Cytokine Expression in Large Cell Lymphoma Associated with Acquired Immunodeficiency Syndrome

1995 ◽  
Vol 15 (3) ◽  
pp. 261-268 ◽  
Author(s):  
JANE W. MARSH ◽  
BRIAN HERNDIER ◽  
AKIKO TSUZUKI ◽  
VALERIE L. NG ◽  
BRUCE SHIRAMIZU ◽  
...  
Keyword(s):  
Acquired Immunodeficiency Syndrome ◽  
Cell Lymphoma ◽  
Large Cell ◽  
Cytokine Expression ◽  
Acquired Immunodeficiency ◽  
Large Cell Lymphoma ◽  
Immunodeficiency Syndrome

Primary Anaplastic Lymphoma Kinase–Negative Anaplastic Large Cell Lymphoma of the Brain in a Patient With Acquired Immunodeficiency Syndrome

2004 ◽  
Vol 128 (3) ◽  
pp. 324-327
Author(s):  
Edward H. Rowsell ◽  
Nazila Zekry ◽  
Boleslaw H. Liwnicz ◽  
Jeffrey D. Cao ◽  
Qin Huang ◽  
...  
Keyword(s):  
Anaplastic Large Cell Lymphoma ◽  
Acquired Immunodeficiency Syndrome ◽  
Anaplastic Lymphoma Kinase ◽  
Cell Lymphoma ◽  
Large Cell ◽  
Anaplastic Lymphoma ◽  
Acquired Immunodeficiency ◽  
Large Cell Lymphoma ◽  
Immunodeficiency Syndrome ◽  
The Brain

Abstract Anaplastic large cell lymphoma is a unique diagnostic subcategory of the T-cell lymphomas in the current World Health Organization classification. Representing approximately 3% of adult and 10% to 30% of childhood non-Hodgkin lymphomas, anaplastic large cell lymphoma classically consists of CD30+ large lymphoid cells with abundant cytoplasm and pleomorphic, often horseshoe-shaped or kidney-shaped nuclei. Among the reported nodal and extranodal sites of occurrence, the gastrointestinal tract and central nervous system have rarely been noted. We report a case of primary anaplastic lymphoma kinase–negative anaplastic large cell lymphoma in the brain of a 46-year-old patient with acquired immunodeficiency syndrome. T-cell lineage was confirmed by T-cell receptor γ chain gene rearrangements using polymerase chain reaction, and extra copies of the anaplastic lymphoma kinase gene of chromosome 2 were demonstrated by fluorescence in situ hybridization analysis. To our knowledge, primary anaplastic large cell lymphoma of the brain has not previously been reported in acquired immunodeficiency syndrome.

Angiotropic (Intravascular) Large Cell Lymphoma of T-Cell Phenotype Presenting as Acute Appendicitis in a Patient With Acquired Immunodeficiency Syndrome

1999 ◽  
Vol 123 (4) ◽  
pp. 335-337 ◽  
Author(s):  
Denise M. Malicki ◽  
Yae K. Suh ◽  
Gregory N. Fuller ◽  
Sung S. Shin
Keyword(s):  
T Cell ◽  
Acute Appendicitis ◽  
Acquired Immunodeficiency Syndrome ◽  
Cell Lymphoma ◽  
Immunohistochemical Analysis ◽  
Large Cell ◽  
Cell Phenotype ◽  
Acquired Immunodeficiency ◽  
Large Cell Lymphoma ◽  
Immunodeficiency Syndrome

Abstract We describe a patient with acquired immunodeficiency syndrome who presented with acute appendicitis but was found to have angiotropic large cell lymphoma (ALCL) by pathologic examination of the appendectomy specimen, without acute inflammation. Very rare cases of angiotropic large cell lymphoma have been reported in patients with human immunodeficiency virus infection, and most cases of this rare lymphoma are of B-cell origin, but in this instance immunohistochemical analysis showed a T-cell phenotype.

scholarly journals Mutations in the coding region of c-myc occur frequently in acquired immunodeficiency syndrome-associated lymphomas

Blood ◽  
1994 ◽  
Vol 84 (3) ◽  
pp. 883-888 ◽  
Author(s):  
K Bhatia ◽  
G Spangler ◽  
G Gaidano ◽  
N Hamdy ◽  
R Dalla-Favera ◽  
...  
Keyword(s):  
Acquired Immunodeficiency Syndrome ◽  
Cell Lymphoma ◽  
Regulatory Region ◽  
Large Cell ◽  
Coding Region ◽  
Intermediate Grade ◽  
Myc Gene ◽  
Acquired Immunodeficiency ◽  
Immunodeficiency Syndrome ◽  
Histologic Subtypes

