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1. Inoue S, Miyamoto T, Yoshino T, Yamadori I, Hagari Y, Yamamoto O: Primary effusion lymphoma with skin involvement. J Clin Pathol; 2006 Nov;59(11):1221-2
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  • Primary effusion lymphoma (PEL) was once defined as a body cavity-based lymphoma without identifiable contiguous tumour mass, but is now recognised as an independent clinicopathological entity.
  • The histopathological findings showed a diffuse infiltration of large neoplastic B cells from the dermis to the subcutis.
  • After the disappearance of pericardial effusion without any treatment, she received several rounds of chemotherapy to resolve the skin eruption, but she finally died from multiple organ failure.
  • No tumour mass was observed during the course of her disease.

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  • (PMID = 17071811.001).
  • [ISSN] 0021-9746
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC1860519
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2. Nedrebø T, Karlsen TV, Salvesen GS, Reed RK: A novel function of insulin in rat dermis. J Physiol; 2004 Sep 1;559(Pt 2):583-91
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  • [Title] A novel function of insulin in rat dermis.
  • In this study we present a novel function of insulin in rat dermis.
  • We investigated local effects of insulin on interstitial fluid pressure (Pif), and capillary albumin leakage and pro-inflammatory cytokine production in skin and serum after intravenous lipopolysaccharide (LPS), tumour necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) challenge treated with a glucose-insulin-potassium regimen (GIK).
  • [MeSH-major] Dermis / drug effects. Insulin / pharmacology. Insulin / therapeutic use
  • [MeSH-minor] Animals. Edema / chemically induced. Edema / drug therapy. Extracellular Fluid / drug effects. Extracellular Fluid / physiology. Female. Lipopolysaccharides / toxicity. Rats. Rats, Wistar

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  • (PMID = 15235083.001).
  • [ISSN] 0022-3751
  • [Journal-full-title] The Journal of physiology
  • [ISO-abbreviation] J. Physiol. (Lond.)
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Insulin; 0 / Lipopolysaccharides
  • [Other-IDs] NLM/ PMC1665113
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3. Goedkoop AY, Kraan MC, Picavet DI, de Rie MA, Teunissen MB, Bos JD, Tak PP: Deactivation of endothelium and reduction in angiogenesis in psoriatic skin and synovium by low dose infliximab therapy in combination with stable methotrexate therapy: a prospective single-centre study. Arthritis Res Ther; 2004;6(4):R326-34
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  • [Title] Deactivation of endothelium and reduction in angiogenesis in psoriatic skin and synovium by low dose infliximab therapy in combination with stable methotrexate therapy: a prospective single-centre study.
  • Psoriasis and psoriatic arthritis are inflammatory diseases that respond well to anti-tumour necrosis factor-alpha therapy.
  • To evaluate the effects of anti-tumour necrosis factor-alpha treatment on expression of adhesion molecules and angiogenesis in psoriatic lesional skin and synovial tissue, we performed a prospective single-centre study with infliximab therapy combined with stable methotrexate therapy.
  • In addition, patients continued to receive stable methotrexate therapy in dosages ranging from 5 to 20 mg/week.
  • In addition, skin biopsies from a target psoriatic plaque and synovial tissue biopsies from a target joint were taken before treatment and at week 4.
  • We found some fluctuations in DAS response as compared with the change in PASI, with the latter exhibiting a steady decrease over time.
  • There was a significant reduction in the number of blood vessels in dermis and synovium at week 4.
  • In conclusion, low-dose infliximab treatment leads to decreased neoangiogenesis and deactivation of the endothelium, resulting in decreased cell infiltration and clinical improvement in psoriasis and psoriatic arthritis.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Arthritis, Psoriatic / drug therapy. Endothelium, Vascular / drug effects. Methotrexate / therapeutic use. Neovascularization, Pathologic / drug therapy. Psoriasis / drug therapy. Skin / pathology. Synovial Membrane / pathology
  • [MeSH-minor] Adult. Aged. Drug Therapy, Combination. Female. Humans. Immunohistochemistry / methods. Infliximab. Male. Middle Aged. Prospective Studies. Tumor Necrosis Factor-alpha / immunology. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 15225368.001).
  • [ISSN] 1478-6362
  • [Journal-full-title] Arthritis research & therapy
  • [ISO-abbreviation] Arthritis Res. Ther.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Tumor Necrosis Factor-alpha; B72HH48FLU / Infliximab; YL5FZ2Y5U1 / Methotrexate
  • [Other-IDs] NLM/ PMC464872
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4. Weisser H, Hartschuh W, Greiner A, Bischof M, Enk A, Helmbold P: [Merkel cell carcinoma--clinically often misjudged]. Dtsch Med Wochenschr; 2007 Jul 30;132(30):1581-6
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  • Merkel cell carcinoma is a rare, rapidly growing, highly malignant dermal tumor which occurs preferentially on light-exposed skin in advanced age.
  • The course of the disease is frequently characterized by the occurrence of lymph node metastases and local recurrences, even in the first year after removal of the primary tumour.
  • The five-year overall survival rate is only about 65 %, despite rigorous therapy.
  • The excision of the primary tumor is regarded as first-line therapy.
  • Adjuvant chemotherapy can be applied in this stage, as in small-cell bronchial carcinoma.
  • Despite good response to radiatiotherapy and chemotherapy, with at least prolonged recurrence-free intervals, Merkel cell carcinoma is rarely curable at the distant metastasizing stage.
  • Individually defined, aggressive treatment,including radiatiotherapy, may in future considerably improve the prognosis, especially in the early stages of the disease.
  • [MeSH-major] Carcinoma, Merkel Cell / pathology. Carcinoma, Merkel Cell / therapy. Neoplasm Recurrence, Local / pathology. Neoplasm Recurrence, Local / therapy. Skin Neoplasms / pathology. Skin Neoplasms / therapy
  • [MeSH-minor] Chemotherapy, Adjuvant. Combined Modality Therapy. Diagnosis, Differential. Humans. Immunohistochemistry / methods. Lymphatic Metastasis. Neoplasm Staging. Prognosis. Survival Rate

