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6. Ding L, Chen XP, Zhang ZW, Guan J, Zhang WG, Wang HP, Wang ZH, Li CL: Synergistic effect of bromocriptine and tumor necrosis factor-alpha on reversing hepatocellular carcinoma multidrug resistance in nude mouse MDR1 model of liver neoplasm. World J Gastroenterol; 2005 Sep 28;11(36):5621-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Synergistic effect of bromocriptine and tumor necrosis factor-alpha on reversing hepatocellular carcinoma multidrug resistance in nude mouse MDR1 model of liver neoplasm.
  • AIM: To investigate the effect of bromocriptine (BCT) and tumor necrosis factor-alpha (TNF-alpha) on hepatocellular carcinoma (HCC) multidrug resistance (MDR) in nude mouse MDR model of liver neoplasm.
  • METHODS: Human hepatocarcinoma cell line HepG(2), drug resistant hepatocarcinoma cell line HepG(2)/adriamycin (ADM) and hepatocarcinoma cell line transfected with TNF-alpha gene HepG(2)/ADM/TNF were injected into the liver of nude mice via orthotopic implantation and MDR model of liver neoplasm in vivo was established (HepG(2), ADM, TNF, BCT groups).
  • Size and weight of the tumor were measured.
  • Furthermore, tumor histological character and growth of the nude mice were observed and their chemosensitivity was tested.
  • MDR-associated genes and proteins (MRP, LRP) of implanted tumors were detected by immunohistochemistry, reverse transcriptase polymerase chain reaction, and apoptosis rate of hepatocarcinoma cells was detected by TUNEL assay.
  • RESULTS: The nude mouse model of each cell line was inoculated successfully.
  • The tumor growth rate and weight were significantly different among groups.
  • After chemotherapy, abdominal cavity tumor growth inhibition rate was higher in BCT group (67%) compared to ADM and TNF groups, and similar to HepG(2) group (54%).
  • MDR1 and LRPmRNA could be detected in all groups, but TNF-alpha was detected only in TNF and BCT groups.
  • Furthermore, MDR1 and LRP protein expression of tumors in TNF and BCT groups was low similar to HepG(2) group.
  • The apoptosis rate of hepatocarcinoma cells was much higher in BCT group than in other groups with TUNEL assay.
  • CONCLUSION: BCT and TNF-alpha can reverse HCC MDR in nude mouse MDR1 model of liver neoplasm.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Bromocriptine / pharmacology. Drug Resistance, Neoplasm / drug effects. Liver Neoplasms / drug therapy. P-Glycoprotein / metabolism. Tumor Necrosis Factor-alpha / pharmacology
  • [MeSH-minor] Animals. Apoptosis. Cell Line, Tumor. Drug Synergism. Female. Gene Expression Regulation, Neoplastic. Genes, MDR / genetics. Genes, MDR / physiology. Humans. Mice. Mice, Nude. Neoplasm Transplantation. RNA, Messenger / metabolism

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  • (PMID = 16237754.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / P-Glycoprotein; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; 3A64E3G5ZO / Bromocriptine
  • [Other-IDs] NLM/ PMC4481477
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7. Hurrell DP, McCluggage WG: Uterine tumour resembling ovarian sex cord tumour is an immunohistochemically polyphenotypic neoplasm which exhibits coexpression of epithelial, myoid and sex cord markers. J Clin Pathol; 2007 Oct;60(10):1148-54
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  • [Title] Uterine tumour resembling ovarian sex cord tumour is an immunohistochemically polyphenotypic neoplasm which exhibits coexpression of epithelial, myoid and sex cord markers.
  • AIMS: To describe the clinicopathological and immunohistochemical findings in four cases of uterine tumour resembling ovarian sex cord tumour (UTROSCT).
  • METHODS: Four UTROSCTs were stained with a wide range of antibodies, including epithelial (AE1/3, epithelial membrane antigen), myoid (desmin, alpha smooth muscle actin, h-caldesmon), sex cord (alpha inhibin, calretinin, melan A, CD99) and neuroendocrine (chromogranin, CD56) markers as well as hormone receptors (oestrogen receptor, progesterone receptor, androgen receptor), vimentin, CD10, WT1 and HMB45.
  • RESULTS: The tumours ranged from 0.8 to 19.5 cm.
  • The tumours were variably composed of solid, corded, trabecular, nested, glandular and retiform arrangements of tumour cells.
  • In three cases, cells with eccentric nuclei and abundant eosinophilic cytoplasm, resulting in a rhabdoid appearance, were a prominent feature.
  • Positivity with myoid markers was common with 3, 4 and 1 case respectively staining with desmin, alpha smooth muscle actin and h-caldesmon; 2, 4, 1 and 2 cases respectively were positive with alpha inhibin, calretinin, melan A and CD99.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Ovarian Neoplasms / diagnosis. Sex Cord-Gonadal Stromal Tumors / diagnosis. Uterine Neoplasms / diagnosis
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Diagnosis, Differential. Female. Humans. Immunophenotyping. Middle Aged. Neoplasm Proteins / metabolism

