scholarly journals Breast implant‐associated anaplastic large cell lymphoma and other rare T‐cell lymphomas

2019 ◽  
Vol 37 (S1) ◽  
pp. 24-29 ◽  
Author(s):  
Laurence Leval
Keyword(s):  
T Cell ◽  
Anaplastic Large Cell Lymphoma ◽  
Cell Lymphoma ◽  
Breast Implant ◽  
Large Cell ◽  
T Cell Lymphomas ◽  
Large Cell Lymphoma

scholarly journals Transcriptional analysis distinguishes breast implant-associated anaplastic large cell lymphoma from other peripheral T-cell lymphomas

2018 ◽  
Vol 32 (2) ◽  
pp. 216-230 ◽  
Author(s):  
Arianna Di Napoli ◽  
Loris De Cecco ◽  
Pier Paolo Piccaluga ◽  
Mohsen Navari ◽  
Valeria Cancila ◽  
...  
Keyword(s):  
T Cell ◽  
Anaplastic Large Cell Lymphoma ◽  
Cell Lymphoma ◽  
Breast Implant ◽  
Large Cell ◽  
Transcriptional Analysis ◽  
T Cell Lymphomas ◽  
Large Cell Lymphoma ◽  
Peripheral T Cell Lymphomas

scholarly journals How I treat breast implant–associated anaplastic large cell lymphoma

Blood ◽  
2018 ◽  
Vol 132 (18) ◽  
pp. 1889-1898 ◽  
Author(s):  
Neha Mehta-Shah ◽  
Mark W. Clemens ◽  
Steven M. Horwitz
Keyword(s):  
T Cell ◽  
Anaplastic Large Cell Lymphoma ◽  
Cell Lymphoma ◽  
Breast Implant ◽  
Large Cell ◽  
World Health ◽  
Team Approach ◽  
Textured Surface ◽  
Complete Surgical Excision ◽  
Large Cell Lymphoma

Abstract Breast implant–associated anaplastic large cell lymphoma (BIA-ALCL) is a recently described form of T-cell non-Hodgkin lymphoma now formally recognized by the World Health Organization classification of lymphoid neoplasms. The disease most often presents with a delayed seroma around the breast implant, almost exclusively with a textured surface, and manifests with breast pain, swelling or asymmetry, capsular contracture, but can also present with a breast mass, and lymph node involvement. The prognosis of BIA-ALCL is favorable compared with many other subtypes of systemic T-cell lymphoma; however, unlike other non-Hodgkin lymphomas, complete surgical excision for localized disease is an important part of the management of these patients. In this paper, we share our recommendations for a multidisciplinary team approach to the diagnosis, workup, and treatment of BIA-ALCL in line with consensus guidelines by the National Comprehensive Cancer Network.

scholarly journals IL-10, IL-13, Eotaxin and IL-10/IL-6 ratio distinguish breast implant-associated anaplastic large-cell lymphoma from all types of benign late seromas

2020 ◽  
Author(s):  
Arianna Di Napoli ◽  
Daniele Greco ◽  
Giorgia Scafetta ◽  
Francesca Ascenzi ◽  
Alessandro Gulino ◽  
...  
Keyword(s):  
T Cell ◽  
Anaplastic Large Cell Lymphoma ◽  
Cell Lymphoma ◽  
Breast Implant ◽  
Large Cell ◽  
Mediators Of Inflammation ◽  
Cytokine Milieu ◽  
Large Cell Lymphoma ◽  
T Cell Clonality ◽  
Cell Clonality

Abstract Breast implant-associated anaplastic large-cell lymphoma (BI-ALCL) is an uncommon peripheral T cell lymphoma usually presenting as a delayed peri-implant effusion. Chronic inflammation elicited by the implant has been implicated in its pathogenesis. Infection or implant rupture may also be responsible for late seromas. Cytomorphological examination coupled with CD30 immunostaining and eventual T-cell clonality assessment are essential for BI-ALCL diagnosis. However, some benign effusions may also contain an oligo/monoclonal expansion of CD30 + cells that can make the diagnosis challenging. Since cytokines are key mediators of inflammation, we applied a multiplexed immuno-based assay to BI-ALCL seromas and to different types of reactive seromas to look for a potential diagnostic BI-ALCL-associated cytokine profile. We found that BI-ALCL is characterized by a Th2-type cytokine milieu associated with significant high levels of IL-10, IL-13 and Eotaxin which discriminate BI-ALCL from all types of reactive seroma. Moreover, we found a cutoff of IL10/IL-6 ratio of 0.104 is associated with specificity of 100% and sensitivity of 83% in recognizing BI-ALCL effusions. This study identifies promising biomarkers for initial screening of late seromas that can facilitate early diagnosis of BI-ALCL.