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  • (PMID = 17628844.001).
  • [ISSN] 1439-4413
  • [Journal-full-title] Deutsche medizinische Wochenschrift (1946)
  • [ISO-abbreviation] Dtsch. Med. Wochenschr.
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Germany
  • [Number-of-references] 50
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5. Boussen H, Zwik J, Mili-Boussen I, Rammeh N, Bouaouina N, Gritli S, el May A, Kammoun MR, Ouertani A, Ladgham A: [Therapeutic results of 5-fluorouracil in multiple and unresectable facial carcinoma secondary to xeroderma pigmentosum]. Therapie; 2001 Nov-Dec;56(6):751-4
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  • [Title] [Therapeutic results of 5-fluorouracil in multiple and unresectable facial carcinoma secondary to xeroderma pigmentosum].
  • [Transliterated title] Résultats thérapeutiques du 5-fluorouracile dans les carcinomes multiples ou non resécables de la face secondaires au xeroderma pigmentosum (XP).
  • Evaluation was done by clinical examination every two months for topical therapy and after every cycle for systemic treatment.
  • Median treatment duration was 12 months (2 to 36 months).
  • Treatment was well tolerated excluding episodes of pruritus in the treated areas.
  • We observed mainly superficial tumour regression followed by dryness and crusting.
  • In 5 cases, we performed biopsies after treatment showing in one case an extensive fibrosis with absence of tumour.
  • However in the remaining 4 cases, despite a superficial reduction of tumour and a reconstitution of the epidermis, viable and unmodified squamous cell carcinoma remained in the deeper dermis.
  • Despite a dissociation between a good cosmetic result and a relatively superficial effect, topical 5-FU represents a useful therapeutic option in multiple unresectable facial SCC in patients with XP.
  • Systemic chemotherapy is recommended in the event of more extended or profound lesions.
  • [MeSH-major] Antimetabolites, Antineoplastic / therapeutic use. Carcinoma, Squamous Cell / drug therapy. Carcinoma, Squamous Cell / secondary. Facial Neoplasms / drug therapy. Facial Neoplasms / secondary. Fluorouracil / therapeutic use. Skin Neoplasms / pathology. Xeroderma Pigmentosum / pathology

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  • (PMID = 11878102.001).
  • [ISSN] 0040-5957
  • [Journal-full-title] Thérapie
  • [ISO-abbreviation] Therapie
  • [Language] fre
  • [Publication-type] Clinical Trial; English Abstract; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; U3P01618RT / Fluorouracil
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6. Strachan AJ, Shiels IA, Reid RC, Fairlie DP, Taylor SM: Inhibition of immune-complex mediated dermal inflammation in rats following either oral or topical administration of a small molecule C5a receptor antagonist. Br J Pharmacol; 2001 Dec;134(8):1778-86
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  • [Title] Inhibition of immune-complex mediated dermal inflammation in rats following either oral or topical administration of a small molecule C5a receptor antagonist.
  • 1. Initiation of a peritoneal Arthus reaction by deposition of immune-complexes results in vascular leakage, polymorphonuclear leukocyte (PMN) infiltration, and tumour necrosis factor alpha (TNFalpha) and interleukin-6 (IL-6) production.
  • 2. Initiation of a dermal Arthus reaction resulted in a significant increase in vascular leakage, PMN infiltration, systemic production of TNFalpha and pathological changes in the dermis.
  • 3. Pretreatment of rats with AcF-[OPdChaWR] either intravenously (1 mg kg(-1) 10 min prior to immune-complex deposition) or orally (1 - 10 mg kg(-1) 30 min prior to immune-complex deposition) significantly inhibited immune-complex mediated dermal vascular leakage and systemic cytokine production.
  • Topical pretreatment with AcF-[OPdChaWR] (400 microg site(-1) in 10% dimethyl sulphoxide 10 min prior to immune-complex deposition) also inhibited vascular leakage, as well as histopathological changes associated with a dermal Arthus reaction.
  • 4. Oral administration of 3 mg kg(-1) AcF-[OPdChaWR] resulted in the appearance of the drug in plasma within 5 min, with peak blood levels approximately 0.3 microM reached within 20 min.
  • The oral activity and bioavailability of AcF-[OPdChaWR], its activity when applied topically to the skin, suggest that small molecule C5a receptor antagonists may have therapeutic utility in dermal inflammatory disorders involving complement activation.
  • 5. This is the first demonstration for either an orally or topically active C5a receptor antagonist, and suggests that small molecule C5a antagonists may have therapeutic utility when given by multiple routes of application.
  • [MeSH-major] Arthus Reaction / drug therapy. Immunosuppressive Agents / pharmacology. Peptides, Cyclic / pharmacology. Receptors, Complement / antagonists & inhibitors
  • [MeSH-minor] Administration, Oral. Administration, Topical. Animals. Antigens, CD. Biological Availability. Biomarkers / analysis. Complement C5a / antagonists & inhibitors. Complement C5a / metabolism. Complement Inactivator Proteins / administration & dosage. Complement Inactivator Proteins / pharmacokinetics. Complement Inactivator Proteins / pharmacology. Cytokines / blood. Female. Half-Life. Infusions, Intravenous. Rats. Rats, Wistar. Receptor, Anaphylatoxin C5a. Time Factors

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  • (PMID = 11739255.001).
  • [ISSN] 0007-1188
  • [Journal-full-title] British journal of pharmacology
  • [ISO-abbreviation] Br. J. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / AcPhe(ornithine-Pro-cyclohexylamine-Trp-Arg); 0 / Antigens, CD; 0 / Biomarkers; 0 / Complement Inactivator Proteins; 0 / Cytokines; 0 / Immunosuppressive Agents; 0 / Peptides, Cyclic; 0 / Receptor, Anaphylatoxin C5a; 0 / Receptors, Complement; 80295-54-1 / Complement C5a
  • [Other-IDs] NLM/ PMC1572898
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7. Proost P, Struyf S, Loos T, Gouwy M, Schutyser E, Conings R, Ronsse I, Parmentier M, Grillet B, Opdenakker G, Balzarini J, Van Damme J: Coexpression and interaction of CXCL10 and CD26 in mesenchymal cells by synergising inflammatory cytokines: CXCL8 and CXCL10 are discriminative markers for autoimmune arthropathies. Arthritis Res Ther; 2006;8(4):R107
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  • Stimulation of fibroblasts and human microvascular endothelial cells with the inflammatory cytokines interleukin-1beta (IL-1beta) or tumour necrosis factor alpha (TNF-alpha) combined with either interferon-alpha (IFN-alpha), IFN-beta or IFN-gamma resulted in a synergistic induction of the CXC chemokine CXCL10, but not of the neutrophil chemoattractant CXCL8.
  • In contrast, simultaneous stimulation with different IFN types did not result in a synergistic CXCL10 protein induction.
  • Synovial concentrations of the neutrophil chemoattractant CXCL8 may therefore be useful to discriminate between autoimmune arthritis types.
  • [MeSH-minor] Autoimmune Diseases / metabolism. Biomarkers / metabolism. Cells, Cultured. Chemokine CXCL10. Dermis / blood supply. Drug Combinations. Humans. Infant, Newborn. Interleukin-8 / metabolism. Joint Diseases / metabolism. Ligands. Peptide Fragments / metabolism. Protein Isoforms / metabolism. Receptors, CXCR3. Receptors, Chemokine / metabolism. Rheumatic Diseases / metabolism. Signal Transduction

