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Biomedical subjects

B Dreno

Publications and source records attributed to B Dreno.

At least 73 records · Page 4Linked to original sources
PubMed1995

[Lymphomatoid papulosis].

Lymphomatoid papulosis is a distinct entity in which recurring crops of haemorragic and necrotic papules display a cytologically malignant infiltrate. The aberrent cell is now generally accepted to be an active T helper phenotype. The expression of Ki-1 (CD30) on a significant portion of the infiltrating cells characterizes lymphomatoid papulosis and relates this disorder with Hodgkin's disease, mycosis fungoides and anaplasic T cell lymphoma which may be associated in 10 to 20% of lymphomatoid papulosis. The categorization of this disease as a benign disorder versus lymphoma remains controversial. Studies of T cell receptor gene rearrangement demonstrate clonality in many cases. So, this monoclonal population could have a malignant transformation induced by a triggering stimulus such as genetic translocation, or viral infection. Finally, recent opinions consider that lymphomatoid papulosis and Ki-1 (CD30) lymphomas are different parts of a clinical and histological spectrum constituted by cutaneous Ki-1 lymphoid infiltrates.

Antigens, CD↗
PubMed1995

HLA class II-restricted recognition of common tumor epitopes on human melanoma cells by CD4+ melanoma-infiltrating lymphocytes.

CD4+ T cell clones derived from lymphocytes infiltrating four human melanomas specifically recognized melanoma-derived tumor epitopes as shown by secretion of tumor necrosis factor (TNF) in vitro upon interaction with autologous melanoma cells, whereas they did not recognize HLA class II-expressing autologous lymphoblasts or HLA class II mismatched allogeneic melanoma cells. Specificity was further established by demonstrating that TNF responses to tumor cells were inhibited by HLA-DR or HLA-DQ monoclonal antibodies. Most of these clones cross-reacted with allogeneic melanoma cells expressing a potentially restricting HLA allele or a structurally similar one. These data show that shared epitopes of human melanoma cells presented on HLA class II molecules are frequently recognized by autologous CD4+ T lymphocytes.

Alleles↗
PubMed1995

[Gene therapy applied to melanoma].

Cellular immunotherapy combined with genetic therapy, a new therapeutic approach to melanoma, is aimed at destroying the tumour by stimulating the organism's immune defences (indirect method) or by transfecting genes directly into the tumoural cells (direct methods). The first method is the most widely used for melanoma. Lymphocytes extracted from the tumour are transfected with genes capable of increasing their cytotoxic action in situ when reinjected (TNF, interleukin 2, interferon gamma). Likewise, immunostimulation by genetic therapy can be applied to tumour cells with transfection, notably cytokins or genes inducing antigen expression on the susceptible surface to modify the tumour cells' immunogeneicity. This method uses oligonucleotide nonsense sequences with suicide genes replacing a suppressor gene. Clinical trials for genetic therapy on melanoma are still in the pilot stage. This clinical evaluation must take into account the patient's quality of life and treatment costs.

Genetic Therapy↗
PubMed1995

[Development of interferon antibodies during the treatment of skin diseases with low-dose recombinant interferon alpha-2a].

In this study, we determined the frequency of interferon antibodies in patients with skin diseases treated with low doses of recombinant interferon alpha 2a (1.5 - 18 x 10(6) IU). We assayed serum specimens from 181 patients with malignant melanoma or cutaneous T cell lymphomas (78 patients treated with recombinant interferon alpha 2a and 103 patients in control group) for interferon antibodies before treatment and every 6 months for at least 18 months. Neutralizing interferon alpha 2a antibodies were detected in 27 of 77 treated patients (35%), but none in control group (p < 10(-6)): 38.2% in melanoma and 12.5% in T cell lymphomas. However antibody formation was not correlated with nonresponse or with frequency of interferon antibodies in patients receiving the combined therapy: interleukin-2 and interferon alpha 2a.

