RESUMO
CD8+ cutaneous T-cell lymphoma (CTCL) is a relatively rare subset of the non-Hodgkins lymphomas. Bexarotene has been FDA-approved for the treatment of CTCL, but previous studies have been conducted on CD4+ CTL and there have been no reports about its use in CD8+ CTCL. Herein, we report on a patient whose CD8+ CTCL completely responded to treatment with bexarotene.
Assuntos
Linfócitos T CD8-Positivos/patologia , Micose Fungoide/tratamento farmacológico , Neoplasias Cutâneas/tratamento farmacológico , Tetra-Hidronaftalenos/uso terapêutico , Antineoplásicos/efeitos adversos , Antineoplásicos/uso terapêutico , Azetidinas/uso terapêutico , Bexaroteno , Carcinoma de Células Renais/cirurgia , Contraindicações , Exantema/etiologia , Ezetimiba , Humanos , Inibidores de Hidroximetilglutaril-CoA Redutases/efeitos adversos , Inibidores de Hidroximetilglutaril-CoA Redutases/uso terapêutico , Hiperlipidemias/induzido quimicamente , Hipolipemiantes/uso terapêutico , Hipotireoidismo/induzido quimicamente , Achados Incidentais , Neoplasias Renais/cirurgia , Masculino , Pessoa de Meia-Idade , Micose Fungoide/diagnóstico , Micose Fungoide/patologia , Neoplasias Primárias Múltiplas , Sinvastatina/uso terapêutico , Neoplasias Cutâneas/diagnóstico , Neoplasias Cutâneas/patologia , Tetra-Hidronaftalenos/efeitos adversos , Tiroxina/uso terapêuticoRESUMO
Aberrant expression of bcl-2 , caused by a t(14;18) translocation, is most commonly associated with follicular lymphoma. In a subset of these tumors, additional acquisition of a translocation involving c-myc leads to transformation to a high-grade lymphoma. We report a case of follicular lymphoma containing a t(14;18) translocation transforming into a Burkitt-like lymphoma containing the original t(14;18) as well as an additional t(8;14). The latter translocation resulted in the phenotype of Burkitt-like lymphoma, and the transformation from follicular lymphoma to Burkitt-like lymphoma was demonstrable within a single lymph node. To the best of our knowledge, this is the first report of a case documenting direct transformation of follicular lymphoma into Burkitt-like lymphoma in the same lymph node. This case illustrates the dramatic oncogenic stimulus that results from the inhibition of apoptosis by bcl-2 combined with the deregulation of cell growth by c-myc .
Assuntos
Linfoma de Burkitt/genética , Linfoma de Burkitt/patologia , Linfonodos/patologia , Linfoma Folicular/genética , Linfoma Folicular/patologia , Translocação Genética , Feminino , Citometria de Fluxo , Genes bcl-2/genética , Genes myc/genética , Humanos , Hibridização in Situ Fluorescente , Pessoa de Meia-IdadeRESUMO
Peripheral T-cell lymphoma primary to the central nervous system is a rare occurrence. The authors report a case of an 89-year-old woman who presented with a 3-month history of worsening confusion and recent onset of headache, nausea and vomiting, and upper limb tremors. Computed tomography and magnetic resonance imaging examinations demonstrated a 4.5-cm solitary brain mass in the right basal ganglia with compression along the ventricular system. No other lesion was found in the patient. Histologic and immunohistochemical studies of a stereotactic biopsy of the mass showed a T-cell lymphoproliferative lesion positive for CD3, CD8, CD57, and T-cell intracellular antigen 1 and negative for CD4, CD56, CD30, anaplastic lymphoma kinase, and CD20. A monoclonal T-cell receptor-gamma gene rearrangement was detected by polymerase chain reaction analysis of genomic DNA isolated from paraffin-embedded tumor tissue sections. These findings were consistent with peripheral T-cell lymphoma of cytotoxic/suppressor phenotype, resembling the phenotype of T-cell large granular cell leukemia. To the authors' best knowledge, this represents the first reported case of primary brain T-cell lymphoma with a cytotoxic/suppressor immunophenotype. A brief review of the literature of primary brain T-cell lymphoma is also presented.
Assuntos
Neoplasias Encefálicas/patologia , Linfoma de Células T Periférico/patologia , Subpopulações de Linfócitos T/patologia , Linfócitos T Citotóxicos/patologia , Linfócitos T Reguladores/patologia , Idoso , Idoso de 80 Anos ou mais , Antígenos CD/análise , Biomarcadores Tumorais/análise , Encéfalo/patologia , Neoplasias Encefálicas/química , Neoplasias Encefálicas/genética , DNA de Neoplasias/análise , Evolução Fatal , Feminino , Rearranjo Gênico do Linfócito T/genética , Genes Codificadores dos Receptores de Linfócitos T/genética , Humanos , Imuno-Histoquímica , Linfoma de Células T Periférico/química , Linfoma de Células T Periférico/genética , Imageamento por Ressonância Magnética , Reação em Cadeia da Polimerase , Subpopulações de Linfócitos T/química , Linfócitos T Citotóxicos/química , Linfócitos T Reguladores/química , Tomografia Computadorizada por Raios XRESUMO
We report a case involving a 45-year-old man with a 12-year history of Wegener granulomatosis, who developed a carcinosarcoma of the urinary bladder after long-term cyclophosphamide therapy. Cyclophosphamide is well recognized as an etiologic agent for urothelial carcinoma of the urinary bladder. However, only 5 cases of carcinosarcoma of the urinary bladder following cyclophosphamide therapy have been reported. We used loss of heterozygosity studies and microsatellite markers to define the molecular basis of this rare neoplasm. These studies revealed evidence supporting a monoclonal origin for the 2 components of this tumor. We also demonstrated allelic loss of chromosome 9p. This loss associated with carcinosarcoma of the urinary bladder is in agreement with previous studies, suggesting a possible role for the tumor suppressor gene p16 in the pathogenesis of this tumor.