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  • (PMID = 16846531.001).
  • [ISSN] 1478-6362
  • [Journal-full-title] Arthritis research & therapy
  • [ISO-abbreviation] Arthritis Res. Ther.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers; 0 / CXCL10 protein, human; 0 / CXCR3 protein, human; 0 / Chemokine CXCL10; 0 / Chemokines, CXC; 0 / Cytokines; 0 / Drug Combinations; 0 / Inflammation Mediators; 0 / Interleukin-8; 0 / Ligands; 0 / Peptide Fragments; 0 / Protein Isoforms; 0 / Receptors, CXCR3; 0 / Receptors, Chemokine; EC 3.4.14.5 / Dipeptidyl Peptidase 4
  • [Other-IDs] NLM/ PMC1779382
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8. Schnurr M, Toy T, Stoitzner P, Cameron P, Shin A, Beecroft T, Davis ID, Cebon J, Maraskovsky E: ATP gradients inhibit the migratory capacity of specific human dendritic cell types: implications for P2Y11 receptor signaling. Blood; 2003 Jul 15;102(2):613-20
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  • [Title] ATP gradients inhibit the migratory capacity of specific human dendritic cell types: implications for P2Y11 receptor signaling.
  • Dendritic cells (DCs) are specialized antigen-presenting cells residing in tissues, from which they take up antigen.
  • Exposure of monocyte-derived DCs (MoDCs) and CD1a+ dermal DCs to gradients of ATP inhibited their migratory capacity in a dose-dependent manner.
  • Although all 4 DC populations expressed mRNA for P2Y11R, calcium-flux studies showed that blood DC types were unresponsive to P2Y11R agonists.
  • The formation of ATP gradients at sites of inflammation may transiently inhibit the migration of local DCs, thus prolonging the time of antigen encounter.
  • [MeSH-major] Adenosine Triphosphate / pharmacology. Chemotaxis / drug effects. Dendritic Cells / drug effects. Receptors, Purinergic P2 / physiology. Signal Transduction / drug effects
  • [MeSH-minor] Antigens, CD1 / analysis. Calcium Signaling / drug effects. Depression, Chemical. Dermis / cytology. Dinoprostone / pharmacology. Dose-Response Relationship, Drug. Drug Resistance. Glycoproteins / analysis. Humans. Inflammation. Interferon-alpha / pharmacology. Melanoma / blood. Melanoma / drug therapy. Melanoma / immunology. Membrane Proteins / pharmacology. Membrane Proteins / therapeutic use. Monocytes / cytology. Phosphatidylinositol Diacylglycerol-Lyase. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. Receptors, Interleukin-3 / analysis. Tumor Necrosis Factor-alpha / pharmacology. Type C Phospholipases / physiology

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  • (PMID = 12649135.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD1; 0 / CD1C protein, human; 0 / Glycoproteins; 0 / Interferon-alpha; 0 / Membrane Proteins; 0 / P2RY11 protein, human; 0 / RNA, Messenger; 0 / Receptors, Interleukin-3; 0 / Receptors, Purinergic P2; 0 / Tumor Necrosis Factor-alpha; 0 / flt3 ligand protein; 8L70Q75FXE / Adenosine Triphosphate; EC 3.1.4.- / Type C Phospholipases; EC 4.6.1.13 / Phosphatidylinositol Diacylglycerol-Lyase; K7Q1JQR04M / Dinoprostone
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9. Lawenda BD, Thiringer JK, Foss RD, Johnstone PA: Merkel cell carcinoma arising in the head and neck: optimizing therapy. Am J Clin Oncol; 2001 Feb;24(1):35-42
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  • [Title] Merkel cell carcinoma arising in the head and neck: optimizing therapy.
  • Merkel cell carcinoma (MCC) is a rare and aggressive neuroendocrine dermal neoplasm.
  • Because of the limited number of cases described in the literature (approximately 600 to date), statistically significant data regarding treatment are difficult to obtain.
  • This study evaluates cases of head and neck MCC at Naval Medical Center San Diego (NMCSD) and compares the treatment regimens and outcomes from multiple institutions.
  • The records of the NMCSD Tumor Registry were searched for patients with that diagnosis, and supplemental information was retrieved from the Radiation Oncology and Head & Neck Surgery Clinic charts.
  • Subsequent therapy varied among the patients.
  • Survey of the available literature revealed inconsistency in terms of which treatment regimens are optimal.
  • Tumor resections are recommended by most groups to include a 2-cm to 3-cm tumor-free margin around the primary lesion when possible, but this is often difficult to achieve in the head and neck.
  • Data, which do not reach statistical significance, suggest improved outcomes with tumor-free margins.
  • Treatment of the regional draining lymph nodes is also recommended in most series.
  • Prophylactic lymph node dissection or radiation therapy to the nodal chain may decrease local recurrence but does not consistently affect overall survival.
  • Adjuvant chemotherapy is advocated by most groups in the treatment of metastatic disease because MCC is pathologically similar to small-cell lung carcinoma.
  • However, no chemotherapy protocol has been shown to improve survival.
  • Head and neck MCC is a rare and aggressive dermal tumor of neuroendocrine origin that requires multimodality therapy, including surgery, radiation therapy, and possibly adjuvant chemotherapy.
  • Multiinstitutional studies are crucial to obtain sufficiently large populations to investigate and optimize therapy in this disease.
  • [MeSH-major] Carcinoma, Merkel Cell / therapy. Head and Neck Neoplasms / therapy
  • [MeSH-minor] Aged. Aged, 80 and over. Combined Modality Therapy. Female. Humans. Male. Middle Aged. Neoplasm Staging. Retrospective Studies. Treatment Outcome