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  • (PMID = 17182656.001).
  • [ISSN] 0021-9746
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Neoplasm Proteins
  • [Other-IDs] NLM/ PMC2014850
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8. Williams LE, DeNardo GL, Meredith RF: Targeted radionuclide therapy. Med Phys; 2008 Jul;35(7Part1):3062-3068

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Targeted radionuclide therapy (TRT) seeks molecular and functional targets within patient tumor sites.
  • A number of agents have been constructed and labeled with beta, alpha, and Auger emitters.
  • Uptake, in percent-injected dose per gram of malignant tissue, is used to evaluate the specificity of the targeting vehicle.
  • Lymphoma (B-cell) has been the primary clinical application.
  • Extension to solid tumors will require raising the macroscopic absorbed dose by several-fold over values found in present technology.

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  • [Copyright] © 2008 American Association of Physicists in Medicine.
  • (PMID = 28513035.001).
  • [ISSN] 2473-4209
  • [Journal-full-title] Medical physics
  • [ISO-abbreviation] Med Phys
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Keywords] NOTNLM ; Anatomy / Auger effect / Cancer / Computed tomography / Conformal radiation treatment / Dosimetry / Medical imaging / Positron emission tomography / Positron emission tomography (PET) / Proteins / Single photon emission computed tomography / Single photon emission computed tomography (SPECT) / Tissue engineering / Tissues / absorbed dose / alpha-particle sources / antibodies / beta-ray sources / blood / cellular biophysics / positron emission tomography / radiation therapy / radioisotopes / radionuclide therapy / single photon emission computed tomography / tumours
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9. Zhu X, Palmer MR, Makrigiorgos GM, Kassis AI: Solid-tumor radionuclide therapy dosimetry: New paradigms in view of tumor microenvironment and angiogenesis. Med Phys; 2010 Jun;37(6Part1):2974-2984

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Solid-tumor radionuclide therapy dosimetry: New paradigms in view of tumor microenvironment and angiogenesis.
  • PURPOSE: The objective of this study is to evaluate requirements for radionuclide-based solid tumor therapy by assessing the radial dose distribution of beta-particle-emitting and alpha-particle-emitting molecules localized either solely within endothelial cells of tumor vasculature or diffusing from the vasculature throughout the adjacent viable tumor cells.
  • METHODS: Tumor blood vessels were modeled as a group of microcylindrical layers comprising endothelial cells (one-cell thick, 10μm diameter), viable tumor cells (25-cell thick, 250μm radius), and necrotic tumor region (>250μm from any blood vessel).
  • Sources of radioactivity were assumed to distribute uniformly in either endothelial cells or in concentric cylindrical 10μm shells within the viable tumor-cell region.
  • The EGSnrc Monte Carlo simulation code system was used for beta particle dosimetry and a dose-point kernel method for alpha particle dosimetry.
  • The radioactive decays required to deposit cytocidal doses (≥100Gy) in the vascular endothelial cells (endothelial cell mean dose) or, alternatively, at the tumor edge [tumor-edge mean dose (TEMD)] of adjacent viable tumor cells were then determined for six beta (P32, P33, C67u, Y90, I131, and R188e) and two alpha (A211t and B213i) particle emitters.
  • RESULTS: Contrary to previous modeling in targeted radionuclide therapy dosimetry of solid tumors, the present work restricts the region of tumor viability to 250μm around tumor blood vessels for consistency with biological observations.
  • For delivering ≥100Gy at the viable tumor edge (TEMD) rather than throughout a solid tumor, energetic beta emitters Y90, P32, and R188e can be effective even when the radionuclide is confined to the blood vessel (i.e., no diffusion into the tumor).
  • Furthermore, the increase in tumor-edge dose consequent to beta emitter diffusion is dependent on the energy of the emitted beta particles, being much greater for lower-energy emitters I131, C67u, and P33 relative to higher-energy emitters Y90, P32, and R188e.
  • Compared to alpha particle emitters, a ∼150-400 times higher number of beta-particle-emitting radioactive atoms is required to deposit the same dose in tumor neovasculature.
  • However, for the alpha particle emitters A211t and B213i to be effective in irradiating viable tumor-cell regions in addition to the vasculature, the carrier molecules must diffuse substantially from the vasculature into the viable tumor.
  • CONCLUSION: The presented data enable comparison of radionuclides used for antiangiogenic therapy on the basis of their radioactive decay properties, tumor neovasculature geometry, and tumor-cell viability.
  • For alpha particle emitters or low-energy beta particle emitters, the targeting carrier molecule should be chosen to permit the radiopharmaceutical to diffuse from the endothelial wall of the blood vessel, while for long-range energetic beta particle emitters that target neovasculature, a radiopharmaceutical that binds to newly formed endothelial cells and does not diffuse is preferable.
  • The work is a first approximation to modeling of tumor neovasculature that ignores factors such as pharmacokinetics and targeting capability of carrier molecules.
  • The calculations quantify the interplay between irradiation of neovasculature, the surrounding viable tumor cells, and the physical properties of commonly used radionuclides and can be used to assist estimation of radioactivity to be administered for neovasculature-targeted tumor therapy.