Adult↗
PubMed1995

[Conjugal mycosis fungoides].

INTRODUCTION: The pathophysiology of mycosis fungoides remains uncertain but HTLV I or a similar virus could be involved. We observed a couple who developed mycosis fungoides suggesting the infectious hypothesis might indeed be valid. CASE REPORT: A 70-year-old man who had often travelled in foreign countries developed parapsoriasis en plaques, lymphomatoid papulosis and mycosis fungoides successively over a thirty year period. Several years after the first manifestation of mycosis fungoides, his wife also developed a single plaque of mycosis fungoides. The diagnosis was confirmed on pathology slides and immunohistochemistry tests as well as on the basis of T-receptor gene rearrangement in both patients. Search for HTLV I was negative using serology tests and PCR on circulating lymphocytes. COMMENTS: The epidemiological situation in our observation (several trips in foreign countries and the delayed development of mycosis fungoides in the wife) favours the hypothesis of an infectious mechanism. Search for HTLV I was unsuccessful with classical virology methods. Certain recent work suggests a virus similar but different from the HTLV I virus could be involved in the pathogenesis of mycosis fungoides.

Aged↗
PubMed1994

Presence of Epstein-Barr virus in cutaneous lesions of mycosis fungoides and Sézary syndrome.

It has been suggested that prolonged antigenic stimulation contributes to the development of epidermotropic cutaneous T cell lymphoma (CTCL), mycosis fungoides and Sézary syndrome, characterized by a cutaneous infiltration of proliferating helper T cells. Since Epstein-Barr virus (EBV) antibodies were increased in CTCL sera, we investigated a possible etiologic role for EBV in epidermotropic CTCL by looking for the EBV genome in 25 cutaneous biopsies of mycosis fungoides or Sézary syndrome and 12 reactional inflammatory skin lesions. The use of a non-isotopic in situ hybridization procedure based on the detection of Epstein-Barr encoded RNAs with biotinylated oligonucleotide probes (EBER) revealed 32% of the lesions with CTCL to be positive for EBV (3 in dermis, 3 in epidermis, 2 both in dermis and epidermis), as compared to no detection of the EBV genome in the reactional inflammatory skin lesions. Moreover, a combined hybridization (EBER probe) and immunochemistry technique (anti-CD3 or anti-Kil monoclonal antibody) permitted the identification of EBV in T cells of dermis and in keratinocytes, respectively. The identification of EBV in epidermotropic CTCL suggests that this virus could play a role in the development of these CTCLs, either as an etiological agent or more probably as a chronic activating agent. Indeed, the infection of keratinocytes by EBV could activate them and so induce the production of in situ cytokines (IL1a, IL6, TNFa) playing a role in the development of tumoral infiltrate.

Adult↗
PubMed1994

Serum selenium in melanoma and epidermotropic cutaneous T-cell lymphoma.

As several studies have demonstrated a relationship between decreased serum selenium concentrations and the frequency of certain cancers, we studied these concentrations in two kinds of cutaneous tumour cancer: melanoma and epidermotropic cutaneous lymphoma. We first determined the predictive value of the selenium assay for the frequency of recurrences in stage I and II melanomas and then considered the relationship between serum selenium concentrations before treatment and therapeutic response. Two hundred melanomas (81 stage I, 63 stage II, 56 stage III) and 51 epidermotropic cutaneous T-cell lymphomas (CTCL) (8 stage I, 24 stage II, 10 stage III, 9 stage IV) were included in the study. Selenium assays were performed by atomic absorption spectrophotometry (92 +/- 16 micrograms/l in 30 normal subjects). Our study showed decreased serum selenium concentrations for melanoma (81 +/- 27 micrograms/l) and lymphoma (78 +/- 36 micrograms/l) relative to disease severity. The concentration was significantly lower (76 +/- 22) for stage I and II melanomas with recurrence within 2 years (31 patients), compared to those without recurrence (113 patients) (p < 0.05). Before treatment, it was higher in CTCL with good response to treatment (89 +/- 36) than in those without response (62 +/- 30) (p < 0.01). This study thus demonstrates the prognostic value of selenium assays in the follow-up of melanoma and CTCL.