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  • (PMID = 11232947.001).
  • [ISSN] 0277-3732
  • [Journal-full-title] American journal of clinical oncology
  • [ISO-abbreviation] Am. J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 33
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10. Thomison J, McCarter M, McClain D, Golitz LE, Goldenberg G: Hyalinized collagen in a dermatofibrosarcoma protuberans after treatment with imatinib mesylate. J Cutan Pathol; 2008 Nov;35(11):1003-6
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  • [Title] Hyalinized collagen in a dermatofibrosarcoma protuberans after treatment with imatinib mesylate.
  • We report a novel histological finding in a dermatofibrosarcoma protuberans (DFSP) after treatment with imatinib mesylate: copious amounts of hyalinized collagen.
  • A 57-year-old female was referred for evaluation and treatment of a 7 x 8 x 10 cm tumor on the right anterior shoulder.
  • Histological evaluation of the incisional biopsy showed a highly cellular dermal neoplasm composed of spindle cells arranged in a storiform pattern with minimal collagen.
  • A CD34 immunohistochemical stain was strongly positive, highlighting atypical spindle cells in the dermis.
  • At the end of therapy, the DFSP decreased in size to 5.5 x 4 x 4 cm.
  • The tumor was excised.
  • Histological evaluation showed a residual dermal neoplasm composed of atypical spindle cells and a copious amount of hyalinized collagen.
  • A procollagen I stain was strongly positive, confirming the presence of abundant collagen in the dermis.
  • A similar finding has been reported in gastrointestinal stromal tumor, which shows deposition of myxohyaline stroma after treatment with imatinib mesylate.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Collagen / metabolism. Dermatofibrosarcoma / drug therapy. Hyalin / metabolism. Piperazines / therapeutic use. Pyrimidines / therapeutic use. Skin Neoplasms / drug therapy
  • [MeSH-minor] Antigens, CD34 / metabolism. Benzamides. Biomarkers, Tumor / metabolism. Combined Modality Therapy. Female. Humans. Imatinib Mesylate. Immunohistochemistry. Magnetic Resonance Imaging. Middle Aged

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  • (PMID = 18544062.001).
  • [ISSN] 1600-0560
  • [Journal-full-title] Journal of cutaneous pathology
  • [ISO-abbreviation] J. Cutan. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Biomarkers, Tumor; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; 9007-34-5 / Collagen
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11. Makino S, Mitsutake N, Nakashima M, Saenko VA, Ohtsuru A, Umezawa K, Tanaka K, Hirano A, Yamashita S: DHMEQ, a novel NF-kappaB inhibitor, suppresses growth and type I collagen accumulation in keloid fibroblasts. J Dermatol Sci; 2008 Sep;51(3):171-80

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  • [Title] DHMEQ, a novel NF-kappaB inhibitor, suppresses growth and type I collagen accumulation in keloid fibroblasts.
  • BACKGROUND: Keloid is a benign dermal tumor characterized by proliferation of dermal fibroblasts and overproduction of extracellular matrix (ECM).
  • METHODS: Primary normal and keloid dermal fibroblasts were used for this study.
  • The effect of DHMEQ was evaluated by cell viability, cell growth and type I collagen accumulation.
  • DHMEQ markedly reduced cell proliferation and type I collagen accumulation in keloid fibroblasts.
  • CONCLUSION: The inhibition of NF-kappaB by DHMEQ may be an attractive therapeutic approach for keloids.
  • [MeSH-major] Benzamides / pharmacology. Collagen Type I / metabolism. Cyclohexanones / pharmacology. Keloid / drug therapy. Keloid / metabolism. NF-kappa B / antagonists & inhibitors
  • [MeSH-minor] Cell Division / drug effects. Cells, Cultured. DNA / metabolism. Fibroblasts / drug effects. Fibroblasts / metabolism. Fibroblasts / pathology. Humans. Immunohistochemistry. Transcription Factor RelA / antagonists & inhibitors. Transcription Factor RelA / metabolism

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  • (PMID = 18406579.001).
  • [ISSN] 0923-1811
  • [Journal-full-title] Journal of dermatological science
  • [ISO-abbreviation] J. Dermatol. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Benzamides; 0 / Collagen Type I; 0 / Cyclohexanones; 0 / NF-kappa B; 0 / RELA protein, human; 0 / Transcription Factor RelA; 0 / dehydroxymethylepoxyquinomicin; 9007-49-2 / DNA
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12. Burcoş T, Popa E, Ivăşcanu A, Ardeleanu C, Zodieru I: [Merkel cell carcinoma]. Chirurgia (Bucur); 2001 Sep-Oct;96(5):509-16
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  • Merkel Cell Carcinoma (MCC) is a rare and aggressive neuroendocrine dermal neoplasm.
  • This study is a retrospective outcomes analysis of two cases of MCC with data regarding clinical, histopathological, immunohistochemistry and also surgical, chimio and radiological treatment.
  • MCC is a rare dermal tumors, this tumors are most predictable found on sunexposed sites.
  • Diagnosis is best accomplished by a thorough clinical evaluation coupled with light microscopy and defined panel of immunohistochemical studies which are necessary for the definitive diagnosis of Merkel cell carcinoma (cytokeratins, neuron specific enoiase and chromogranin).
  • MCC is an aggressive tumor with local or locoregionale extension and distant spread by hematogen or lymphatic way.
  • Surgical excision of tumor and regional lymphadenectomy is the first step of treatment completed with radiotherapy and chemotherapy bat in advanced studies the rate of local or distant recidives is high.
  • [MeSH-minor] Aged. Arm. Axilla. Female. Humans. Lymph Node Excision / methods. Male. Middle Aged. Treatment Outcome

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  • (PMID = 12731194.001).
  • [ISSN] 1221-9118
  • [Journal-full-title] Chirurgia (Bucharest, Romania : 1990)
  • [ISO-abbreviation] Chirurgia (Bucur)
  • [Language] rum
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Romania
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13. Murakami T, Fukasawa T, Fukayama M, Usui K, Ohtsuki M, Nakagawa H: Gene expression profile in a case of primary cutaneous CD30-negative large T-cell lymphoma with a blastic phenotype. Clin Exp Dermatol; 2001 Mar;26(2):201-4
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  • Histological examination showed diffuse and dense infiltrates located in the dermis and subcutis, composed of large pleomorphic T lymphocytes.
  • Despite systemic chemotherapy, the patient died 7 months after diagnosis.
  • MCP-1, MCP-2, IP-10, and IL-2R gamma) in the tumour-indurated skin.

