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)

The mechanism of the occurrence of natural antikeratin antibodies in human sera was studied using hybrid spleen cells obtained from experimentally naive or from immunized mice. Antikeratin antibodies were detected by enzyme-linked immunosorbent assay (ELISA) in 5.9-9.5% of the culture supernatants of fused spleen cells taken from naive mice. When mice were immunized with keratins, the number of supernatants containing antikeratin antibodies was increased to eight out of 51 (15.7%). When immunized with non-keratin materials such as activated human T cells, adult T-cell leukaemia cell lysates, and human T-cell lymphotropic virus type-I (HTLV-I), 16.7-20.8% of the supernatants were found to contain antikeratin antibodies by ELISA. The antikeratin antibodies in the supernatants showed cytoplasmic staining of keratinocytes in human as well as mouse skin by indirect immunofluorescence. The antibodies reacted with extracted human epidermal keratins by dot-blot and Western blot analysis. Most antikeratin antibodies in the supernatants did not show cross-reactivity with exogenous antigens used for immunization and vimentin-type intermediate-sized filaments. These findings demonstrate that B cells producing antikeratin antibodies are common in naive mice, and produce various types of antikeratin antibodies following specific activation with epidermal keratins and non-specific immunological stimuli.
Br J Dermatol 1990 Dec
PMID:Production of antikeratin autoantibodies by hybrid spleen cells of naive mice. 170 8

Stimulation of T cells by superantigenic bacterial toxins is selective for cells bearing particular B chain variable (VB) gene segments of T-cell receptor (TCR). In humans, staphylococcal exfoliating toxin (ExT) and toxic shock syndrome toxin-1 (TSST-1) are known to stimulate VB 2-bearing T cells and staphylococcal enterotoxin B (SEB) does not activate VB 2-bearing T cells. We examined the proliferative response of cutaneous T-cell lymphoma (CTCL) cells to ExT, TSST-1, and SEB. Leukemic VB 2.1-bearing CTCL cells were reactive to ExT and TSST-1, but not SEB. In addition, two leukemia CTCL-VB 2- cell samples (one of which was VB 8) showed no substantial response to ExT. Thus, it was shown that Sezary cells proliferate in response to bacterial superantigens in a manner that is restricted by their VB usage. The addition of interleukin-1 (IL-1) in combination with ExT enhanced the stimulative response of VB 2.1-bearing CTCL cells that were pre-cultured with ExT for 7 d, suggesting that IL-1 can be a co-factor for the stimulation. The present study indicates that the superantigen reaction occurs with CTCL cells and implies a possible involvement of bacterial toxins in the pathogenesis of CTCL.
J Invest Dermatol 1992 Jan
PMID:Stimulation of cutaneous T-cell lymphoma cells with superantigenic staphylococcal toxins. 172 39

We report the development of acute, tender, erythematous plaques in a 65 year old female with Myelodysplastic Syndrome transforming to Acute Myeloid Leukaemia. The clinical presentation strongly suggested Sweet's syndrome. Histopathological examination of the plaques showed a normal epidermis, dermal and subcutaneous oedema, and large numbers of polymorphs in the panniculus. The eruption responded quickly to systemic steroids, with recrudescence when steroid dosage was reduced. She remained symptom free when prednisolone dosage was reduced more slowly.
Australas J Dermatol 1991
PMID:Sweet's panniculitis. 178 56

Various samples from lymphoproliferative diseases in the skin were analyzed by Southern blotting technique with probes from the T cell receptor gene, immunoglobulin genes, and human T cell leukemia virus-I genome. Samples were taken from 10 mycosis fungoides (MF) patients, 1 parapsoriasis en plaque patient, 10 Adult T cell leukemia/lymphoma (ATL) patients, 1 cutaneous T cell lymphoma (CTCL) patient, 4 lymphomatoid papulosis (LP) patients, 4 B cell lymphoma patients, and 2 actinic reticuloid (AR) patients. In MF, the monoclonality of the T cells became detectable first in the skin when plaques develop to tumors then in lymph nodes, and finally in the blood lymphocytes, indicating this disease develops from local (skin) malignancy to systemic malignancy. In parapsoriasis en plaque, no monoclonality was detected in any sample. We could distinguish cutaneous ATL from the carrier state by detecting the T cell monoclonality and HTLV-I integration with these probes. One patient with CTCL showed detectable T cell monoclonality; 1 out of 4 patients with LP did the same. Four samples from patients with B cell lymphoma revealed detectable monoclonal rearrangement of immunoglobulin heavy and light chain genes. In AR, no monoclonality was detected in any sample. From these data, we conclude that DNA analysis is useful in determining the monoclonality, cell origin, and distribution of monoclonal cells from skin samples.
J Dermatol 1991 Nov
PMID:Characterization of the lymphoproliferative diseases in the skin by DNA analysis. 180 May 28