Adolescent↗
PubMed1994

[Combination of dacarbazine, vindesine and interferon alpha in the treatment of metastatic melanoma].

INTRODUCTION: The aim of this work was to study the effectiveness and safety of a combined therapy with dacarbazine, vindesine and alpha-interferon in the treatment of metastatic melanoma. PATIENTS AND METHODS: Thirty-one patients (20 with visceral metastases and 11 with regional skin and lymph nodes metastases) were treated with dacarbazine (400 mg/m2 i.v. every 28 days), vindesine (3 mg/m2 i.v. every 14 days) and recombinant interferon alpha 2b (Introna) 10 x 10(6) UI subcutaneously three times weekly. RESULTS: All patients at least received 3 cures of chemotherapy. The response rate was 22.6 p. 100 with an average of 3.6 months and an average deviation of 7.2 months. The responders were predominantly patients with lymph nodes (50 p. 100) and lung metastases (25 p. 100). Response was better in patients with no more than two metastatic sites. The treatment was well tolerated. DISCUSSION: This combined chemotherapy with 3 drugs not significantly increase either the response rate or its duration. However, the quality of life was good.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1993

Cutaneous anaplastic T-cell lymphoma in a patient with human immunodeficiency virus infection: detection of Epstein-Barr virus DNA.

The Epstein-Barr virus (EBV) genome exists in tumour cells of T-cell lymphomas in non-immunosuppressed patients. We identified EBV-DNA by in situ hybridization in a case of anaplastic T-cell lymphoma associated with acquired immunodeficiency syndrome (AIDS). EBV-DNA has been reported in AIDS-related Hodgkin's disease or B-cell lymphoma, but never in T-cell lymphoma. Although our results suggest that EBV could play a role in the development of these anaplastic T-cell lymphomas, the mechanism of EBV penetration into T-cells remains uncertain.

DNA, Viral↗
PubMed1993

Roferon-A in combination with Tigason in cutaneous T-cell lymphomas.

In cutaneous T-cell lymphomas (CTCL; mycosis fungoides and Sézary syndrome), the standard therapies tend to be effective but not curative. Single drug therapy with either interferon-alpha or retinoids shows a response rate of about 45%. In this article, we report the results obtained in the treatment of CTCL with a combined therapy. To date, four clinical studies have been carried out using a combination of low doses of interferon-alpha and retinoids for treatment in the early stages of CTCL. The mechanism of action of this combination therapy is unknown.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1993

[Combination of fotemustine-dacarbazine and interferon alpha in the treatment of metastatic malignant melanoma].

In the treatment of disseminated malignant melanoma (DMM), the results obtained with fotemustine associated or not with dacarbazine are promising and those obtained with interféron alpha are also interesting. Therefore, we have investigated the efficacy and the toxicity of a combined chemotherapy with fotemustine-dacarbazine and interferon alpha in DMM. We present in this work our results on 44 patients who entered into this opened study. 37 patients were evaluable. 29 (78.4 p. 100) had previously received one or more cytotoxic chemotherapy. The regimen consisted of an induction treatment with fotemustine (100 mg/m2) on days 1.8, and 60 dacarbazine (400 mg/m2) on days 1, and 60 and subcutaneous injections of interféron (9.10(6) UI) alpha three times weekly. Responding and stabilized patients were given maintenance treatment with a monthly infusion of fotemustine (100 mg/m2) and dacarbazine (400 mg/m2) and interferon alpha carried on at the same dose. The response rate was 10.8 p. 100 (3 PR + 1 CR). Responses have depended on metastatic sites (cerebral site 18,2 p. 100). The median duration of response was 28 weeks. Toxicity was mainly hematologic and was acceptable. These results are not as good as those reported before with fotemustine and dacarbazine. Even if reasons related to patients and protocol could be discussed, the association of interferon alpha, fotemustine and dacarbazine seems devoid of interest during induction treatment.