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  • (PMID = 11298116.001).
  • [ISSN] 0307-6938
  • [Journal-full-title] Clinical and experimental dermatology
  • [ISO-abbreviation] Clin. Exp. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD30; 0 / CASP8 and FADD-Like Apoptosis Regulating Protein; 0 / CCL8 protein, human; 0 / CFLAR protein, human; 0 / Carrier Proteins; 0 / Chemokine CCL2; 0 / Chemokine CCL8; 0 / Chemokine CXCL10; 0 / Cytokines; 0 / Intracellular Signaling Peptides and Proteins; 0 / Monocyte Chemoattractant Proteins; 0 / Proliferating Cell Nuclear Antigen; 0 / Receptors, Cytokine
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14. Bandara M, Arun SJ, Allanson M, Widyarini S, Chai Z, Reeve VE: Topical isoflavonoids reduce experimental cutaneous inflammation in mice. Immunol Cell Biol; 2010 Oct;88(7):727-33
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  • This study uses ultraviolet (UV)B irradiation to induce inflammation in the mouse skin, as a model for some symptoms of cutaneous inflammatory and hyperproliferative diseases such as psoriasis in humans, with the objective of testing two topically applied isoflavonoid compounds for therapeutic properties.
  • UVB exposure resulted in the overexpression of the cytokines, tumour necrosis factor (TNF)-α, interleukin (IL)-6 and the adhesion molecule P-cadherin.
  • Infiltration into the dermal compartment of mast cell populations was also induced.
  • Expression of IL-6 mRNA and protein was also decreased, and the number of infiltrating mast cells into the dermis was reduced by both isoflavonoids.
  • These results suggest that this class of compounds has the potential for useful, innocuous anti-inflammatory therapy from topical application in human cutaneous diseases.
  • [MeSH-major] Anti-Inflammatory Agents, Non-Steroidal / therapeutic use. Cadherins / radiation effects. Dermatitis / drug therapy. Isoflavones / pharmacology. Skin / drug effects
  • [MeSH-minor] Administration, Cutaneous. Animals. Equol. Humans. Interleukin-6 / antagonists & inhibitors. Interleukin-6 / metabolism. Mast Cells. Mice. Mice, Hairless. Mice, Inbred C3H. Mice, Inbred C57BL. Models, Animal. Psoriasis / drug therapy. Tumor Necrosis Factor-alpha / antagonists & inhibitors. Tumor Necrosis Factor-alpha / metabolism. Ultraviolet Rays. Up-Regulation / drug effects. Up-Regulation / radiation effects

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  • (PMID = 20212509.001).
  • [ISSN] 1440-1711
  • [Journal-full-title] Immunology and cell biology
  • [ISO-abbreviation] Immunol. Cell Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 4',7-dihydroxy-3,4-dihydroisoflavone; 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Cadherins; 0 / Interleukin-6; 0 / Isoflavones; 0 / Tumor Necrosis Factor-alpha; 531-95-3 / Equol
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15. Zoli A, Massi G, Pinnelli M, Lo Cuccio CD, Castri F, Ferraccioli G: Interstitial granulomatous dermatitis in rheumatoid arthritis responsive to etanercept. Clin Rheumatol; 2010 Jan;29(1):99-101
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  • It may be associated with drug-related adverse reactions and autoimmune diseases.
  • We report a case of RA patient with persistent erythematous plaques who did not respond to traditional disease-modifying anti-rheumatic drugs with a persistent skin condition of erythematous plaque eruptions.
  • A biopsy showed a homogeneous inflammatory infiltrate in the deep dermis composed of large epithelioid histiocytes with occasional granulocytes, leading us to consider a diagnosis of IGD.
  • The cutaneous lesions disappeared after a 3-month treatment with the tumour necrosis factor-alpha (TNF-alpha) inhibitor etanercept.
  • Anti-TNF-alpha agents can antagonise the multiple effects of TNF-alpha on the immune system, effects that are required for the continued maintenance of granulomatous structure, and offer a therapeutic strategy in the treatment of IGD associated with arthritis.
  • [MeSH-major] Antirheumatic Agents / adverse effects. Arthritis, Rheumatoid / drug therapy. Granuloma / chemically induced. Immunoglobulin G / adverse effects. Receptors, Tumor Necrosis Factor / therapeutic use
  • [MeSH-minor] Anti-Inflammatory Agents / therapeutic use. Drug Eruptions / drug therapy. Drug Eruptions / etiology. Etanercept. Female. Humans. Male. Treatment Outcome. Tumor Necrosis Factor-alpha / antagonists & inhibitors

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  • (PMID = 19802716.001).
  • [ISSN] 1434-9949
  • [Journal-full-title] Clinical rheumatology
  • [ISO-abbreviation] Clin. Rheumatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents; 0 / Antirheumatic Agents; 0 / Immunoglobulin G; 0 / Receptors, Tumor Necrosis Factor; 0 / Tumor Necrosis Factor-alpha; OP401G7OJC / Etanercept
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16. Di Paolo S, Teutonico A, Ranieri E, Gesualdo L, Schena PF: Monitoring antitumor efficacy of rapamycin in Kaposi sarcoma. Am J Kidney Dis; 2007 Mar;49(3):462-70
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  • BACKGROUND: The clinical challenge for the application of rapamycin and its derivatives as anticancer drugs is the ability to prospectively identify which tumors will be sensitive to mammalian target of rapamycin (mTOR) inhibition.
  • The present study is designed to explore mTOR signaling in peripheral-blood mononuclear cells (PBMCs) from renal transplant recipients with Kaposi sarcoma and ascertain whether it would reflect deregulation of the AKT-mTOR pathway in skin cancer tissue and might help identify which patients would benefit from rapamycin treatment, as well as to monitor their clinical response.
  • METHODS: We measured basal and in vivo stimulated AKT and P70 S6 kinase (P70(S6K)) phosphorylation in PBMCs from 37 cyclosporine A-treated patients, 10 of whom had Kaposi sarcoma, before and 6 months after conversion to rapamycin therapy.
  • Long-term treatment with rapamycin was associated with marked inhibition of basal and stimulated phosphorylation of both AKT and P70(S6K), in parallel with regression of the dermal neoplasm.
  • CONCLUSION: Overactivation of basal P70(S6K) in PBMCs from renal transplant recipients appears to be associated with the presence of Kaposi sarcoma dermal lesions; conversely, kinase inhibition is linked to regression of skin cancer lesions.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Protein Kinases / metabolism. Sarcoma, Kaposi / drug therapy. Sirolimus / therapeutic use. Skin Neoplasms / drug therapy
  • [MeSH-minor] Adult. Biomarkers / metabolism. Female. Humans. Kidney Transplantation / adverse effects. Male. Middle Aged. Monocytes / physiology. Patient Selection. Phosphorylation. Predictive Value of Tests. Proto-Oncogene Proteins c-akt / physiology. Ribosomal Protein S6 Kinases, 70-kDa / physiology. Signal Transduction / physiology. TOR Serine-Threonine Kinases. Treatment Outcome