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  • [Copyright] © 2010 American Association of Physicists in Medicine.
  • (PMID = 28512969.001).
  • [ISSN] 2473-4209
  • [Journal-full-title] Medical physics
  • [ISO-abbreviation] Med Phys
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Keywords] NOTNLM ; Alpha particles / Beta particles / Cancer / Cell growth / Cell processes / Diffusion / Dose-volume analysis / Dosimetry / Monte Carlo methods / Nutrients / Radiation treatment / Radioactivity / Radiopharmaceuticals / alpha particle emitter / blood vessels / cellular biophysics / dosimetry / electron emitter / neovasculature targeting / radiation therapy / targeted radionuclide therapy / tumor targeting / tumor vascularity / tumours
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10. Bilbao EA, Chirife AM, Florio D, Giménez LB, Marino L, Rosso DA: [Hematodermic CD4+ CD56+ neoplasm in childhood]. Medicina (B Aires); 2008;68(2):147-50
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  • [Title] [Hematodermic CD4+ CD56+ neoplasm in childhood].
  • [Transliterated title] Neoplasia hematodérmica CD4+ CD56+ en la infancia.
  • Hematodermic CD4+ CD56+ neoplasm with plasmacytoid dendritic cell phenotype is a rare and aggressive neoplasm recently recognized by the WHO-EORTC classification.
  • Histologically the nodules showed diffuse dermal infiltrate of medium and small cells and expression of CD4, CD56, CD43, S100 and plasmacytoid dendritic markers: CD123, BDCA-2 under flow cytometry study.
  • [MeSH-major] Antigens, CD4. Antigens, CD56. Biomarkers, Tumor. Lymphoma / pathology. Skin Neoplasms / pathology
  • [MeSH-minor] Child. Dendritic Cells / immunology. Dendritic Cells / pathology. Diagnosis, Differential. Female. Flow Cytometry. Humans. Interleukin-3 Receptor alpha Subunit / analysis. Killer Cells, Natural / immunology. Lectins, C-Type / analysis. Membrane Glycoproteins / analysis. Receptors, Immunologic / analysis

