: the cerberus of glioblastoma

2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Alice Buonfiglioli ◽  
Dolores Hambardzumyan
Keyword(s):  
Tumor Cells ◽  
Innate Immune System ◽  
Tumor Heterogeneity ◽  
Expression Profiles ◽  
Brain Parenchyma ◽  
Innate Immune ◽  
Malignant Growth ◽  
Neoplastic Cells ◽  
Functional Roles ◽  
The Brain

AbstractGlioblastoma (GBM) is the most aggressive and deadliest of the primary brain tumors, characterized by malignant growth, invasion into the brain parenchyma, and resistance to therapy. GBM is a heterogeneous disease characterized by high degrees of both inter- and intra-tumor heterogeneity. Another layer of complexity arises from the unique brain microenvironment in which GBM develops and grows. The GBM microenvironment consists of neoplastic and non-neoplastic cells. The most abundant non-neoplastic cells are those of the innate immune system, called tumor-associated macrophages (TAMs). TAMs constitute up to 40% of the tumor mass and consist of both brain-resident microglia and bone marrow-derived myeloid cells from the periphery. Although genetically stable, TAMs can change their expression profiles based upon the signals that they receive from tumor cells; therefore, heterogeneity in GBM creates heterogeneity in TAMs. By interacting with tumor cells and with the other non-neoplastic cells in the tumor microenvironment, TAMs promote tumor progression. Here, we review the origin, heterogeneity, and functional roles of TAMs. In addition, we discuss the prospects of therapeutically targeting TAMs alone or in combination with standard or newly-emerging GBM targeting therapies.

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