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  • (PMID = 17336708.001).
  • [ISSN] 1523-6838
  • [Journal-full-title] American journal of kidney diseases : the official journal of the National Kidney Foundation
  • [ISO-abbreviation] Am. J. Kidney Dis.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Biomarkers; EC 2.7.- / Protein Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.1 / Ribosomal Protein S6 Kinases, 70-kDa; W36ZG6FT64 / Sirolimus
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17. Sirvent N, Maire G, Pedeutour F: Genetics of dermatofibrosarcoma protuberans family of tumors: from ring chromosomes to tyrosine kinase inhibitor treatment. Genes Chromosomes Cancer; 2003 May;37(1):1-19
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  • [Title] Genetics of dermatofibrosarcoma protuberans family of tumors: from ring chromosomes to tyrosine kinase inhibitor treatment.
  • Dermatofibrosarcoma protuberans (DP) is a rare, slow-growing, infiltrating dermal neoplasm of intermediate malignancy, made up of spindle-shaped tumor cells often positive for CD34.
  • The preferred treatment is wide surgical excision with pathologically negative margins.
  • Both the rings and linear der(22) contain a specific fusion of COL1A1 with PDGFB.
  • DP is therefore a unique example of a tumor in which (i) the same molecular event occurs either on rings or linear translocation derivatives, (ii) the chromosomal abnormalities display an age-related pattern, and (iii) the presence of the specific fusion gene is associated with the gain of chromosomal segments, probably taking advantage of gene dosage effects.
  • Recent studies have determined the molecular identity of "classical" DP, giant cell fibroblastoma, Bednar tumor, adult superficial fibrosarcoma, and the granular cell variant of DP.
  • It is encouraging that inhibitory effects of the PDGF receptor tyrosine kinase antagonist imatinib mesylate have been demonstrated in vivo; such targeted therapies might be warranted in the near future for treatment of the few DP cases not manageable by surgery.
  • [MeSH-major] Dermatofibrosarcoma / drug therapy. Dermatofibrosarcoma / genetics. Enzyme Inhibitors / therapeutic use. Ring Chromosomes. Skin Neoplasms / drug therapy. Skin Neoplasms / genetics. src-Family Kinases / antagonists & inhibitors

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  • [Copyright] Copyright 2003 Wiley-Liss, Inc.
  • (PMID = 12661001.001).
  • [ISSN] 1045-2257
  • [Journal-full-title] Genes, chromosomes & cancer
  • [ISO-abbreviation] Genes Chromosomes Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; EC 2.7.10.2 / src-Family Kinases
  • [Number-of-references] 109
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18. Wolf K, Friedl P: Molecular mechanisms of cancer cell invasion and plasticity. Br J Dermatol; 2006 May;154 Suppl 1:11-5

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  • Cancer cell interactions with the extracellular matrix and the migration therein involve the function of adhesion receptors of the integrin family, a dynamic cytoskeleton, as well as proteolytic mechanisms to overcome tissue barriers.
  • Recent progress in investigating tumour cell migration and associated matrix remodelling was made using three-dimensional (3D) dermis equivalents such as 3D collagen lattices or dermal explant cultures, prompting new concepts in molecular tumour invasion mechanisms and related adaptation responses.
  • Depending on the context of invasion, treatment with protease inhibitors or integrin antagonists can cause the mesenchymal-amoeboid transition and the collective-amoeboid transition, both generating sustained dissemination of single cells.
  • These adaptation responses show an unexpected degree of plasticity resulting in migratory 'escape' strategies after pharmacotherapeutic intervention by prompting alternative mechanisms of cancer cell dissemination in tissues.
  • [MeSH-major] Neoplasm Invasiveness / pathology
  • [MeSH-minor] Antineoplastic Agents / pharmacology. Cell Movement / drug effects. Extracellular Matrix / pathology. Humans. Integrins / physiology

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  • (PMID = 16712711.001).
  • [ISSN] 0007-0963
  • [Journal-full-title] The British journal of dermatology
  • [ISO-abbreviation] Br. J. Dermatol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Integrins
  • [Number-of-references] 40
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19. Parise-Fortes MR, Marques SA, Soares AM, Kurokawa CS, Marques ME, Peracoli MT: Cytokines released from blood monocytes and expressed in mucocutaneous lesions of patients with paracoccidioidomycosis evaluated before and during trimethoprim-sulfamethoxazole treatment. Br J Dermatol; 2006 Apr;154(4):643-50
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  • [Title] Cytokines released from blood monocytes and expressed in mucocutaneous lesions of patients with paracoccidioidomycosis evaluated before and during trimethoprim-sulfamethoxazole treatment.
  • BACKGROUND: Mucocutaneous lesions in paracoccidioidomycosis are granulomatous and result from tissue responses to Paracoccidioides brasiliensis, the aetiological agent.
  • OBJECTIVES AND METHODS: In this study we investigate the expression of tumour necrosis factor (TNF)-alpha, interleukin (IL)-10 and transforming growth factor (TGF)-beta1 by immunohistochemistry in skin and mucosa lesions from patients with the chronic form of paracoccidioidomycosis, evaluated before and at day 20 of trimethoprim-sulfamethoxazole treatment.
  • RESULTS: Intense immunostaining for TNF-alpha was detected in mononuclear cells that infiltrated granulomas in all skin and mucosa lesions before treatment simultaneously with low IL-10 granular deposits in these cells.
  • At day 20 of treatment, there was reduced TNF-alpha and IL-10 deposition.
  • Immunoreactive TGF-beta1 was observed diffusely in the dermis and generally in the cytoplasm of macrophages and giant cells, before treatment, and as increased TGF-beta1 deposits in the fibrosis area at day 20 of treatment.
  • Peripheral blood monocytes from patients with paracoccidioidomycosis, evaluated before treatment, produced high endogenous levels of TNF-alpha, TGF-beta1 and IL-10 in relation to healthy controls.
  • CONCLUSIONS: Trimethoprim-sulfamethoxazole therapy was effective in decreasing fungal load in the lesions, allowing patient immune response to control the infection leading to the healing of the lesions.
  • [MeSH-major] Antifungal Agents / therapeutic use. Cytokines / metabolism. Monocytes / immunology. Paracoccidioidomycosis / immunology. Trimethoprim, Sulfamethoxazole Drug Combination / therapeutic use
  • [MeSH-minor] Adult. Aged. Cells, Cultured. Female. Humans. Immunoenzyme Techniques. Interleukin-10 / metabolism. Male. Middle Aged. Mouth Mucosa / immunology. Mouth Mucosa / pathology. Skin / immunology. Skin / pathology. Transforming Growth Factor beta / metabolism. Transforming Growth Factor beta1. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 16536806.001).
  • [ISSN] 0007-0963
  • [Journal-full-title] The British journal of dermatology
  • [ISO-abbreviation] Br. J. Dermatol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antifungal Agents; 0 / Cytokines; 0 / TGFB1 protein, human; 0 / Transforming Growth Factor beta; 0 / Transforming Growth Factor beta1; 0 / Tumor Necrosis Factor-alpha; 130068-27-8 / Interleukin-10; 8064-90-2 / Trimethoprim, Sulfamethoxazole Drug Combination
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20. Wu JK, Siller G, Whitehead K: Treatment of Bowen's disease and basal cell carcinoma of the nose with imiquimod 5% cream. Australas J Dermatol; 2003 May;44(2):123-5
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  • [Title] Treatment of Bowen's disease and basal cell carcinoma of the nose with imiquimod 5% cream.
  • Treatment was applied on a once-a-day regimen, and a total of 32 applications over 9 weeks were used.
  • A florid local skin reaction occurred early in the treatment, necessitating a rest period and decreasing the frequency of application.
  • Persistent BCC at 4 weeks post treatment was surgically excised.
  • This tumour showed an unusual histological picture, with normal epidermis overlying residual BCC in the papillary dermis.
  • [MeSH-major] Aminoquinolines / administration & dosage. Bowen's Disease / drug therapy. Carcinoma, Basal Cell / drug therapy. Skin Neoplasms / drug therapy
  • [MeSH-minor] Administration, Topical. Biopsy, Needle. Dose-Response Relationship, Drug. Drug Administration Schedule. Female. Follow-Up Studies. Humans. Immunohistochemistry. Middle Aged. Treatment Outcome

