Transformation in Mycosis Fungoides: The Role of Methotrexate

2002 ◽  
Vol 6 (2) ◽  
pp. 109-116 ◽  
Author(s):  
Jasmin Abd-El-Baki ◽  
Marie-France Demierre ◽  
Ning Li ◽  
Francine M. Foss
Keyword(s):  
Mycosis Fungoides ◽  
Cell Transformation ◽  
Cell Lymphoma ◽  
Cell Clone ◽  
Small Sample Size ◽  
Large Cell ◽  
Small Sample ◽  
T Cell Clone ◽  
Large Cell Lymphoma

Background: Large cell transformation in patients with mycosis fungoides (MF) has been well reported in the literature. Although the risk factors have not been clearly elucidated, advanced stage seems to be associated with a higher incidence of transformation. Because MF is a rare disorder, little is known about the influence of other factors such as immunosuppressive therapy in the occurrence of transformation. Objective: We questioned the role of methotrexate (MTX) in the transformation of MF to large cell lymphoma (LCL). Methods: We identified all patients with MF who were registered in our cutaneous lymphoma database. Transformation was defined by the presence of large cells exceeding 25% of the infiltrate in at least one skin biopsy. In one patient, we followed the histologic, immunophenotypic, and genotypic changes taking place as transformation occurred. Results: A total of 134 patients with MF were identified. Of 21 patients who received MTX, 3 transformed, and of the 113 patients in the non-MTX group, only 2 transformed. The incidence of transformation in the patients who received MTX was significantly higher than in those who did not receive the drug (14.3% vs. 1.8%; p = 0.03). This significance was maintained, even after controlling for stage and sex. For one patient who transformed, we demonstrated an identical dominant T-cell clone in all skin specimens, including the large cell lymphoma. Conclusion: Our results demonstrate a significant association between MTX exposure and transformation to LCL in patients with MF. In light of the small sample size, short followup of patients, and the inherent tendency of mycosis fungoides to transform, the role for MTX in transformation is unproven and needs to be confirmed in a multicenter study.

Large-cell transformation following detection of minimal residual disease in cutaneous T-cell lymphoma: molecular and in situ analysis of a single neoplastic T-cell clone expressing the identical T-cell receptor.

1995 ◽  
Vol 13 (7) ◽  
pp. 1751-1757 ◽  
Author(s):  
J T Wolfe ◽  
L Chooback ◽  
D T Finn ◽  
C Jaworsky ◽  
A H Rook ◽  
...  
Keyword(s):  
T Cell ◽  
Cell Transformation ◽  
Residual Disease ◽  
Cell Lymphoma ◽  
Cell Clone ◽  
Large Cell ◽  
Cell Receptor ◽  
Clinical Relapse ◽  
T Cell Clone ◽  
Large Cell Transformation

PURPOSE One of the unique characteristics of cutaneous T-cell lymphoma (CTCL) is its ability to undergo cytologic transformation in which the malignant T cells develop the morphologic appearance of a large-cell lymphoma. Reported to occur in up to 20% of advanced cases, large-cell transformation (LCT) is associated with an aggressive clinical course. Little is known about the risk factors or the molecular mechanisms of LCT. Before current immunohistochemical and molecular techniques, it was not possible to determine if LCT represented changes of the initial neoplastic T-cell clone or, in fact, was a distinct second malignancy. The goal of this study was to define the clonal evolution of LCT in CTCL. PATIENTS AND METHODS Polymerase chain reaction (PCR) amplification of T-cell receptor-beta (TCR-beta) gene rearrangements and immunohistochemistry with monoclonal antibodies to TCR-V beta regions were used as markers of T-cell clonality to analyze the skin and peripheral blood of a patient with CTCL and LCT. RESULTS We first detected the presence of minimal residual disease (MRD) in a CTCL patient with a complete clinical response to biologic response modifiers (BRMs). When clinical relapse occurred and demonstrated LCT, TCR-beta-PCR and in situ immunohistochemistry with a specific TCR-V beta monoclonal antibody identified a single neoplastic T-cell clone that expressed the identical TCR as the original clone. CONCLUSION Our results confirm a common clonal origin for CTCL and LCT. We also provide evidence of MRD in CTCL by molecular analysis, implying that residual malignant cells maintain a potential for clinical relapse and possibly LCT. The role of MRD detection remains to be defined in the clinical assessment of CTCL. LCT in CTCL provides a unique model to investigate the molecular events that underlie terminal-stage tumor progression.