Adult↗
PubMed1993

[Methylprednisolone versus prednisolone methylsulfobenzoate in pemphigoid: a comparative multicenter study].

Bullous pemphigoid is a bullous skin disease associated with basal membrane antibodies. At present, the first treatment of these lesions is with corticosteroids. In this randomized study we compared the clinical results obtained with methylprednisolone (MePr) in 28 patients and with prednisolone methylsulfobenzoate (MsPr) in 29 patients. Both drugs were administered orally in daily doses of 1 to 1.5 mg/kg bodyweight. Three clinical data were examined: the number of bullous lesions, the intensity of pruritus and the extent of erythema after 5 then 10 days of treatment. After 10 days, the number of bullous lesions had decreased by 83 p. 100 with MePr and by 78 p. 100 with MsPr, and the decrease of pruritus had been significantly more pronounced in the MePr group than in the Ms group (p < 0.05). There had been no difference between treatments in the regression of erythema. Altogether, good results were obtained in 22/28 patients under MsPr (78.6 p. 100) and 18/29 patients under MePr (62.1 p. 100). This raises the question of the value of pharmacokinetic studies not only with these two corticosteroids, but also with prednisone which seems to be better absorbed.

Administration, Oral↗
PubMed1992

Induction of myelo-monocytic My7 antigen (CD13) expression by interferon-alpha in basal cells of cutaneous T-cell lymphomas.

The My7 antigen that is expressed on the basal cells in normal skin and inflammatory disorders is absent in the lesions of cutaneous T-cell lymphoma (CTCL). Induction of My7 expression in basal cells in the cutaneous lesions of 12 patients with mycosis fungoides and three with Sézary syndrome treated with interferon-alpha 2a (IFN-alpha 2a) for 10 months was investigated. Biopsies were taken from the same area before treatment and after 2, 6 and 10 months of therapy with IFN-alpha 2a. My7 antigen was expressed on the basal cells only in those patients who showed either a complete or partial response to therapy with IFN-alpha 2a.

Antigens, CD↗
PubMed1992

Zinc salts effects on granulocyte zinc concentration and chemotaxis in acne patients.

To explore the mechanism by which zinc acts on cutaneous inflammatory lesions, we studied granulocyte zinc levels and in vitro polymorphonuclear leukocyte chemotaxis in 20 acne patients before and after 2 months of zinc therapy (200 mg/day zinc gluconate). The zinc level was assayed by flame absorption spectrophotometry and chemotaxis was performed by agarose assay. After 2 months of treatment, a significant decrease in granulocyte zinc level associated with inhibition of chemotaxis (r = 0.69) was observed in 16 patients. This suggests that zinc anti-inflammatory action is related to inhibition of polymorphonuclear leukocyte chemotaxis induced by a decreased granulocyte zinc level.

Acne Vulgaris↗
PubMed1992

[Changes in cutaneous zinc during skin aging].

Variations of epidermal zinc concentration with aging were studied by measuring zinc levels in the epidermis of two groups of healthy subjects: group A aged less than 35 years; group B aged more than 65 years. The epidermis was obtained from a suction blister, and zinc levels measurements were performed by absorption spectrophotometry. There was a significant decrease (p less than 0.01) of epidermal zinc concentration with aging, and zinc contents of the epidermis were the same in men and women. On the other hand, no significant difference was found in zinc blister fluid levels between the two groups, confirming the absence of relationship between plasma zinc and epidermal zinc. The decrease of epidermal zinc concentrations observed in elderly subjects might be due to a decrease of enzyme activities in the epidermis induced by aging; conversely, a low epidermal zinc level might induce, by itself, a fall in enzyme activities. Thus, zinc might play an important role in the development of alterations in keratinocytes with aging.

Adult↗