FDG-PET Scans as a Staging Study for T-Cell Lymphomas: High Rates of Positivity Do Not Result in Frequent Changes in Stage.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 2399-2399 ◽  
Author(s):  
Steven M. Horwitz ◽  
Francine Foss ◽  
Shari Goldfarb ◽  
Ana Molina ◽  
Paul A. Hamlin ◽  
...  
Keyword(s):  
Lymph Node ◽  
T Cell ◽  
Anaplastic Large Cell Lymphoma ◽  
Fdg Pet ◽  
Cell Lymphoma ◽  
Large Cell ◽  
T Cell Lymphoma ◽  
T Cell Lymphomas ◽  
Large Cell Lymphoma ◽  
Pet Scans

Abstract FDG-PET is emerging as a standard staging study for diffuse large B-cell lymphoma and Hodgkin’s disease. There is little experience with PET in staging T-cell lymphomas (TCL). TCL often involve extranodal sites not well imaged by standard CT. We hypothesized that PET would add to staging by detecting additional sites of disease. To address this question we reviewed our TCL database to identify patients (pt) who had PET as part of complete staging at initial diagnosis or at relapse. Each pt was included once. Staging included physical exam, CT scan of the chest/abdomen/pelvis alone or as part of a PET/CT combination, and bone marrow (BM) biopsy. Studies such as MRI of the sinus or ultrasound of the testes were done as clinically indicated. We reviewed 107 pt who met the above criteria. Histologies were as follows: peripheral T-cell lymphoma NOS (PTCL), angioimmunoblastic T-cell lymphoma (AILT), anaplastic large cell lymphoma, ALK-1-, (ALCL−), anaplastic large cell lymphoma, ALK-1+, (ALCL+), mycosis fungoides (MF), subcutaneous panniculitis-like T-cell lymphoma (SPTCL), adult T-cell lymphoma (ATL), NK lymphoma nasal type (NK-Nas), lymphoblastic lymphoma (LL), enteropathy associated T-cell lymphoma (EATCL), blastic NK lymphoma (BLNK), primary cutaneous ALCL (ALCL-Cut), and hepatosplenic T-cell lymphoma (HSPTCL). All pt with MF had suspicion of extracutaneous disease. Overall 95/107 (89%) had a PET interpreted as positive by visual review. Standard uptake values (SUV) varied from 1.1–20.5 g/ml. Of the 12 pt with negative PET scans, 7(58%) had no evidence of disease on CT including PTCL (n=3, stage I resected), HSPTCL (n=2, liver, spleen, BM disease only), ALCL-Cut (n=2, skin only). T-cell Lymphoma-PET Results Histology N PET + % positive SUV Range (g/ml) ALL PT 107 95 89% 1.1–20.5 PTCL 27 24 88% 2–20 AILT 19 16 84% 2–11.7 ALCL− 12 12 100% 3–19.6 ALCL+ 4 4 100% 4–12 MF 12 10 83% 1.8–17.6 SPTCL 8 8 100% 1.4–13.1 ATL 5 5 100% 2.9–19.7 NK-Nas 5 5 100% 3.4–13.1 LL 3 3 100% 5.5–20.5 EATCL 3 3 100% 3.5–9.9 ALCL-Cut 5 3 60% 1.1–1.4 BLNK 2 2 100% 1.929.5 HSPTCL 2 0 0 N/A PET detected additional sites of disease in 34/107 (32%). These sites detected by PET were skin/subcut (n=9), bone (n=7), lymph node (n=6), spleen (n=3), nasopharynx/sinus (n=2), liver (n=2), BM (n=1), bowel (n=1), muscle (n=1), kidney (n=1), tonsil (n=1), testes (n=1). Three new malignancies were incidentally detected by PET including lung cancer (n=1), metastatic renal cell to the parotid (n=1), and mantle cell lymphoma (n=1 in a pt with ALCL-cut). Despite these additional sites, stage was changed in only 10/107 (9%). We did not use negative PET to downstage. Sites resulting in higher stage included bone (n=3), lymph node (n=2), subcut/muscle (n=3), testes (n=1), liver (n=1). Skin lesions were noted on physical exam and therefore did not change stage. In conclusion, TCL are almost universally PET positive. PET often adds information by identifying extranodal disease. However, partly due to many pt being stage IV by other modalities, PET resulted in a change of stage in <10% of pt. PET may be particularly useful in assessing of skin sites. These data suggest that it may be beneficial to include PET in the response assessment of TCL, as has been proposed for DLBCL and HL in revised NHL response criteria.

scholarly journals Hemophagocytic Lymphohistiocytosis in Association with Primary Cutaneous Anaplastic Large Cell Lymphoma