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  • (PMID = 18499965.001).
  • [ISSN] 0025-7680
  • [Journal-full-title] Medicina
  • [ISO-abbreviation] Medicina (B Aires)
  • [Language] spa
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Argentina
  • [Chemical-registry-number] 0 / Antigens, CD4; 0 / Antigens, CD56; 0 / Biomarkers, Tumor; 0 / CLEC4C protein, human; 0 / Interleukin-3 Receptor alpha Subunit; 0 / Lectins, C-Type; 0 / Membrane Glycoproteins; 0 / Receptors, Immunologic
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11. Lu J, Herrera PL, Carreira C, Bonnavion R, Seigne C, Calender A, Bertolino P, Zhang CX: Alpha cell-specific Men1 ablation triggers the transdifferentiation of glucagon-expressing cells and insulinoma development. Gastroenterology; 2010 May;138(5):1954-65
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  • [Title] Alpha cell-specific Men1 ablation triggers the transdifferentiation of glucagon-expressing cells and insulinoma development.
  • BACKGROUND & AIMS: The tumor suppressor menin is recognized as a key regulator of pancreatic islet development, proliferation, and beta-cell function, whereas its role in alpha cells remains poorly understood.
  • The purpose of the current study was to address this issue in relation to islet tumor histogenesis.
  • METHODS: We generated alpha cell-specific Men1 mutant mice with Cre/loxP technology and carried out analyses of pancreatic lesions developed in the mutant mice during aging.
  • RESULTS: We showed that, despite the alpha-cell specificity of the GluCre transgene, both glucagonomas and a large amount of insulinomas developed in mutant mice older than 6 months, accompanied by mixed islet tumors.
  • Interestingly, the cells sharing characteristics of both alpha and beta cells were identified shortly after the appearance of menin-deficient alpha cells but well before the tumor onset.
  • Using a genetic cell lineage tracing analysis, we demonstrated that insulinoma cells were directly derived from transdifferentiating glucagon-expressing cells.
  • CONCLUSIONS: Our work shows cell transdifferentiation as a novel mechanism involved in islet tumor development and provides evidence showing that menin regulates the plasticity of differentiated pancreatic alpha cells in vivo, shedding new light on the mechanisms of islet tumorigenesis.
  • [MeSH-major] Cell Transdifferentiation. Cell Transformation, Neoplastic / metabolism. Glucagon / metabolism. Glucagon-Secreting Cells / metabolism. Glucagonoma / metabolism. Insulinoma / metabolism. Pancreatic Neoplasms / metabolism. Proto-Oncogene Proteins / deficiency
  • [MeSH-minor] Age Factors. Aging / metabolism. Aging / pathology. Animals. Biomarkers / metabolism. Cell Fusion. Cell Lineage. Cell Proliferation. Gene Deletion. Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Genotype. Insulin / metabolism. Insulin-Secreting Cells / metabolism. Insulin-Secreting Cells / pathology. Mice. Mice, Knockout. Phenotype. Transcription Factors / metabolism


12. Allison KH, Love JE, Garcia RL: Epithelioid trophoblastic tumor: review of a rare neoplasm of the chorionic-type intermediate trophoblast. Arch Pathol Lab Med; 2006 Dec;130(12):1875-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Epithelioid trophoblastic tumor: review of a rare neoplasm of the chorionic-type intermediate trophoblast.
  • We present a brief review of epithelioid trophoblastic tumor, a rare trophoblastic neoplasm derived from chorionic-type intermediate trophoblastic cells that typically presents in reproductive-age women between 1 and 18 years following a previous gestation.
  • Histologic features include a nodular growth pattern of monomorphic, epithelioid cells within a hyaline matrix.
  • Areas of necrosis and mitotic activity (0-9 mitoses per 10 high-power fields) are additional features of this neoplasm.
  • Positive immunostaining for p63 and cytokeratin, frequent location in the lower uterine segment and endocervix, as well as the epithelioid appearance can lead to confusion with squamous cell carcinoma.
  • Inhibin-alpha is typically expressed, as well as focal, more variable expression of other trophoblastic markers including beta-human chorionic gonadotropin, human placental lactogen, placental alkaline phosphate, and Mel-CAM (CD148).
  • The clinical behavior of this rare form of gestational trophoblastic disease is difficult to predict.
  • Although most cases follow a benign course following resection, there is a potential for metastatic disease.
  • [MeSH-major] Epithelioid Cells / pathology. Trophoblastic Tumor, Placental Site / pathology. Uterine Neoplasms / pathology
  • [MeSH-minor] Adult. Biomarkers, Tumor / analysis. Carcinoma, Squamous Cell / pathology. Diagnosis, Differential. Female. Humans. Immunohistochemistry. Keratins / analysis. Membrane Proteins / analysis. Mitosis. Necrosis. Pregnancy