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  • (PMID = 12752186.001).
  • [ISSN] 0004-8380
  • [Journal-full-title] The Australasian journal of dermatology
  • [ISO-abbreviation] Australas. J. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Aminoquinolines; 99011-02-6 / imiquimod
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21. Avramidis G, Krüger-Krasagakis S, Krasagakis K, Fragiadaki I, Kokolakis G, Tosca A: The role of endothelial cell apoptosis in the effect of etanercept in psoriasis. Br J Dermatol; 2010 Nov;163(5):928-34
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  • BACKGROUND: Psoriasis is a chronic inflammatory skin disease associated with abnormal vascular expansion in the papillary dermis.
  • Tumour necrosis factor (TNF)-α is a proinflammatory cytokine that can induce antiapoptotic proteins and endothelial cell activation factors in psoriasis.
  • The terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labelling (TUNEL) assay was applied for apoptosis detection.
  • RESULTS: Etanercept caused a statistically significant time-dependent reduction in the number of dermal blood vessels, the number of CD31+ cells and VEGF in psoriatic lesions, with induction of endothelial cell apoptosis and statistically significant upregulation of TSP-1 in psoriatic vessels.
  • Immunohistochemical analysis showed significant reduction of NF-κB, Bcl-2 and Bcl-xL expression in endothelial cells during treatment.
  • CONCLUSIONS: The present findings suggest that treatment with etanercept induces apoptosis, reduces apoptosis-inhibiting factors in psoriatic endothelial cells, and decreases angiogenesis in psoriatic skin.
  • [MeSH-major] Apoptosis / drug effects. Endothelial Cells / drug effects. Immunoglobulin G / pharmacology. Immunologic Factors / pharmacology. Psoriasis / drug therapy
  • [MeSH-minor] Adult. Antigens, CD31 / metabolism. Biopsy. Etanercept. Female. Humans. Immunohistochemistry. Male. Middle Aged. NF-kappa B / metabolism. Proto-Oncogene Proteins c-bcl-2 / metabolism. Receptors, Tumor Necrosis Factor. Thrombospondin 1 / metabolism. Vascular Endothelial Growth Factor A / metabolism. bcl-X Protein / metabolism

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  • [Copyright] © 2010 The Authors. BJD © 2010 British Association of Dermatologists.
  • (PMID = 20633014.001).
  • [ISSN] 1365-2133
  • [Journal-full-title] The British journal of dermatology
  • [ISO-abbreviation] Br. J. Dermatol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD31; 0 / BCL2L1 protein, human; 0 / Immunoglobulin G; 0 / Immunologic Factors; 0 / NF-kappa B; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Receptors, Tumor Necrosis Factor; 0 / Thrombospondin 1; 0 / Vascular Endothelial Growth Factor A; 0 / bcl-X Protein; OP401G7OJC / Etanercept
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22. Huang PY, Chu CY, Hsiao CH: Multiple eruptive dermatofibromas in a patient with dermatomyositis taking prednisolone and methotrexate. J Am Acad Dermatol; 2007 Nov;57(5 Suppl):S81-4
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  • Dermatofibroma (DF) is a common, benign, dermal tumor, often occurring as a single lesion.
  • Multiple eruptive DFs are rare and usually associated with autoimmune diseases, immunosuppressant therapy, or both.
  • We present the case of a 28-year-old woman with dermatomyositis who developed multiple eruptive DFs after undergoing methotrexate and corticosteroid treatment.
  • [MeSH-major] Dermatomyositis / drug therapy. Glucocorticoids / adverse effects. Histiocytoma, Benign Fibrous / chemically induced. Immunosuppressive Agents / adverse effects. Methotrexate / adverse effects. Prednisolone / adverse effects. Skin Neoplasms / chemically induced