Abstract We have analyzed 30 cases of high- and intermediate-grade acquired immunodeficiency syndrome-associated non-Hodgkin's lymphoma (AIDS-NHL) for mutations in the c-myc coding region. In addition, in these same tumors, we have sought the presence of mutations in a regulatory region within the first c-myc intron defined by the binding to a factor that inhibits c-myc transcription (MYC intron factor, or mif). Mutations in the c-myc coding region were present in 10 of 16 small noncleaved cell lymphoma (SNCL), but in only 3 of 14 other histologic subtypes tested (0/3 large non-cleaved cell, 2/8 immunoblastic, and 1/3 anaplastic large cell lymphomas). Nineteen of the AIDS-NHLs analyzed contained a c- myc rearrangement and in 10 of these the c-myc gene was mutated in its coding region. In contrast, we could detect a mutation in the coding region in only 2 of 8 AIDS-NHL without a c-myc rearrangement. Mutations in the mif region were detected in 5 of 16 SNCL. Among AIDS-NHL carrying mutations in the c-myc coding region, only 4 carried mutations in the regulatory region. These results suggest that the mutations in the coding region of the c-myc protein may either be a consequence of the translocations involving c-myc, or may be necessary only in tumors where c-myc is deregulated as a result of a c-myc/lg translocation.

scholarly journals Mutations in the coding region of c-myc occur frequently in acquired immunodeficiency syndrome-associated lymphomas

Blood ◽  
1994 ◽  
Vol 84 (3) ◽  
pp. 883-888 ◽  
Author(s):  
K Bhatia ◽  
G Spangler ◽  
G Gaidano ◽  
N Hamdy ◽  
R Dalla-Favera ◽  
...  
Keyword(s):  
Acquired Immunodeficiency Syndrome ◽  
Cell Lymphoma ◽  
Regulatory Region ◽  
Large Cell ◽  
Coding Region ◽  
Intermediate Grade ◽  
Myc Gene ◽  
Acquired Immunodeficiency ◽  
Immunodeficiency Syndrome ◽  
Histologic Subtypes

We have analyzed 30 cases of high- and intermediate-grade acquired immunodeficiency syndrome-associated non-Hodgkin's lymphoma (AIDS-NHL) for mutations in the c-myc coding region. In addition, in these same tumors, we have sought the presence of mutations in a regulatory region within the first c-myc intron defined by the binding to a factor that inhibits c-myc transcription (MYC intron factor, or mif). Mutations in the c-myc coding region were present in 10 of 16 small noncleaved cell lymphoma (SNCL), but in only 3 of 14 other histologic subtypes tested (0/3 large non-cleaved cell, 2/8 immunoblastic, and 1/3 anaplastic large cell lymphomas). Nineteen of the AIDS-NHLs analyzed contained a c- myc rearrangement and in 10 of these the c-myc gene was mutated in its coding region. In contrast, we could detect a mutation in the coding region in only 2 of 8 AIDS-NHL without a c-myc rearrangement. Mutations in the mif region were detected in 5 of 16 SNCL. Among AIDS-NHL carrying mutations in the c-myc coding region, only 4 carried mutations in the regulatory region. These results suggest that the mutations in the coding region of the c-myc protein may either be a consequence of the translocations involving c-myc, or may be necessary only in tumors where c-myc is deregulated as a result of a c-myc/lg translocation.

scholarly journals Multiple genetic lesions in acquired immunodeficiency syndrome-related non-Hodgkin‧s lymphoma

Blood ◽  
1993 ◽  
Vol 81 (1) ◽  
pp. 166-176 ◽  
Author(s):  
P Ballerini ◽  
G Gaidano ◽  
JZ Gong ◽  
V Tassi ◽  
G Saglio ◽  
...  
Keyword(s):  
Tumor Suppressor ◽  
Acquired Immunodeficiency Syndrome ◽  
Tumor Suppressor Genes ◽  
Cell Lymphoma ◽  
Large Cell ◽  
Suppressor Genes ◽  
Ebv Infection ◽  
Short Period ◽  
Acquired Immunodeficiency ◽  
Immunodeficiency Syndrome

