Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Enlargement of the cheeks may be due to a multitude of disorders, congenital, neoplastic, and in particular inflammatory. Congenital facial anomalies include cutaneous (and osseous) hemihypertrophy of the face and unilateral angiomatous malformations (e.g. Sturge-Weber-Krabbe Syndrome). Buccal enlargement due to dermal tumours include localized haemangiomas and lymphangiomas, lipomas and other benign connective tissue neoplasms, generalized disorders of the lymphatic or reticuloendothelial system including mycosis fungoides, reticulum cell sarcoma and other soft tissue malignancies, and cutaneous manifestations of malignant haemoblastoses, in particular chronic lymphatic leukaemia. Within the very large group of inflammatory skin swellings of the face a review is made of some bacterial pyodermias, severe forms of acne vulgaris, herpes zoster, lupus vulgaris, erysipelas, rosacea, steroid dermatitis, lupus erythematosus (discoid and systemic), toxic dermatitis, allergic eczema, urticaria, Quincke's oedema, and the Melkersson-Rosenthal syndrome. The importance of prevention and early detection of steroid-induced dermatitis is emphasized. This disorder, which is a pseudo-inflammatory disfiguring complication of prolonged topical steroid abuse, ranks in frequency with the skin problems most often seen in dermatological practice.
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PMID:[Differential diagnosis of facial skin swellings (author's transl)]. 37 16

In Jamaican children infective dermatitis is a chronic eczema associated with refractory nonvirulent Staphylococcus aureus or beta-haemolytic streptococcus infection of the skin and nasal vestibule. 14 children between the ages of 2 and 17 years with typical infective dermatitis, attending the dermatology clinic at the University Hospital of the West Indies in Jamaica, were tested for antibody to human T-lymphotropic virus type 1 (HTLV-1). All were seropositive, whereas 11 children of similar age with atopic eczema were all negative. In 2 of 2 cases of infective dermatitis, the biological mother was HTLV-1 seropositive. None of the 14 patients showed signs of adult T-cell leukaemia/lymphoma, though experience with previous cases of infective dermatitis indicates the possibility of such progression.
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PMID:Infective dermatitis of Jamaican children: a marker for HTLV-I infection. 167 Nov 53

Adult T cell leukemia, an endemic disease in the southwestern part of Japan, is characterized (1) by a short survival, (2) by leukemic T cells in peripheral blood that have lobulated nuclei and helper/inducer surface phenotypes, and (3) by cutaneous involvement. A 34-year-old man who had a history of atopic dermatitis was seen at our clinic because of generalized erythroderma and lymphadenopathy. His clinical course was rather chronic as compared with that of prototypic adult T cell leukemia; however, typical leukemia cells were observed in specimens taken from his peripheral blood and skin. The diagnosis of adult T cell leukemia was established by the patient's positive serum antibody reaction to adult T cell leukemia-associated antigen and monoclonal integration of virus genome in the patient's leukemia cell DNA. Interesting and characteristic of the patient were the very high levels of serum immunoglobulin E. With the use of an in vitro immunoglobulin production system with mitogen, the patient's T lymphocytes enhanced the differentiation of B cells, both from the patient and from a normal adult, into immunoglobulin E-producing cells. Therefore it may be speculated that T cells functioning as immunoglobulin E-specific helpers were transformed to leukemia cells by human T-lymphotropic virus type I. Continuous antigen stimulation of the patient's atopic diathesis also may be a factor.
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PMID:Adult T cell leukemia: a case with massive hyperimmunoglobulinemia E. 252 15

Natural-killer (NK)-cell activity was measured in the peripheral blood of twenty patients with atopic dermatitis and in a group of thirteen age-matched non-atopic controls (nine subjects on thirteen occasions). The method uses a chromium-release assay with the human leukaemia cell line, K562, labelled with 51Cr as the target cell. A highly significant reduction in NK-cell activity was found in the patients with atopic dermatitis.
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PMID:Natural-killer-cell activity in atopic dermatitis. 648 14

