Second primary cutaneous T-cell lymphoma in patients with non-Hodgkin lymphoma: a chicken-or-the-egg issue

2017 ◽  
Vol 57 (1) ◽  
pp. 113-113
Author(s):  
Joseph G. Kamel ◽  
Kyle T. Amber
Keyword(s):  
T Cell ◽  
Hodgkin Lymphoma ◽  
Cell Lymphoma ◽  
T Cell Lymphoma ◽  
Second Primary ◽  
Cutaneous T Cell Lymphoma ◽  
Non Hodgkin Lymphoma

scholarly journals Risk of cutaneous T-cell lymphoma in patients with chronic lymphocytic leukemia and other subtypes of non-Hodgkin lymphoma

2017 ◽  
Vol 56 (11) ◽  
pp. 1125-1129 ◽  
Author(s):  
Timothy W. Chang ◽  
Amy L. Weaver ◽  
Tait D. Shanafelt ◽  
Thomas M. Habermann ◽  
Cooper C. Wriston ◽  
...  
Keyword(s):  
T Cell ◽  
Chronic Lymphocytic Leukemia ◽  
Hodgkin Lymphoma ◽  
Cell Lymphoma ◽  
Lymphocytic Leukemia ◽  
T Cell Lymphoma ◽  
Cutaneous T Cell Lymphoma ◽  
Non Hodgkin Lymphoma

scholarly journals Imaging of Chemokine Receptor-4 Targeted PET/CT with 68Ga-Pentixafor in Non-Hodgkin Lymphoma: Comparison to 18F-FDG

2020 ◽  
Author(s):  
Qingqing Pan ◽  
Yaping Luo ◽  
Yan Zhang ◽  
Long Chang ◽  
Ji Li ◽  
...  
Keyword(s):  
T Cell ◽  
B Cell ◽  
Hodgkin Lymphoma ◽  
Marginal Zone ◽  
Cell Lymphoma ◽  
B Cell Lymphoma ◽  
T Cell Lymphoma ◽  
Lymphoplasmacytic Lymphoma ◽  
Non Hodgkin Lymphoma ◽  
Pet Ct

Abstract Background: In order to study the CXCR4 expression with 68Ga-Pentixafor PET in different types of non-Hodgkin lymphoma, we performed a retrospective study to describe the 68Ga-Pentixafor PET/CT imaging in a spectrum of lymphomas and to compare it with 18F-FDG PET/CT. Results: Twenty-seven patients with newly diagnosed non-Hodgkin lymphoma were recruited retrospectively. 68Ga-Pentixafor PET showed increased radioactivity in lymphoplasmacytic lymphoma (n = 8), marginal zone lymphoma (n = 4), diffuse large B cell lymphoma (n = 3), follicular lymphoma (n = 2), mantle cell lymphoma (n = 1), unclassified indolent B cell lymphoma (n = 3) and enteropathy associated T cell lymphoma (n = 3). However, peripheral T cell lymphoma, not otherwise specified (n = 1), and NK/T cell lymphoma (n = 2) were not avid for 68Ga-Pentixafor. In comparison to 18F-FDG PET, 68Ga-Pentixafor PET demonstrated more extensive disease and higher radioactivity in lymphoplasmacytic lymphoma and marginal zone lymphoma. Conclusion: CXCR4 expression varies in different types of non-Hodgkin lymphoma. Overexpression of CXCR4 was detected with 68Ga-Pentixafor PET/CT in lymphoplasmacytic lymphoma, marginal zone lymphoma, diffuse large B cell lymphoma, follicular lymphoma, mantle cell lymphoma, unclassified indolent B cell lymphoma, and enteropathy associated T cell lymphoma.