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  • (PMID = 17149967.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CKAP4 protein, human; 0 / Membrane Proteins; 68238-35-7 / Keratins
  • [Number-of-references] 12
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13. Cajaiba MM, Chojniak MM, Cunha IW: Unusual primary ocular neoplasm in a child: leiomyosarcoma of the ciliary body. Pediatr Dev Pathol; 2008 Nov-Dec;11(6):479-81
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Unusual primary ocular neoplasm in a child: leiomyosarcoma of the ciliary body.
  • Primary uveal-tract neoplasms are extremely rare in childhood; the most common lesions found are melanocytic.
  • We report here the case of a 7-year-old girl who underwent enucleation of the right eye with clinical suspicion of choroid melanoma as a result of a ciliary body mass that extended to the posterior chamber.
  • Histologically, the neoplasm featured spindle cell morphology, atypia, and mitoses.
  • The tumor expressed smooth muscle alpha actin, pan-actin HHF-35, and desmin, whereas immunohistochemistry for melanocytic markers, such as S-100, Melan-A, and HMB-45, was negative.
  • Based on these features, the diagnosis of leiomyosarcoma of the ciliary body was firmly established.
  • Immunohistochemical expression of muscle proteins allowed distinction from the most common melanocytic tumors arising in this location.
  • [MeSH-major] Ciliary Body / pathology. Leiomyosarcoma / pathology. Uveal Neoplasms / pathology
  • [MeSH-minor] Biomarkers, Tumor / analysis. Cell Proliferation. Child. Choroid / pathology. Diagnosis, Differential. Eye Enucleation. Female. Humans. Immunohistochemistry. Melanoma / diagnosis

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  • (PMID = 17990912.001).
  • [ISSN] 1093-5266
  • [Journal-full-title] Pediatric and developmental pathology : the official journal of the Society for Pediatric Pathology and the Paediatric Pathology Society
  • [ISO-abbreviation] Pediatr. Dev. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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4. Warren GW, Kudrimoti M, McGarry R, Arnold S, Rangnekar V: Mechanisms of nicotine-induced resistance to treatment with chemotherapy and radiotherapy. J Clin Oncol; 2009 May 20;27(15_suppl):e22008

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • : e22008 Background: Nicotine (NIC), used for smoking cessation in cancer patients, is associated with increased tumor growth, angiogenesis, migration, invasion, growth factor production, and inhibition of apoptosis.
  • METHODS: A review of the literature produced a construct demonstrating that NIC generates more than 100 interactions with 40 proteins involved in tumor promotion and progression.
  • The effect of NIC on cell proliferation, cell survival, and protein activation was analyzed following CT, XRT, or chemoradiotherapy (CRT) in FaDu, A549, and H460 human cancer cell lines.
  • RESULTS: Proliferation measured with the WST-1 (tetrazolium) assay demonstrated that NIC increased proliferation following cisplatin, XRT, and cisplatin with XRT.
  • NIC administration increased cell survival (colony survival) following XRT and following CT (cisplatin, doxorubicin, or etoposide) regimens in all cell lines. nAChR expression was verified in each cell line using Western blot.
  • Non-specific inhibition of nAChR demonstrated no consistent effect on preventing NIC induced resistance to CT, XRT, or CRT; however, specific inhibition of the alpha-3- or alpha-7-nAChR had variable cell specific ability to prevent NIC induced resistance.
  • Inhibition of MAPK activity (using PD98059) produced marked reduction in proliferation of all cell lines, but generally had no effect on NIC induced resistance.
  • These findings have significant clinical implications including smoking cessation, treatment efficacy, and outcomes research in cancer patients.

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  • (PMID = 27963179.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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15. Sumiyoshi Y, Hashine K, Niwakawa M, Yamaguchi R, Fujii H, Hamamoto Y, Fukino K: Phase I trial of sorafenib in combination with interferon-alpha in Japanese patients with unresectable or metastatic renal cell carcinoma. J Clin Oncol; 2009 May 20;27(15_suppl):e16107

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase I trial of sorafenib in combination with interferon-alpha in Japanese patients with unresectable or metastatic renal cell carcinoma.
  • Interferon-α (IFN) is most commonly used for metastatic renal cell carcinoma (RCC) in Japan.
  • In this phase I study, we investigated the safety profile, pharmacokinetics (PK), and tumor response of SOR/(recombinant)IFN combination in Japanese patients (pts) with RCC.
  • Objectives were safety/tolerability and recommended dose of SOR/IFN as primary, and tumor response and PK as secondary.
  • RESULTS: Pt characteristics were: median 64.5 y.o.
  • At data cut-off (September 30, 2008), dose-limiting toxicities were reported in all cohorts, including G3 fatigue, G3 anorexia, and G3 skin disorders.
  • Five PR (1 in C1 and 4 in C3) and 11 SD (4 in C1, 5 in C2, and 2 in C3) were achieved as the best response.

