Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.24.11 (CD10)
 9,792 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 31 year-old male who was treated with radiation under the diagnosis of malignant lymphoma was admitted to our hospital because of systemic erythema and tumor of bilateral upper arms in October, 1987. Leucocyte count of peripheral blood showed 4,400/microliters with 36% leukemic cells and bone marrow was hypercellular with 85.6% leukemic cells. Leukemic cells were negative for peroxidase reaction and lineage specific monoclonal antibodies such as CD3, CD4, CD8, CD10, CD19 and CD20. T cell receptor (TCR) delta gene was rearranged but TCR beta, TCR gamma and immunoglobulin (Ig) genes were in germline configuration. He was treated with combination regimen of doxorubicin, vindesine, prednisolone and L-asparaginase, and complete remission was obtained. These observations suggest that TCR delta gene rearrangement is useful for determination of clonality in cases without rearrangements of the other TCR and Ig genes.
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PMID:[T cell receptor delta chain gene rearrangement in acute unclassified leukemia]. 260 18

1. We have investigated the mechanism of capsaicin-induced mouse ear oedema compared with that of arachidonic acid (AA)-induced ear oedema, and evaluated the possible involvement of neuropeptides in the development of capsaicin-induced oedema. 2. Topical application of capsaicin (0.1-1.0 mg per ear) to the ear of mice produced immediate vasodilatation and erythema followed by the development of oedema which was maximal at 30 min after the treatment. This oedema was of shorter duration with less swelling than AA-induced oedema (2.0 mg per ear). 3. Capsaicin-induced ear oedema was unaffected when inhibitors of arachidonate metabolites including platelet activating factor (PAF) were administered before capsaicin (250 micrograms per ear) application, while these agents significantly prevented AA-induced oedema. Dexamethasone, histamine H1 and/or 5-hydroxytryptamine (5-HT) antagonists, and substance P (SP) antagonists were effective in inhibiting both models. Furthermore, a Ca(2+)-channel blocker and the capsaicin inhibitor, ruthenium red, were effective inhibitors of capsaicin oedema but had no effect on AA-induced oedema. 4. Phosphoramidon (50 micrograms kg-1, i.v.), an endopeptidase inhibitor, markedly (P < 0.001) enhanced only capsaicin-induced ear oedema, but bestatin (0.5 mg kg-1, i.v.), an aminopeptidase, failed to enhance oedema formation. 5. Neuropeptides (1-100 pmol per site) such as rat calcitonin gene-related peptide (CGRP), SP, neurokinin A (NKA), and vasoactive intestinal peptide (VIP), which are released from capsaicin-sensitive neurones, caused ear oedema by intradermal injection. Furthermore, a synergistic effect of CGRP (10 fmol per site) and SP (10 pmol per site) on oedema formation was observed. 6. The oedema induced by neuropeptides was significantly (P<0.05 or P<0.001) inhibited when cyproheptadine (20 mg kg-1, p.o.), a histamine H, and 5-HT antagonist, was administered before injection. In contrast, nifedipine (50 mg kg-1, p.o.), a Ca2+-channel blocker, and indomethacin(10 mg kg-1, p.o., except for NKA), a cyclo-oxygenase inhibitor, had little effect on neuropeptide induced oedema.7. These results suggest that the mechanism of capsaicin-induced ear oedema is different from that of AA-induced oedema and suggest that the development of capsaicin-induced ear oedema is primarily mediated by neuropeptides. The neuropeptides released after activation of sensory nerves cause an increase of vascular permeability by interactions with endothelial cells and by histamine (and 5-HT)release from mast cells.