The intravenous administration of recombinant human granulocyte-macrophage colony-stimulating factor to three patients with leukemia who were receiving marrow aplasia-inducing chemotherapy resulted in the development of wide-spread erythematous macules and papules. The course of the eruption paralleled the time of infusion of the granulocyte-macrophage colony-stimulating factor. Skin biopsy specimens taken from two of the eruptions displayed characteristic changes consisting of a variable mixture of granulocytes and lymphocytes, increased number and size of dermal macrophages, mild to moderate epidermal exocytosis, intercellular edema, and rare dyskeratotic keratinocytes. Immunophenotypic analysis of one specimen was notable for keratinocyte intercellular adhesion molecule-1 expression. Administration of the recombinant human cytokine in pharmacologic doses is postulated to induce changes in the immunologic status of the skin, resulting in the expression of a cutaneous eruption.
Arch Dermatol 1991 Jan
PMID:Intravenous administration of recombinant human granulocyte-macrophage colony-stimulating factor causes a cutaneous eruption. 182 45

Leukaemic skin infiltration is uncommon in hairy-cell leukaemia (HCL), a neoplasm characterized by the presence of uniform mononuclear cells with cytoplasmic projections in the blood, bone marrow and spleen. A case is reported in which leukaemia cutis was a transient phenomenon, appearing soon after the onset of a continuous pyrexia associated with marked systemic upset which was subsequently shown to be due to pulmonary tuberculosis.
Clin Exp Dermatol 1991 May
PMID:Transient leukaemia cutis in hairy-cell leukaemia. 193 76

A case of Sweet syndrome in a patient with an acute myelomonocytic leukemia is reported. It is an unusual case simulating a facial erysipela. This case illustrates the difficulty in differentiating infection from Sweet syndrome in an immunocompromised patient. The negative cultures, ineffective antibiotics, and histopathologic examination results allowed the onset of corticosteroid therapy. The phagocytic function of the neutrophils studied by chemoluminescence was normal in the patient. The physiopathology of Sweet syndrome is discussed, in particular the role of cytokines in the accumulation of granulocytes.
Int J Dermatol 1991 Sep
PMID:Sweet syndrome associated with acute myelogenous leukemia. Atypical form simulating facial erysipelas. 142 59

We describe a patient with acute myelomonocytic leukemia who demonstrated leukemic cell infiltration to scratched wounds and scars from trauma. A 65-year-old Japanese woman developed low grade fever, headache and exanthema. Hematology testing disclosed leukocytosis of 95,600/mm3 with 65% monocytes and 9% blast cells. Infiltrated erythema and nodules were disseminated over most of her body. Moreover, linear scratched wounds and traumatic scars were indurated. Skin biopsy showed dense atypical mononuclear cell infiltration with monocytic characteristics. We discuss the possible reasons for the infiltration of leukemia cells into the wounds and scars from trauma.
J Dermatol 1991 May
PMID:Leukemia cutis in acute myelomonocytic leukemia: infiltration to minor traumas and scars. 193 54

Graft-versus-host disease (GVHD) is an immunologically mediated disease occurring most frequently after allogeneic bone marrow transplantation. The aim of this study was to evaluate the contribution of immunohistochemistry in the diagnosis of cutaneous GVHD. Patients transplanted for either leukemia or beta-thalassemia were included in the study. Skin lesions of acute and chronic GVHD were examined both by direct immunofluorescence to detect immunoglobulin deposits and by an avidin-biotin-peroxidase complex technique to evaluate the inflammatory cell infiltrate. Epidermal and dermal fluorescent bodies (IgG and IgM) were frequently found in both acute and chronic GVHD. Most of the infiltrating cells were CD3+ T lymphocytes, with CD8+ cells representing the major cell population invading the epidermis both in acute GVHD and in chronic lichenoid GVHD. A small proportion of the dermal cells were CD14+ macrophages; no B cells were detected. HLA-DR, but not HLA-DQ antigens, were variably expressed by keratinocytes in all cases of acute GVHD and in chronic lichenoid GVHD. KL-1, a monoclonal antikeratin antibody specific for the 56.5 KD acidic polypeptide usually present in suprabasal keratinocytes, stained all epidermal layers, including the basal layer. Langerhans cells were dramatically reduced in number in the epidermis of both acute and chronic lichenoid GVHD. It is concluded that immunohistologic analysis may be supportive in the diagnosis of acute and early chronic lichenoid cutaneous GVHD.
J Dermatol 1991 Jun
PMID:Immunohistochemistry of cutaneous graft-versus-host disease after allogeneic bone marrow transplantation. 193 60

The various clinical features of adult T-cell leukemia/lymphoma (ATL) are frequently accompanied by skin eruptions. Recently, a cutaneous type of ATL has been proposed by clinical studies. We analyzed the viral integration of human T-cell leukemia virus-I (HTLV-I) and monoclonal rearrangement of T-cell receptor (TCR) gene in blood lymphocytes and the cutaneous infiltrated cells of nine ATL patients with various clinical features and skin eruptions. We classified them by the results of Southern blot analysis and propose a cutaneous-type ATL accordingly. In two of them, we could detect the monoclonal integration of HTLV-I and T-cell monoclonality only in the skin but not in the peripheral lymphocytes. We also demonstrated the time course study in one patient. Clinicians should be aware of the HTLV-I positive cutaneous T cell lymphoma that can be named cutaneous-type ATL. Examination of viral integration and T-cell monoclonality in skin lesions is required to make an exact diagnosis of cutaneous ATL.
J Invest Dermatol 1991 Feb
PMID:Examination of HTLV-I integration in the skin lesions of various types of adult T-cell leukemia (ATL): independence of cutaneous-type ATL confirmed by Southern blot analysis. 199 79


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