2014 ◽  
Vol 2014 ◽  
pp. 1-7
Author(s):  
Aneesh Basheer ◽  
Somanath Padhi ◽  
Ramesh Nagarajan ◽  
Vinoth Boopathy ◽  
Sudhagar Mookkappan ◽  
...  
Keyword(s):  
T Cell ◽  
Anaplastic Large Cell Lymphoma ◽  
Hemophagocytic Lymphohistiocytosis ◽  
Cell Lymphoma ◽  
Large Cell ◽  
Lymphoproliferative Disorders ◽  
Elderly Male ◽  
Anaplastic Lymphoma ◽  
T Cell Lymphomas ◽  
Large Cell Lymphoma

Hemophagocytic lymphohistiocytosis (HLH) has a well known association with lymphomas, especially of T cell origin. Prognosis of lymphoma associated HLH is very poor, especially in T cell lymphomas; and, therefore, early diagnosis might alter the outcome. Though association of HLH with systemic anaplastic large cell lymphoma (ALCL) is known, its occurrence in primary cutaneous ALCL (C-ALCL) is distinctly rare. We aim to describe a case of C-ALCL (anaplastic lymphoma kinase (ALK)−) in an elderly male who succumbed to the complication of associated HLH, which was possibly triggered by coexistent virus infection. We briefly present the literatures on lymphoma associated HLH and discuss the histopathological differentials of cutaneous CD30+ lymphoproliferative disorders. We do suggest that HLH may pose diagnostic challenges in the evaluation of an underlying lymphoma and hence warrants proper evaluation for the underlying etiologies and/or triggering factors.

scholarly journals Peripheral T-cell lymphoma, NOS, and anaplastic large cell lymphoma

Hematology ◽  
2015 ◽  
Vol 2015 (1) ◽  
pp. 550-558 ◽  
Author(s):  
Anne W. Beaven ◽  
Louis F. Diehl
Keyword(s):  
T Cell ◽  
Anaplastic Large Cell Lymphoma ◽  
Cell Lymphoma ◽  
Large Cell ◽  
Brentuximab Vedotin ◽  
Response To Therapy ◽  
Anaplastic Lymphoma ◽  
T Cell Lymphomas ◽  
First Remission ◽  
Large Cell Lymphoma

AbstractPeripheral T-cell lymphomas (PTCL), with the exception of anaplastic lymphoma kinase (ALK)-positive anaplastic large cell lymphoma (ALCL), have a very poor prognosis. Although current first line chemotherapy continues to be a CHOP-like (cyclophosphamide, doxorubicin, vincristine, prednisone) regimen there is now data suggesting that the addition of etoposide in younger patients improves outcomes. Even for those patients who do have a response to therapy, the risk of relapse remains quite high. Although autologous transplant in first remission is often used, its role as consolidation therapy in first remission remains unclear and may preferentially benefit low-risk patients. In the relapsed setting, major advances have occurred with Food and Drug Administration (FDA) approval of 4 new agents (pralatrexate, romidepsin, belinostat, brentuximab vedotin) for relapsed/refractory PTCL since 2009. These 4 drugs represent the first agents ever approved specifically for this indication. Unfortunately, with the exception of ALCL for which brentuximab vedotin will likely substantially change our approach to treatment, there are still many patients for whom available drugs will not be effective, and it is for these patients that further advances are urgently needed.

scholarly journals Breast implant-associated, ALK-negative, T-cell, anaplastic, large-cell lymphoma: Establishment and characterization of a model cell line (TLBR-1) for this newly emerging clinical entity

Cancer ◽  
2010 ◽  
Vol 117 (7) ◽  
pp. 1478-1489 ◽  
Author(s):  
Melissa G. Lechner ◽  
Stephen Lade ◽  
Daniel J. Liebertz ◽  
H. Miles Prince ◽  
Garry S. Brody ◽  
...  
Keyword(s):  
T Cell ◽  
Cell Line ◽  
Anaplastic Large Cell Lymphoma ◽  
Cell Lymphoma ◽  
Breast Implant ◽  
Large Cell ◽  
Clinical Entity ◽  
Model Cell ◽  
Large Cell Lymphoma

scholarly journals Etiology of Breast Implant-Associated Anaplastic Large Cell Lymphoma (BIA-ALCL): Current Directions in Research

Cancers ◽  
2020 ◽  
Vol 12 (12) ◽  
pp. 3861
Author(s):  
Anand K. Deva ◽  
Suzanne D. Turner ◽  
Marshall E. Kadin ◽  
Mark R. Magnusson ◽  
H. Miles Prince ◽  
...  
Keyword(s):  
T Cell ◽  
Anaplastic Large Cell Lymphoma ◽  
Cell Lymphoma ◽  
Breast Implant ◽  
Bacterial Load ◽  
Locally Advanced ◽  
Large Cell ◽  
Future Research ◽  
Anaplastic Lymphoma ◽  
Large Cell Lymphoma