Non-Hodgkin's lymphoma (NHL) develops in about 5% to 10% of acquired immunodeficiency syndrome (AIDS) patients. The vast majority of AIDS- NHL are clinically aggressive B-cell NHL that are histologically classified as small noncleaved cell lymphoma (SNCCL), large cell immunoblastic plasmacytoid lymphoma (LC-IBPL), and large noncleaved cell lymphoma (LNCCL). In an attempt to understand the molecular pathogenesis of these tumors, we have investigated the involvement of dominantly acting oncogenes (c-myc, N-, K-, H-Ras), tumor suppressor genes (p53, RB1), and Epstein-Barr virus (EBV) infection in 27 AIDS-NHL samples (16 SNCCL, 5 LC-IBP, and 6 LNCCL). The following lesions were detected in AIDS-NHL: EBV infection (10/24; 41.6%), c-myc rearrangement (19/24; 79.1%), Ras mutation (4/27; 14.8%), and p53 loss/mutation (10/27; 37.0%). These lesions are not uniformly distributed, but, rather, cluster with specific types of AIDS-NHL: EBV infection is preferentially associated with LC-IBPL (4/4; 100%), while it is present in only a fraction of SNCCL (5/16; 31.2%) and LNCCL (1/4; 25%); c-myc oncogene activation clusters with SNCCL (16/16; 100%), whereas it is less frequent in LC-IBPL (1/4; 25%) and LNCCL (2/4; 50%); p53 inactivation is restricted to SNCCL (10/16; 62.5%) and consistently associated with c-myc activation. These data show that AIDS-NHL are associated with multiple genetic lesions that involve both proto- oncogenes and tumor suppressor genes and may accumulate in the relatively short period of time (4 to 6 years) between human immunodeficiency virus infection and AIDS-NHL development. These genetic lesions differ in the various AIDS-NHL subtypes, suggesting the involvement of distinct molecular pathway.

scholarly journals Rearrangements of the BCL-6 gene in acquired immunodeficiency syndrome- associated non-Hodgkin's lymphoma: association with diffuse large-cell subtype

Blood ◽  
1994 ◽  
Vol 84 (2) ◽  
pp. 397-402 ◽  
Author(s):  
G Gaidano ◽  
F Lo Coco ◽  
BH Ye ◽  
D Shibata ◽  
AM Levine ◽  
...  
Keyword(s):  
Acquired Immunodeficiency Syndrome ◽  
Cell Lymphoma ◽  
Large Cell ◽  
Suppressor Gene ◽  
Barr Virus ◽  
Ebv Infection ◽  
Genetic Lesion ◽  
Acquired Immunodeficiency ◽  
Hodgkin's Lymphomas ◽  
Immunodeficiency Syndrome

Acquired immunodeficiency syndrome (AIDS)-associated non-Hodgkin's lymphomas (AIDS-NHL), a major source of morbidity and mortality among AIDS patients, are derived from B cells and can be classified into two main histologic categories, small noncleaved cell lymphoma (SNCCL) and diffuse large-cell lymphoma (DLCL). DLCL includes two histologic subsets, ie, large noncleaved cell lymphoma (LNCCL) and large cell- immunoblastic plasmacytoid lymphoma (LC-IBPL). Several studies have shown that AIDS-SNCCL is associated with the clonal accumulation of multiple genetic lesions, including Epstein-Barr virus (EBV) infection, activation of the c-MYC and RAS oncogenes, as well as inactivation of the p53 tumor suppressor gene at variable frequencies. On the contrary, the molecular pathogenesis of AIDS-DLCL is largely obscure, because no genetic lesion other than EBV infection has been specifically identified in this group. In this study, we have tested a panel of 40 AIDS-NHL for structural alterations of BCL-6, a putative proto-oncogene that is frequently altered in DLCL in the immunocompetent host. Our results show that rearrangements of BCL-6 are present in 20% of AIDS- DLCL (5 of 24), including 2 of 8 LNCCL and 3 of 16 LC-IBPL, but in no case of AIDS-SNCCL. BCL-6 rearrangements were detected both in the presence and in the absence of EBV infection of the tumor clone, but in no case were associated with activation of c-MYC or mutations of p53. These data identify a novel genetic lesion in AIDS-DLCL and corroborate the notion that lymphomagenesis in AIDS follows two distinct molecular pathways that are associated with the development of histologically distinct types of AIDS-NHL.

scholarly journals Multiple genetic lesions in acquired immunodeficiency syndrome-related non-Hodgkin‧s lymphoma

Blood ◽  
1993 ◽  
Vol 81 (1) ◽  
pp. 166-176 ◽  
Author(s):  
P Ballerini ◽  
G Gaidano ◽  
JZ Gong ◽  
V Tassi ◽  
G Saglio ◽  
...  
Keyword(s):  
Tumor Suppressor ◽  
Acquired Immunodeficiency Syndrome ◽  
Tumor Suppressor Genes ◽  
Cell Lymphoma ◽  
Large Cell ◽  
Suppressor Genes ◽  
Ebv Infection ◽  
Short Period ◽  
Acquired Immunodeficiency ◽  
Immunodeficiency Syndrome