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  • (PMID = 17097372.001).
  • [ISSN] 1097-6787
  • [Journal-full-title] Journal of the American Academy of Dermatology
  • [ISO-abbreviation] J. Am. Acad. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Glucocorticoids; 0 / Immunosuppressive Agents; 9PHQ9Y1OLM / Prednisolone; YL5FZ2Y5U1 / Methotrexate
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23. Woo KJ, Choi YL, Jung HS, Jung G, Shin YK, Jang KT, Han J, Pyon JK: Merkel cell carcinoma: our experience with seven patients in Korea and a literature review. J Plast Reconstr Aesthet Surg; 2010 Dec;63(12):2064-70
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The purpose of this study was to retrospectively review our experience with the surgical treatment of MCC in Korea and to study its management and outcome.
  • We analysed patient characteristics, tumour location and size, staging, treatment methods and outcomes.
  • We performed polymerase chain reaction (PCR) to detect Merkel cell polyomavirus (MCPyV) from formalin-fixed paraffin-embedded tissue specimens.
  • RESULTS: Two patients had stage I tumours, four patients had stage II tumours and one patient had a stage III tumour.
  • Wide local excision with a clear resection margin was the primary modality of treatment in all cases.
  • Adjuvant radiotherapy and chemotherapy were performed for selected patients.
  • Wide excision is the primary modality of treatment, but adjuvant radiotherapy could be positively considered if the tumour is large and the lesion is not confined to the dermis.
  • [MeSH-minor] Adult. Aged. Chemotherapy, Adjuvant. Female. Humans. Lymphatic Metastasis. Male. Middle Aged. Neoplasm Staging. Radiotherapy, Adjuvant. Retrospective Studies. Skin Transplantation. Treatment Outcome

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  • [Copyright] Copyright © 2010 British Association of Plastic, Reconstructive and Aesthetic Surgeons. Published by Elsevier Ltd. All rights reserved.
  • (PMID = 20207211.001).
  • [ISSN] 1878-0539
  • [Journal-full-title] Journal of plastic, reconstructive & aesthetic surgery : JPRAS
  • [ISO-abbreviation] J Plast Reconstr Aesthet Surg
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
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24. Nakaseko H, Kobayashi M, Akita Y, Tamada Y, Matsumoto Y: Histological changes and involvement of apoptosis after photodynamic therapy for actinic keratoses. Br J Dermatol; 2003 Jan;148(1):122-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Histological changes and involvement of apoptosis after photodynamic therapy for actinic keratoses.
  • BACKGROUND: Photodynamic therapy (PDT), which employs a combination of a tumour-localizing photosensitizer and visible light, has been used to treat superficial malignancies in the epidermis.
  • The detection of apoptosis was performed using a terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-biotin nick end labelling (TUNEL) method, antiactivated caspase-3 antibody and anti-Fas antibody.
  • RESULTS: One hour after PDT, cells with eosinophilic cytoplasm and markedly stained nuclei were found, and vacuolation of some tumour cells was noted in the lower layer of the epidermis.
  • An infiltrate of lymphocytes and neutrophils was observed in the upper layer of the dermis.
  • Necrosis in all layers of the epidermis and lymphocyte infiltration in the dermis were found 3 days after PDT.
  • Tumour cells had disappeared and regenerative thickening of the epidermis was observed 7 days after PDT.
  • CONCLUSIONS: Results suggested that apoptosis is involved in tumour cell death after PDT in patients with AK, and that it occurs within 1 day after PDT.
  • [MeSH-major] Apoptosis. Keratosis / drug therapy. Photochemotherapy
  • [MeSH-minor] Aged. Aged, 80 and over. Epidermis / pathology. Facial Dermatoses / drug therapy. Facial Dermatoses / pathology. Female. Humans. Immunoenzyme Techniques. In Situ Nick-End Labeling. Male. Middle Aged

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  • (PMID = 12534605.001).
  • [ISSN] 0007-0963
  • [Journal-full-title] The British journal of dermatology
  • [ISO-abbreviation] Br. J. Dermatol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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25. Barnetson RS, Satchell A, Zhuang L, Slade HB, Halliday GM: Imiquimod induced regression of clinically diagnosed superficial basal cell carcinoma is associated with early infiltration by CD4 T cells and dendritic cells. Clin Exp Dermatol; 2004 Nov;29(6):639-43
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  • The objective was to determine the cellular immune response early in the course of treatment in order to examine whether cell mediated immunity could be responsible for imiquimod mediated regression of BCC.
  • Sixteen adults with clinically diagnosed BCC were openly assigned to 5 days per week of drug (1, 2 or 4 weeks) or placebo (2 weeks) in groups of four.
  • Post-treatment excision specimens were examined by routine and immunohistochemical staining.
  • Treatment was associated with the early appearance of CD4 cells, activated dendritic cells and macrophages, with later infiltration by CD8 T cells.
  • Dendritic cells continually increased with time, while macrophages reached a maximum at 1 week and then declined slightly.
  • Early infiltrates were most prominent in the tumour and upper dermis.
  • Several immune-mediated tumour destruction mechanisms are likely to be involved.
  • [MeSH-major] Aminoquinolines / therapeutic use. Antineoplastic Agents / therapeutic use. Carcinoma, Basal Cell / drug therapy. Lymphocytes, Tumor-Infiltrating / drug effects. Skin Neoplasms / drug therapy
  • [MeSH-minor] Adult. CD4-Positive T-Lymphocytes / drug effects. Dendritic Cells / drug effects. Humans. Treatment Outcome

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  • (PMID = 15550144.001).
  • [ISSN] 0307-6938
  • [Journal-full-title] Clinical and experimental dermatology
  • [ISO-abbreviation] Clin. Exp. Dermatol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Controlled Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Aminoquinolines; 0 / Antineoplastic Agents; 99011-02-6 / imiquimod
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26. Kluger N, Cohen P, Fallet-Bianco C, Guillevin L: Mycobacterium chelonae infection under adalimumab therapy for spondylarthritis. Clin Exp Rheumatol; 2010 Jan-Feb;28(1):101-2
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  • [Title] Mycobacterium chelonae infection under adalimumab therapy for spondylarthritis.
  • Tumour necrosis factor (TNF)-alpha antagonists have been prescribed increasingly over the past few years to manage various inflammatory diseases.
  • We describe a 66-year-old man taking adalimumab for spondyloarthropathy who developed an inflammatory infiltration in his right index finger.
  • A non-necrotising granuloma with epitheloid and giant cells in the dermis and eosinophilic acid-fast bacilli, identified by using Ziehl-Neelsen staining suggested a mycobacterial infection.
  • [MeSH-major] Antibodies, Monoclonal / adverse effects. Antirheumatic Agents / adverse effects. Mycobacterium Infections, Nontuberculous / complications. Mycobacterium chelonae. Spondylarthritis / complications. Spondylarthritis / drug therapy

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  • (PMID = 20346249.001).
  • [ISSN] 0392-856X
  • [Journal-full-title] Clinical and experimental rheumatology
  • [ISO-abbreviation] Clin. Exp. Rheumatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antirheumatic Agents; FYS6T7F842 / Adalimumab
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