The Role of IgM Antibodies in T Cell Lymphoma Protection in a Novel Model Resembling Anaplastic Large Cell Lymphoma

2021 ◽  
pp. ji2001279
Author(s):  
Chuancang Jiang ◽  
Ming-Lang Zhao ◽  
Luis Ramos ◽  
Katarzyna Dobaczewska ◽  
Ronald Herbert ◽  
...  
Keyword(s):  
T Cell ◽  
Anaplastic Large Cell Lymphoma ◽  
Cell Lymphoma ◽  
Large Cell ◽  
T Cell Lymphoma ◽  
Igm Antibodies ◽  
Large Cell Lymphoma ◽  
Novel Model

scholarly journals IGF-IR tyrosine kinase interacts with NPM-ALK oncogene to induce survival of T-cell ALK+ anaplastic large-cell lymphoma cells

Blood ◽  
2009 ◽  
Vol 114 (2) ◽  
pp. 360-370 ◽  
Author(s):  
Ping Shi ◽  
Raymond Lai ◽  
Quan Lin ◽  
Abid S. Iqbal ◽  
Leah C. Young ◽  
...  
Keyword(s):  
T Cell ◽  
Tyrosine Kinase ◽  
Malignant Lymphoma ◽  
Cell Lines ◽  
Anaplastic Large Cell Lymphoma ◽  
Cell Lymphoma ◽  
Large Cell ◽  
Type I ◽  
Large Cell Lymphoma

Abstract Type I insulin-like growth factor receptor (IGF-IR) tyrosine kinase plays important roles in the pathogenesis of several malignancies. Although it promotes the growth of stimulated hematopoietic cells, a direct role of IGF-IR in malignant lymphoma has not been identified. Anaplastic lymphoma kinase-positive anaplastic large-cell lymphoma (ALK+ ALCL) is a unique type of T-cell lymphoma. Approximately 85% of ALK+ ALCL cases harbor the translocation t(2;5)(p23;q35), which generates the chimeric oncogene NPM-ALK. In the present study, we explored a possible role of IGF-IR in ALK+ ALCL. Our results demonstrate that IGF-IR and IGF-I are widely expressed in ALK+ ALCL cell lines and primary tumors. Importantly, we identified novel reciprocal functional interactions between IGF-IR and NPM-ALK. Antagonism of IGF-IR decreased the viability, induced apoptosis and cell-cycle arrest, and decreased proliferation and colony formation of ALK+ ALCL cell lines. These effects could be explained by alterations of cell survival regulatory proteins downstream of IGF-IR signaling. Our findings improve current understanding of the biology of IGF-IR and NPM-ALK and have significant therapeutic implications as they identify IGF-IR signaling as a potential therapeutic target in ALK+ ALCL and possibly other types of malignant lymphoma.

Primary Central Nervous System Anaplastic Large Cell Lymphoma is an Unusual Brain Tumour

2014 ◽  
Vol 10 (01) ◽  
pp. 48
Author(s):  
Dionysis Papadatos-Pastos ◽  
James Hall ◽  
Ruth Pettengell ◽  
Leslie R Bridges ◽  
Barry Newell ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Anaplastic Large Cell Lymphoma ◽  
Potential Role ◽  
Cell Lymphoma ◽  
Large Cell ◽  
Anaplastic Lymphoma ◽  
The Central Nervous System ◽  
Large Cell Lymphoma

We present a case of a 64-year-old man who was diagnosed with a primary anaplastic large cell lymphoma of the central nervous system (PCNSAL). He had received radical chemotherapy and radiotherapy for a non-small cell lung cancer (NSCLC) in the past. There is no known association between NSCLC and PCNSAL. We describe the diagnostic and therapeutic challenges associated with these rare intracranial lymphomas and highlight the potential role of newer biological agents in patients with anaplastic lymphoma kinase (ALK-1) positive PCNSAL.

A Case of Mycosis Fungoides after CD30 Positive Anaplastic Large Cell Lymphoma

2000 ◽  
Vol 27 (7) ◽  
pp. 458-461 ◽  
Author(s):  
Mi-Woo Lee ◽  
Doo-Hyun Chi ◽  
Jee-Ho Choi ◽  
Kyung-Jeh Sung ◽  
Kee-Chan Moon ◽  
...  
Keyword(s):  
Mycosis Fungoides ◽  
Anaplastic Large Cell Lymphoma ◽  
Cell Lymphoma ◽  
Large Cell ◽  
Large Cell Lymphoma
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