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PMID:Profile of capsaicin-induced mouse ear oedema as neurogenic inflammatory model: comparison with arachidonic acid-induced ear oedema. 750 28

The prognosis and clinical and biological characteristics of infant leukemia differ from those of leukemia in children 1 year or older. We reviewed the charts of patients younger than 1 year in whom leukemia was diagnosed from January 1981 through December 2003 at our institution. Fourteen infants had leukemia, 6 had acute lymphoblastic leukemia (ALL), and 8 had acute myeloid leukemia (AML). The age of patients at diagnosis ranged from 2 to 11 months. Five of 8 AML patients presented with cutaneous manifestations, such as erythema and nodules, at diagnosis. Central nervous system (CNS) involvement was seen in 1 AML patient at diagnosis. Hyperleukocytosis of more than 50 x 10(9)/L was seen in 4 of 6 ALL patients and in 4 of 8 AML patients at diagnosis. All ALL patients showed a morphological diagnosis of L1 using the French-America-British classification system. For patients with AML, the morphological diagnoses were M0 for 1 patient, M2 for 1 patient, M4 for 2 patients (1 with eosinophilia), M5b for 2 patients, and M7 for 2 patients. One patient showing M7 morphology had Down syndrome. Surface markers were examined in 5 of 6 ALL patients and all AML patients. Five ALL patients showed a B-cell precursor immunophenotype. Two of 5 patients with ALL had CD10-positive leukemic cells and 3 of 5 patients with ALL had CD10-negative leukemic cells. All AML patients were positive for CD13 or CD33 or both. Three of 5 patients with ALL showed abnormal chromosomes related to 11q. Six of 7 patients with AML showed abnormal karyotypes. MLL gene rearrangements were seen in 3 (2 ALL, 1 AML) of 5 (2 ALL, 3 AML) patients. Serum immunoglobulin M levels were increased in 9 of 14 patients. Complete remission (CR) was achieved in all infants with ALL. Three patients relapsed and then died of the original disease. One of these 3 patients died after cord blood transplantation. Three ALL patients are alive without leukemia. CR was achieved in 6 of 8 AML patients. Four of 6 patients are alive without leukemia. Infant leukemia patients in our institution had some special features. CNS involvement at diagnosis was seen in only 1 patient and serum IgM levels were higher than those in children whose leukemia was diagnosed at 1 to 10 years of age.
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PMID:Clinical aspects of infant leukemia--experiences of a single institution of Japan: high level of serum immunoglobulin M in infant leukemia. 1641 15

Dear Editor, Cutaneous metastases (CM) are detected in about 0.6-10.4% of patients with an internal malignancy (1-3). Excluding melanoma, breast and lung carcinomas are the main source of CM in women and men, respectively (1,4,5). CM can have different clinical features, and a diagnosis of CM is usually suspected before performing a biopsy. However, this can be a pitfall for clinicians when the clinical presentation is not the typical inflammatory nodule or mass. Herein we report 2 cases of cutaneous metastases of breast carcinoma, initially treated as a common skin infection. Case 1 A 51-year-old Caucasian woman presented to our Institute with a four-month history of diffuse and erythematous pustular, lesions on the right arm that were painless and non pruritic (Figure 1). The patient had undergone excision for a breast adenocarcinoma (stage IIIA) 5 years earlier. An initial diagnosis of folliculitis was established, and the patient started systemic and topical antibiotics without any improvement. Based on the clinical features and the patient medical history, we performed a skin biopsy. Pathologically dermal nests of tumor cells, arranged in a glandular-like pattern and involving the perifollicular and follicular areas (Figure 2, Figure 3), were highlighted. The tumor cells were positive to cytokeratin (CK) 7, CK19, and carcinoembryonic antigen (CEA) and negative for CK20, CK5/6, CD10, and thyroid transcription factor-1 (TTF-1) (Figure 4). According to the clinical history and pathology, a final diagnosis of folliculotropic metastatic breast carcinoma was established. Unfortunately, the patient died after 10 months. Case 2 A 61-year old Caucasian woman presented to our Department with a two-month history of pink/violet macular lesions with diffuse telangiectasia on the left breast and arm (Figure 5, Figure 6). Five years earlier she had undergone excision for a breast adenocarcinoma (stage II A). A previous diagnosis of cellulitis had been made, and systemic antibiotic therapy had been started without any improvement. Based on the clinical features and the patient medical history, a punch biopsy was performed. Examination of skin biopsy showed a diffuse, sclerotic, and mixoid stroma with several dense ectatic lymphatic vessels (Figure 7, Figure 8). The dermal and hypodermal lymphatic lumens were filled with neoplastic cells. Thus, a diagnosis of cutaneous lymphangitis carcinomatosa (CLC) was established. Unfortunately, the patient died after 8 months. Discussion CM are present after breast carcinoma in about 23.9% of patients, often involving the chest and abdomen and manifesting on average 5 years after surgical removal of the first malignancy (1,6). CM of breast cancer are usually solitary or multiple nodular pinkish lesions (ranging between 1 and 3 cm) (1). However, several clinical features have