Abstract Non-Hodgkin's lymphoma (NHL) develops in about 5% to 10% of acquired immunodeficiency syndrome (AIDS) patients. The vast majority of AIDS- NHL are clinically aggressive B-cell NHL that are histologically classified as small noncleaved cell lymphoma (SNCCL), large cell immunoblastic plasmacytoid lymphoma (LC-IBPL), and large noncleaved cell lymphoma (LNCCL). In an attempt to understand the molecular pathogenesis of these tumors, we have investigated the involvement of dominantly acting oncogenes (c-myc, N-, K-, H-Ras), tumor suppressor genes (p53, RB1), and Epstein-Barr virus (EBV) infection in 27 AIDS-NHL samples (16 SNCCL, 5 LC-IBP, and 6 LNCCL). The following lesions were detected in AIDS-NHL: EBV infection (10/24; 41.6%), c-myc rearrangement (19/24; 79.1%), Ras mutation (4/27; 14.8%), and p53 loss/mutation (10/27; 37.0%). These lesions are not uniformly distributed, but, rather, cluster with specific types of AIDS-NHL: EBV infection is preferentially associated with LC-IBPL (4/4; 100%), while it is present in only a fraction of SNCCL (5/16; 31.2%) and LNCCL (1/4; 25%); c-myc oncogene activation clusters with SNCCL (16/16; 100%), whereas it is less frequent in LC-IBPL (1/4; 25%) and LNCCL (2/4; 50%); p53 inactivation is restricted to SNCCL (10/16; 62.5%) and consistently associated with c-myc activation. These data show that AIDS-NHL are associated with multiple genetic lesions that involve both proto- oncogenes and tumor suppressor genes and may accumulate in the relatively short period of time (4 to 6 years) between human immunodeficiency virus infection and AIDS-NHL development. These genetic lesions differ in the various AIDS-NHL subtypes, suggesting the involvement of distinct molecular pathway.

scholarly journals Rearrangements of the BCL-6 gene in acquired immunodeficiency syndrome- associated non-Hodgkin's lymphoma: association with diffuse large-cell subtype

Blood ◽  
1994 ◽  
Vol 84 (2) ◽  
pp. 397-402 ◽  
Author(s):  
G Gaidano ◽  
F Lo Coco ◽  
BH Ye ◽  
D Shibata ◽  
AM Levine ◽  
...  
Keyword(s):  
Acquired Immunodeficiency Syndrome ◽  
Cell Lymphoma ◽  
Large Cell ◽  
Suppressor Gene ◽  
Barr Virus ◽  
Ebv Infection ◽  
Genetic Lesion ◽  
Acquired Immunodeficiency ◽  
Hodgkin's Lymphomas ◽  
Immunodeficiency Syndrome

Abstract Acquired immunodeficiency syndrome (AIDS)-associated non-Hodgkin's lymphomas (AIDS-NHL), a major source of morbidity and mortality among AIDS patients, are derived from B cells and can be classified into two main histologic categories, small noncleaved cell lymphoma (SNCCL) and diffuse large-cell lymphoma (DLCL). DLCL includes two histologic subsets, ie, large noncleaved cell lymphoma (LNCCL) and large cell- immunoblastic plasmacytoid lymphoma (LC-IBPL). Several studies have shown that AIDS-SNCCL is associated with the clonal accumulation of multiple genetic lesions, including Epstein-Barr virus (EBV) infection, activation of the c-MYC and RAS oncogenes, as well as inactivation of the p53 tumor suppressor gene at variable frequencies. On the contrary, the molecular pathogenesis of AIDS-DLCL is largely obscure, because no genetic lesion other than EBV infection has been specifically identified in this group. In this study, we have tested a panel of 40 AIDS-NHL for structural alterations of BCL-6, a putative proto-oncogene that is frequently altered in DLCL in the immunocompetent host. Our results show that rearrangements of BCL-6 are present in 20% of AIDS- DLCL (5 of 24), including 2 of 8 LNCCL and 3 of 16 LC-IBPL, but in no case of AIDS-SNCCL. BCL-6 rearrangements were detected both in the presence and in the absence of EBV infection of the tumor clone, but in no case were associated with activation of c-MYC or mutations of p53. These data identify a novel genetic lesion in AIDS-DLCL and corroborate the notion that lymphomagenesis in AIDS follows two distinct molecular pathways that are associated with the development of histologically distinct types of AIDS-NHL.

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