Disease relevance of Lymphoma, T-Cell, Cutaneous

• The T-cell-receptor alpha-chain gene was cloned and sequenced from a cell line derived from the advanced-stage cutaneous T-cell lymphoma, and the polymerase chain reaction was used to search for this rearrangement of the alpha-chain gene in tissues obtained earlier that were affected by Hodgkin's disease or lymphomatoid papulosis [1].
• Treatment of cutaneous T-cell lymphoma (mycosis fungoides) with 13-cis-retinoic acid [2].
• Since certain compounds prevent experimental carcinogenesis by elevating the levels of glutathione and phase II detoxication enzymes, we compared the potencies of several inducers with their ability to inhibit basal levels of HIV-1 replication in H9 cutaneous T-cell lymphoma cells [3].
• Sézary syndrome (SzS) is an advanced form of cutaneous T-cell lymphoma characterized by peripheral blood involvement, impaired cell-mediated immunity, and T-helper 1 (TH1) cytokine production [4].
• Primary CD30(+) cutaneous T-cell lymphomas (CTCLs) represent a spectrum of non-Hodgkin's lymphomas (NHLs) that have been well defined at the clinical, histologic, and immunologic level [5].

High impact information on Lymphoma, T-Cell, Cutaneous

• Treatment of cutaneous T-cell lymphoma with beta carotene [6].
• These results suggest that IL7 may, therefore, represent an important cytokine in the physiopathology of cutaneous T cell lymphoma [7].
• Circulating monocytes disappeared within 1 wk in patients with cutaneous T cell lymphoma or with rheumatoid arthritis during continuous CldAdo infusion [8].
• Cutaneous T-cell lymphoma and calcitriol and isotretinoin treatment [9].
• Treatment of cutaneous T-cell lymphoma by retinoids and calcitriol [10].

Chemical compound and disease context of Lymphoma, T-Cell, Cutaneous

• Remission of cutaneous T-cell lymphoma with combined calcitriol and acitretin [11].
• Isotretinoin in cutaneous T-cell lymphoma [12].
• To determine whether this biomodulatory effect could be recapitulated in vivo, we treated 14 patients with relapsed or refractory cutaneous T-cell lymphoma with escalating doses of bexarotene (75 mg/day-300 mg/day) and denileukin diftitox (18 mcg/kg per day x 3 days every 21 days) in a phase 1 trial [13].
• An investigation of 2'-deoxycoformycin in the treatment of cutaneous T-cell lymphoma [14].
• Phase II trial of 2-chlorodeoxyadenosine for the treatment of cutaneous T-cell lymphoma [15].

Biological context of Lymphoma, T-Cell, Cutaneous

• Interleukin-7 (IL-7) and IL-15 have been recently identified as growth factors for cutaneous T-cell lymphoma (CTCL) cells, and they protect these cells from cell death [16].
• Among the skin lesions tested, MS-1 antigen expression by endothelial cells of continuous origin is frequently observed in wound healing tissue, in cutaneous T-cell lymphoma, in psoriasis, and in melanoma metastasis, ie, in 100%, 80%, 71%, and 71% of cases, respectively [17].
• Arsenic trioxide induces apoptosis of cutaneous T cell lymphoma cells: evidence for a partially caspase-independent pathway and potentiation by ascorbic acid (vitamin C) [18].
• CD4 + /CD7- cell counts were significantly higher in patients with advanced cutaneous T cell lymphomas than in patients with early cutaneous T cell lymphomas [19].
• Application of the new FISH assays to a series of 24 angioimmunoblastic and 12 cutaneous T-cell lymphomas confirmed the cytogenetic evidence of lack of breakpoints in the TCRA/D or TCRB locus [20].

Anatomical context of Lymphoma, T-Cell, Cutaneous

• Long-term growth of lymphoblastoid T cells from tissue samples from six of six patients with cutaneous T-cell lymphoma (CTCL) and six of six patients with acute T-lymphoblastic leukemia (ALL) has been achieved by using partially purified mitogen-free human T-cell growth factor (pp-TCGF) [21].
• Functional characterization of neurotensin receptors in human cutaneous T cell lymphoma malignant lymphocytes [22].
• In patients with cutaneous T-cell lymphomas (CTCL), soluble interleukin-2 receptor serum levels (sIL-2R) were determined by ELISA technique, and natural killer cell (NK) activity, by a 4-h chromium-51 release assay [23].
• The addition of interleukin-12 to cutaneous T cell lymphoma patient peripheral blood cells resulted in the production of interferon-gamma (mean = 7914 pg per ml +/- 2161, n = 15) as did interleukin-2 alone (mean = 7222 pg per ml +/- 2228, n = 15) [24].
• We have previously demonstrated that peripheral blood mononuclear cells from patients with Sézary syndrome, the leukemic form of cutaneous T-cell lymphoma which is accompanied by erythroderma and lymphadenopathy, have a Th2 cell cytokine [interleukin 4 (IL-4) and interleukin 5] production pattern [25].

Gene context of Lymphoma, T-Cell, Cutaneous

• In this study we investigated the role of interleukin-15 (IL-15) in the immunobiology of cutaneous T-cell lymphoma (CTCL) cells [26].
• Interferon-alpha resistance in a cutaneous T-cell lymphoma cell line is associated with lack of STAT1 expression [27].
• Amplification and overexpression of JUNB is associated with primary cutaneous T-cell lymphomas [28].
• Functional expression of the eotaxin receptor CCR3 in CD30+ cutaneous T-cell lymphoma [29].
• Costimulation of cutaneous T-cell lymphoma cells by interleukin-7 and interleukin-2: potential autocrine or paracrine effectors in the Sézary syndrome [30].

Analytical, diagnostic and therapeutic context of Lymphoma, T-Cell, Cutaneous

• TCR delta 1 cellular expression was assessed in skin biopsy specimens of 104 individuals with cutaneous T-cell lymphoma by immunohistochemistry [31].
• Radioimmunotherapy of patients with cutaneous T-cell lymphoma using an iodine-131-labeled monoclonal antibody: analysis of retreatment following plasmapheresis [32].
• The immunogenic epitope of cTAGE-1 was determined by using epitope mapping and sera of two cutaneous T cell lymphoma patients [33].
• We conclude that cTAGE-1 and cTAGE-5 are new cancer germline antigens and that tumor-specific splicing of cTAGE genes may lead to further candidate proteins for specific immunotherapy of cutaneous T cell lymphoma and other malignancies [33].
• CONCLUSIONS: A first generation hypoxic cytotoxin, SR 4233, was able to enhance the tumor growth delay produced by radioimmunotherapy in severe combined immunodeficient phenotype mice with human cutaneous T cell lymphoma xenografts [34].

References