been reported in the literature, including telangiectatic carcinoma, erythema-like, erythema annulare centrifugum-like, morphea-like, erysipelas-like, dermatofibroma-like, herpes-zoster-like, and alopecia-like lesions (1,7-10). Clinical and pathological images of folliculitis-like metastases are rarely reported in the literature, especially after breast cancer (11,13) Clinically, folliculitis-like metastases could resemble a zosteriform-like metastatic lesion (7,14,15) although they do not follow a dermatome and are pustular lesions rather than violaceous indurate papules and/or nodules (13,14) Pathologically, our cases showed an infiltration of the dermis and pilosebaceous units growing through the pilosebaceous unit in a "pseudo-eruptive way". In this regard, folliculitis-like CM could be similar to alopecia neoplastica, where the metastatic process involves and destroys the pilosebaceous units completely, leading to scarring alopecia (9,10). However, in our case, the pilosebaceous unit was still slightly recognizable, and clinically there were no scar-like features. The mechanism of folliculitis-like metastasis formation is currently unknown. As reported in zosteriform-like metastases, the lymphatic and hematogenous spread of malignant cells or the koebnerization at the site of a previous viral and/or bacterial infection could lead to metastasis (7,14-16). However, unlike zosteriform-like metastases, the spread of neoplastic cells from the dorsal root ganglia was not a plausible mechanism of metastasization in our cases because of the absence of dermatome involvement. Furthermore, there were no signs of possible koebnerization in a previous bacterial and/or viral infection site (7,13) In our opinion, folliculitis-like metastasis may be a result of the skin extruding malignant cells through the pilosebaceous unit to limit the neopalstic proliferation. This could explain the clinical and pathological features of folliculitis-like metastasis. Alternatively, the adnexotropic behavior of malignant cells may be explained by homing mechanisms, involving the up-regulation of the intercellular adhesion molecule 1 (ICAM-1) on the follicular epithelium, such as folliculotropic mycosis fungoides (17). In our patient, the folliculitis-like eruption was the first sign of recurrence after 5 years of disease-free survival. It is evident that the unusual folliculitis-like eruption of CM led to a delay in the diagnosis. CLC is a rare presentation of skin metastasis, characterized by an occlusion of dermic lymphatic vessels by neoplastic cells (18). CLC has been reported in the literature in association with several malignancies, including lung, breast, and ovarian cancer (19). CLC shows pink/violet macular lesions with diffuse telangiectasias, often associated with itching and burning sensation. The main differential diagnoses are erysipelas and cellulitis. However, CLC is not associated with fever, chills, and leukocytosis. Furthermore, CLC shows no response to antibiotic therapies. Several clinicopathological types of cutaneous metastasis have been reported in the literature, including telangiectatic metastatic breast carcinoma (TMBC) and carcinoma erysipelatous (CE). TMBC is characterized by yellowish/reddish or violaceous papulo-vesicular lesions. CE usually shows blistering erythematous eruptions resembling erysipelas. However, CLC, TMBC, and CE are different clinical expressions of the same metastatic process, pathologically characterized by edema of the dermis and ectatic lymphatic vessels. Positivity to CD31 and podoplanin in the endothelial cells shows that the tumor metastatises predominantly via lymphatic vessels (20). In conclusion, we stress that every cutaneous lesion should be studied and examined carefully in patients with a personal history of cancer. Indeed, a correct diagnosis remains the pivotal point for a better management of these patients.
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PMID:Folliculotropic Cutaneous Metastases and Lymphangitis Carcinomatosa: When Cutaneous Metastases of Breast Carcinoma Are Mistaken for Cutaneous Infections. 2747 79

Exposure of human skin to ultraviolet (UV) radiation causes significant damage to that tissue. The effects of UV on the skin mainly include acute inflammation (erythema/edema) and abnormal keratinization wherein prostaglandin E2 (produced by cyclooxygenase-2), interleukin-8 and transglutaminase 1 (a major regulatory factor of keratinization) play pivotal roles. Later phases of UV-induced skin reactions include hyperpigmentation, wrinkle formation and carcinogenesis, the former two being associated with the UVB-induced production and/or secretion of endothelin-1, stem cell factor and granulocyte-macrophage colony-stimulating factor by keratinocytes in the epidermis. Those paracrine factors then stimulate expression of the critical melanogenic enzyme tyrosinase by melanocytes in the epidermis and increase expression of neprilysin, an enzyme that degrades elastin, by fibroblasts in the dermis. This review summarizes the biological effects of the xanthophyll carotenoid astaxanthin, which prevents UV-induced cutaneous inflammation, abnormal keratinization and wrinkling as well as pigmentation of the skin even by its postirradiation treatment.
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PMID:The Xanthophyll Carotenoid Astaxanthin has Distinct Biological Effects to Prevent the Photoaging of the Skin Even by its Postirradiation Treatment. 3033 60