The lymphoid component of skin infiltrates from 6 cases of mycosis fungoides and 2 cases of T cell chronic lymphatic leukaemia consisted almost exclusively of T lymphocytes with abnormally high E receptor expression. Such T cells were also found to dominate the skin infiltrates from 10 patients with severe atopic dermatitis. Blood T lymphocyte counts from all types of patients were within the normal range, but even the blood T lymphocytes of the patients had a strong E receptor expression. The bone marrow in atopic dermatitis and in mycosis fungoides showed normal T cell counts with normal E receptor expression. Supported by basic lymphocyte-kinetic considerations it is likely that the skin in T lymphoproliferative diseases is characterized by an abnormal ability to home and/or to trap T lymphocytes with strong E receptor expression.
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PMID:E receptor expression of T lymphocytes in T lymphoproliferative diseases. 698 Dec 1

Ten patients with atopic dermatitis and ten healthy control subjects, matched for age, sex, and skin color, were studied for their peripheral blood natural cell-mediated cytotoxic activity against K-562 human leukemia cell line target cells, using the sodium chromate Cr 51 release assay. There was a great reduction in the natural cytotoxic activity of the patients with atopic dermatitis compared with that of their respective control subjects; the patients with atopic dermatitis had a mean value of 41.9 alpha +/- 28.3% of that of the control subjects.
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PMID:Natural cell-mediated cytotoxic activity in the peripheral blood of patients with atopic dermatitis. 710 26

Fast antigen is a cell surface protein that mediates apoptosis. Using immunohistological, flow cytometry and electron microscopic analyses, we investigated the expression of Fas antigen on various skin tissues, and on cultured SV40-transformed human epidermal keratinocyte cell line KJD and human skin squamous cell carcinoma cell line HSC. The Fas antigen was widely distributed in skin components such as the keratinocytes in the lower portion of the epidermis, epidermal dendritic cells, endothelial cells, fibroblasts, apocrine glands, eccrine sweat glands, sebaceous glands, some normal melanocytes and infiltrating lymphoid cells. It was also strongly expressed on the keratinocytes of lichenoid eruptions seen in lupus erythematosus and lichen planus, and on the spongiotic or acanthotic epidermis seen in chronic eczema, adult T-cell leukaemia/lymphoma (ATLL) and atopic dermatitis. Its expression was closely correlated with lymphoid infiltrating cells and it was strongly expressed in lymphoid neoplastic cells, particularly ATLL cells, and fibroblasts seen in dermatofibroma. However, the antigen was not detected on basal cell epithelioma cells, some malignant melanomas or any junctional naevi. The cell lines KJD and HSC strongly expressed the Fas antigen, and crosslinking of the Fas antigen by an anti-Fas monoclonal antibody induced apoptosis of these cell lines. These results indicate that the apoptosis-mediating Fas antigen may play an important role in normal skin turnover and cell differentiation, in immune regulation of skin tumours, and in the pathogenesis of various skin diseases.
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PMID:Distribution of apoptosis-mediating Fas antigen in human skin and effects of anti-Fas monoclonal antibody on human epidermal keratinocyte and squamous cell carcinoma cell lines. 752 80

A 5-year-old girl was diagnosed as having idiopathic thrombocytopenic purpura (ITP) based on symptoms of nasal bleeding and purpura. The platelet count was 35,000/microliters without anemia or leukopenia. Micromegakaryocytes were observed in normocellular bone marrow without dyserythropoiesis or dysgranulopoiesis. She had periosteal fibroma of the rib and atopic dermatitis with elevated serum IgE. Prednisolone and azathioprine were administered but with no response. The cumulative dose of azathioprine was 20 g for 28 months. Nine years after the diagnosis of ITP, she was admitted because of dyspnea and anemia. The white cell count was 26,900/microliters with 17% monocytes. The hemoglobin was 3.9 g/dl and the platelet count was 9,000/microliters. Dyserythropoiesis, dysgranulopoiesis and micromegakaryocytes were observed in hypercellular bone marrow. The chromosome analysis demonstrated 47, XX, +21. She was diagnosed as having chronic myelomonocytic leukemia (CMMoL) and received bone marrow transplantation (BMT) from an HLA-identical sibling conditioned with high-dose busulfan and melphalan. After 17 months of remission, the disease recurred with an abnormal karyotype of 47, XX, +21, 7q+. Despite a second BMT conditioned with high-dose etoposide, cyclophosphamide and total body irradiation, she died of the disease. Refractory thrombocytopenia as a subgroup of myelodysplastic syndrome, rather than ITP, might have preceded the development of CMMoL, with the possibility of azathioprine-induced leukemia.
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PMID:[Chronic myelomonocytic leukemia developed 9 years after the diagnosis of idiopathic thrombocytopenic purpura in a child]. 807 97