Clinical Applications of the Genomic Landscape of Aggressive Non-Hodgkin Lymphoma

2017 ◽  
Vol 35 (9) ◽  
pp. 955-962 ◽  
Author(s):  
Andrea B. Moffitt ◽  
Sandeep S. Dave
Keyword(s):  
T Cell ◽  
B Cell ◽  
Hodgkin Lymphoma ◽  
Cell Lymphoma ◽  
B Cell Lymphoma ◽  
Large Cell ◽  
T Cell Lymphoma ◽  
Adult T Cell Leukemia ◽  
Non Hodgkin Lymphoma ◽  
T Cell Lymphomas

In this review, we examine the genomic landscapes of lymphomas that arise from B, T, and natural killer cells. Lymphomas represent a striking spectrum of clinical behaviors. Although some lymphomas are curable with standard therapy, the majority of the affected patients succumb to their disease. Here, the genetic underpinnings of these heterogeneous entities are reviewed. We consider B-cell lymphomas, including Burkitt lymphoma, diffuse large B-cell lymphoma, Hodgkin lymphoma, and primary mediastinal B-cell lymphoma. We also examine T-cell lymphomas, including anaplastic large-cell lymphoma, angioimmunoblastic T-cell lymphoma, cutaneous T-cell lymphoma, adult T-cell leukemia/lymphoma, and other peripheral T-cell lymphomas. Together, these malignancies make up most lymphomas diagnosed around the world. Genomic technologies, including microarrays and next-generation sequencing, have enabled a better understanding of the molecular underpinnings of these cancers. We describe the broad genomics findings that characterize these lymphoma types and discuss new therapeutic opportunities that arise from these findings.

scholarly journals Common genetic variants and risk for non-Hodgkin lymphoma and adult T-cell lymphoma/leukemia in Jamaica

2009 ◽  
Vol 125 (6) ◽  
pp. 1479-1482 ◽  
Author(s):  
Sophia S. Wang ◽  
J. Daniel Carreon ◽  
Barrie Hanchard ◽  
Stephen Chanock ◽  
Michie Hisada
Keyword(s):  
T Cell ◽  
Hodgkin Lymphoma ◽  
Genetic Variants ◽  
Cell Lymphoma ◽  
T Cell Lymphoma ◽  
Non Hodgkin Lymphoma ◽  
Common Genetic Variants

Comparison of Autologous Vs. Allogeneic Stem Cell Transplantation for Non-Hodgkin Lymphoma

Blood ◽  
2012 ◽  
Vol 120 (21) ◽  
pp. 2036-2036
Author(s):  
Nishitha M. Reddy ◽  
Olalekan O Oluwole ◽  
John P Greer ◽  
David S Morgan ◽  
Stacey Goodman ◽  
...  
Keyword(s):  
Stem Cell ◽  
T Cell ◽  
Stem Cell Transplantation ◽  
B Cell ◽  
Hodgkin Lymphoma ◽  
Cell Lymphoma ◽  
Conditioning Regimen ◽  
B Cell Lymphoma ◽  
T Cell Lymphoma ◽  
Non Hodgkin Lymphoma

Abstract Abstract 2036 Background: Stem cell transplantation (SCT) is a common indication for patients with Non-Hodgkin lymphoma (NHL). Auto-SCT is recommended for patients with relapsed NHL or as consolidative therapy in first remission. Allo-SCT is reserved for pts with either relapsed or primary refractory disease. The outcomes of these pts in large prospective studies are lacking and current recommendations and timing of selection of auto vs. allo-SCT are influenced by variety of factors including physician bias. Transplant outcomes of auto or allo-SCT have not been elucidated as a single cohort. Methods: We report a retrospective analysis of 270 pts with NHL who underwent auto-SCT or allo-SCT between January 2000- December 2010 after obtaining institutional IRB approval. Data were analyzed using SPSS.19. Results: Of the 270 pts, 238 patients underwent SCT for B-cell lymphoma (178 auto, 60 allo-SCT), and 32 for T-cell lymphoma (21 auto and 11 allo-SCT). Fifteen pts (6%) received prior auto-SCT. The median age of transplant was 52 years for the entire group. For those who underwent allo-SCT, median age was 47 (range 22–65 yrs) and 54 yrs (range 22–77) for auto-SCT. One hundred seventy (62%) were male. Majority of pts (76%) had advanced stage disease (stages III and IV). Fifty four (20%) received radiation therapy either before or after transplantation. The median number of prior regimens for allo-SCT were 3 (range 1–5) and 2 for auto-SCT (range 1 to 4). Within the allo-SCT group (n=71), 45 received matched-related donor transplants, and 26 unrelated donor transplants; majority of pts (n=47) received reduced intensity conditioning regimen. The auto-SCT group predominantly received CBV as their conditioning regimen. Median time from diagnosis to allo-SCT or auto-SCT was 1.4 yrs (range 0.32–13.1 yrs) and 1.69 (range 0.38–13.7 yrs), respectively. The median follow up time for the entire cohort was 6.2 yrs. The overall survival (OS) rates for the B- cell and T-cell NHL were 58% and 50% respectively (allo-SCT 51% vs. 54% for B and T-cell NHL, and auto-SCT 60% vs. 47% for B and T-cell lymphoma, respectively) (p=0.26). Within the allo-SCT group the relapse and non-relapse mortalities were 45% and 16%, respectively. In the auto-SCT group, the relapse and non-relapse mortality were 46% and 7% respectively. In B-cell lymphoma the relapse rate was 48% and 45% for auto and allo-SCT respectively (p=0.80). In T-cell lymphoma the relapse rate was 40% and 45% for auto and allo-SCT (p=0.67). Multivariate analysis of pts receiving auto vs. allo-SCT in NHL will be presented. Conclusions: We conclude that in this highly selected patient population with otherwise minimal comorbidities but chemo-sensitive aggressive lymphomas, about 50% of patients achieve long term survival after either an auto or allo-SCT approach. Despite recent evidence, there are intricate difficulties in patient selection for allo vs. auto-SCT and outcome of either approach is not satisfactory. Post transplant relapse is the most common cause of post-SCT failure. Tandem auto followed by allo-SCT and maintenance strategies need to be explored. We propose a larger prospective analysis on transplant outcomes in both B and T-cell lymphoma and improve strategies to prevent relapses after SCT. Disclosures: No relevant conflicts of interest to declare.