Breast implant-associated anaplastic large cell lymphoma (BIA-ALCL) is a CD30-positive, anaplastic lymphoma kinase-negative T-cell lymphoma. Where implant history is known, all confirmed cases to date have occurred in patients with exposure to textured implants. There is a spectrum of disease presentation, with the most common occurring as a seroma with an indolent course. A less common presentation occurs as locally advanced or, rarely, as metastatic disease. Here we review the immunological characteristics of BIA-ALCL and potential triggers leading to its development. BIA-ALCL occurs in an inflammatory microenvironment with significant lymphocyte and plasma cell infiltration and a prominent Th1/Th17 phenotype in advanced disease. Genetic lesions affecting the JAK/STAT signaling pathway are commonly present. Proposed triggers for the development of malignancy include mechanical friction, silicone implant shell particulates, silicone leachables, and bacteria. Of these, the bacterial hypothesis has received significant attention, supported by a plausible biologic model. In this model, bacteria form an adherent biofilm in the favorable environment of the textured implant surface, producing a bacterial load that elicits a chronic inflammatory response. Bacterial antigens, primarily of Gram-negative origin, may trigger innate immunity and induce T-cell proliferation with subsequent malignant transformation in genetically susceptible individuals. Although much remains to be elucidated regarding the multifactorial origins of BIA-ALCL, future research should focus on prevention and treatment strategies, recognizing susceptible populations, and whether decreasing the risk of BIA-ALCL is possible.

scholarly journals Clonotype pattern in T-cell lymphomas map the cell of origin to immature lymphoid precursors

2021 ◽  
Author(s):  
Aishwarya Iyer ◽  
Dylan Hennessey ◽  
Robert Gniadecki
Keyword(s):  
T Cells ◽  
T Cell ◽  
Anaplastic Large Cell Lymphoma ◽  
Cell Lymphoma ◽  
Large Cell ◽  
T Cell Lymphoma ◽  
Cell Of Origin ◽  
Peripheral T Cell Lymphoma ◽  
T Cell Lymphomas ◽  
Large Cell Lymphoma

Background Mature T-cell lymphomas (TCLs) are rare, clinically heterogeneous hematologic cancers of high medical need. TCLs have inferior prognosis compared with their B-cell counterparts, which is attributed to poor understanding of their pathogenesis. Based on phenotypic similarities between normal and neoplastic lymphocytes it has been assumed that TCLs develop in the periphery, directly from various subtypes of normal T-cells. Methods and findings To address the debated question of the cell of origin in TCLs we analyzed to identify the highly variable complementarity determining regions (CDR3) regions of T-cell receptor (TCR) to trace the clonal history of the T-cells. We have collected previously published whole genome -exome, and -transcriptome sequencing data from 574 TCL patients comprising five nodal lymphomas [anaplastic large cell lymphoma (n=67), peripheral T-cell lymphoma (PTCL, n=55), adult T-cell lymphoma/leukemia (n=135), natural killer T-cell lymphoma (NKCL, n=25), not specified/other (n=30)] and three extranodal, cutaneous T-cell lymphomas [mycosis fungoides (n=122), Sezary syndrome (n=130), and subcutaneous panniculitis like T-cell lymphoma (n=10)]. TCR clonotypes contained in the tumor cell fraction, representing the clonotypes of malignant cells, were identified by de novo assembly of CDR3 regions of TCRγ, β and α. We have found that the vast majority of TCLs are clonotypically oligoclonal, although the pattern oligoclonality varied. Anaplastic large cell lymphoma was most diverse comprising multiple clonotypes of TCRγ, β and α whereas adult T-cell lymphoma/leukemia and peripheral T-cell lymphomas often showed monoclonality for TCRγ and β but had diverse TCRα clonotypes. These patterns of rearrangements were not compatible with the current mature T-cell precursor model and indicated that TCLs are initiated at the level of the lymphoid precursor. In keeping with this hypothesis, TCR rearrangements in TCLs resembled the pattern seen in the human thymus showing biased usage of V and J segments of high combinatorial probability resulting in recurrent, public CDR3 sequences shared between unrelated patients and across different clinical TCL entities. Frequencies of malignant clonotypes followed Zipf-Mandelbrot scaling law suggesting that TCLs comprise an interconnected system of expanding tumor clones. The major limitation of this study is that it is based on the analysis of the TCR clonotypes and does not directly inform about developmental trajectories of cellular clones. Conclusions Lymphoid precursors are the likely cells of origin for mature T-cell lymphomas. Anaplastic large cell lymphoma seems to be derived from the most immature precursors with germline TCR whereas peripheral T-cell lymphoma and adult T-cell lymphoma/leukemia map to the later stages after TCR lower case Greek beta rearrangement stage. Clonotypically diverse initiating cells may seed target tissues being responsible for disease relapses after therapy.

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