Immunohistochemical staining of proliferating cell nuclear antigen (PCNA) was performed in skin from patients with various malignant and nonmalignant skin diseases using anti-PCNA monoclonal antibodies. The malignant diseases included squamous cell carcinoma (SCC), adult T lymphotrophic leukemia (ATL), mycosis fungoides, malignant melanoma and malignant lymphoma, and the nonmalignant diseases included severe treatment-resistant atopic dermatitis (AD), psoriasis vulgaris, verruca vulgaris, and others. The percentage of PCNA-positive cells (the labeling index, LI) was highest for the malignant diseases (56.5+/-7.1%). The LIs for severe treatment-resistant AD, psoriasis, and verruca vulgaris were also significantly higher than those for the normal control or nonlesional skin of the patients. The PCNA LIs were, however, not significantly elevated in eczema and contact dermatitis. The high PCNA LIs in severe AD and psoriasis vulgaris were considerably lower in the skin improved by treatment. Labeling with Ki67, a nuclear protein expressed in cycling cells, was also performed in skin from subsets of each patient group. The results were very similar to those found with PCNA labeling. PCNA-positive cells were found throughout the dermis as well as the basal layer in the malignant diseases, whereas they were found only in the basal layer in the nonmalignant diseases. The results suggest that in human skin diseases, the extent of staining for PCNA, which is a cofactor of DNA polymerase-delta and is essential for cell proliferation, correlates with the extent to which the disease is treatment-resistant. In addition, our findings suggest that the PCNA LI and distribution of PCNA-positive cells in the skin may be helpful in the early diagnosis of skin malignancies.
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PMID:Immunohistochemical staining of proliferating cell nuclear antigen (PCNA) in malignant and nonmalignant skin diseases. 1048 11

Endogenous cellular chromophores absorb ultraviolet A radiation (UVA, 290-320 nm), the major UV component of terrestrial solar radiation, leading to the formation of reactive oxidizing species that initiate apoptosis, gene expression and mutagenesis. UVA-induced apoptosis of T helper cells is believed to underlie the UVA phototherapy for atopic dermatitis and other T cell-mediated inflammatory skin diseases. We have evaluated the involvement of the Fas-Fas ligand (FasL) pathway in rapid UVA-induced apoptosis in human leukemia HL-60 cells. UVA-induced apoptosis was not inhibited by pretreatment with a neutralizing anti-Fas antibody, although the same UVA treatment initiated cleavage of caspase-8 and subsequent processing of Bid and caspase-3-like proteases. Inhibition of caspase-8 by Lle-Glu (OMe)-Thr-Asp(OMe)-fluoromethyl ketone completely blocked caspase-3 cleavage and apoptosis in UVA-treated cells, suggesting that apoptosis was initiated by the Fas pathway. This inference was supported by demonstrating that immunoprecipitates obtained from UVA-treated cells using anti-Fas antibody contained caspase-8 and Fas-associating protein with death domain (FADD). In addition, Fas clustering in response to UVA treatment was observed by immunofluorescence microscopy. These data support a mechanism for rapid, UVA-induced apoptosis in HL-60 cells involving initial formation of the Fas-FADD-caspase-8 death complex in an FasL-independent manner.
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PMID:Ultraviolet A radiation induces rapid apoptosis of human leukemia cells by Fas ligand-independent activation of the Fas death pathways. 1292 50


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