Expression pattern of T-cell–associated chemokine receptors and their chemokines correlates with specific subtypes of T-cell non-Hodgkin lymphoma

Blood ◽  
2000 ◽  
Vol 96 (2) ◽  
pp. 685-690 ◽  
Author(s):  
Dan Jones ◽  
Carl O'Hara ◽  
Madeleine D. Kraus ◽  
Antonio R. Perez–Atayde ◽  
Aliakbar Shahsafaei ◽  
...  
Keyword(s):  
T Cell ◽  
Hodgkin Lymphoma ◽  
Chemokine Receptor ◽  
Chemokine Receptors ◽  
Cell Lymphoma ◽  
Large Cell ◽  
T Cell Lymphoma ◽  
Receptor Expression ◽  
Non Hodgkin Lymphoma ◽  
Alk Positive

Abstract Chemokine receptors mediate the migration of lymphocytes through the binding of soluble ligands, and their expression is differentially regulated in lymphocyte subsets. The pattern of chemokine receptor expression in T-cell non-Hodgkin lymphoma has not been previously studied. Using a panel of mouse monoclonal antibodies, we studied the immunohistochemical expression of the Th1-associated chemokine receptor CXCR3 in 141 patients with T-cell lymphoma, and we studied the receptors CCR4 and CCR5 and some of their ligands in a subset of these tumors. Expression of CXCR3 was typical of the smaller T cells in angioimmunoblastic lymphoma (15 of 18 patients), angiocentric lymphoma (3 of 3 patients), histiocyte-rich tumors (4 of 5 patients), and unspecified T-cell lymphomas (17 of 39 patients). CXCR3 expression was seen in only 1 of 15 patients with anaplastic lymphoma kinase (ALK)-positive anaplastic large-cell lymphoma. In contrast, all ALK-positive tumors showed diffuse reactivity for the Th2-associated receptor CCR4 (5 of 5 patients). CCR4 expression was also a consistent feature of the large-cell transformation of mycosis fungoides. CCR5 expression showed no consistent association with any T-cell tumor type. The chemokines Mig (CXCR3 ligand), TARC (CCR4 ligand), and MCP-2 (CCR5 ligand) were detected in intratumoral blood vessels and histiocytes. Mig was also coexpressed by a subset of CXCR3-positive tumor cells in 6 of 20 lymphomas. MCP-2 was highly expressed in stromal cells in 3 patients with nodal involvement by cutaneous T-cell lymphoma. As with normal T-cell subsets, we demonstrated that there is frequent differential expression of chemokine receptors in T-cell tumors, which may explain, in part, the distinctive patterns of spread in different tumor subtypes.

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