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  • (PMID = 27963330.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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16. Boyle H, You B, Fronton L, Ribba B, Girard P, Tranchand B, Tod M, Coquelin H, Droz J, Flechon A: Major prognostic value of modeled AUC<sub>hCG-AFP</sub>, a dynamic kinetic marker characterizing tumor marker decline of nonseminomatous germ cell tumors (NSGCT) intermediate-poor-risk patients according to the IGCCCG. J Clin Oncol; 2009 May 20;27(15_suppl):5085

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Major prognostic value of modeled AUC<sub>hCG-AFP</sub>, a dynamic kinetic marker characterizing tumor marker decline of nonseminomatous germ cell tumors (NSGCT) intermediate-poor-risk patients according to the IGCCCG.
  • : 5085 Background: The level of human chorionic gonadotrophin (hCG) and alpha-foetoprotein (AFP) serum tumor marker is well established in NSGCT as prognostic factor, the relevance of marker kinetic analysis under treatment is still unclear.
  • We propose to model patient's AFP and hCG decline profiles in order to calculate area under the curve of marker concentrations versus time (AUC<sub>hCG-AFP</sub>) and to test its prognostic value.
  • Survival univariate and multivariate analyses tested the prognostic value of AUC<sub>hCG-AFP</sub> regarding PFS.
  • RESULTS: Mono-exponential models best fitted AFP and hCG decreases: C<sub>AFP</sub> (t) = 381*e <sup>- 0.14 *t</sup> +3.27 and C<sub>hCG</sub> (t) = 1230*e - <sup>0.25 *t</sup> +1.22.
  • These results must be validated in a prospective cohort.

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  • (PMID = 27964275.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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17. Amato R, Hernandez-McClain J, Harrop R, Cen P, Doshi G: Vaccination of renal cell cancer (RCC) patients with modified vaccinia Ankara (MVA) delivering tumor antigen 5T4 administered alone or with interleukin 2 (IL-2) or interferon-alpha (IFN). J Clin Oncol; 2009 May 20;27(15_suppl):3026

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Vaccination of renal cell cancer (RCC) patients with modified vaccinia Ankara (MVA) delivering tumor antigen 5T4 administered alone or with interleukin 2 (IL-2) or interferon-alpha (IFN).
  • : 3026 Background: The attenuated vaccinia virus (MVA) has been engineered to deliver the tumor antigen 5T4 (TroVax).
  • A series of clinical trials were conducted to evaluate the effectiveness of MVA 5T4 as a single agent or in combination with either IL-2 or IFN.
  • METHODS: Eligibility: Pathologic diagnosis of clear cell or papillary RCC, progressive measurable metastases, any prior therapy, adequate physiological parameters, Karnofsky performance status ≥ 80%, and no active CNS involvement.
  • RESULTS: A total of 53 pts received MVA 5T4 alone or in combination with IL-2 or IFN.
  • Clinical responses were assessed by measuring changes in tumor burden via computed tomography or magnetic resonance imaging scan.
  • 20 pts demonstrated disease stabilization for ≥ 3 months.

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  • (PMID = 27962068.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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18. Irigoyen A, Olmedo C, Valdivia J, Comino A, Cano C, Luque R, Conde V, Delgado J, Blanco A, Bueno P: Microarray study of gene expression profiles in peripheral blood samples from lung cancer patients before and after erlotinib treatment. J Clin Oncol; 2009 May 20;27(15_suppl):e19072

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • RESULTS: The selected genes were expressed >3-fold with a false discovery rate =0.05.
  • Before treatment (T0) when patients were compared to healthy volunteers there was an increase in the expression of: histone 1 H4c, transforming growth factor beta 2, endothelial cell growth factor 1 (platelet-derived), glucose-6-phosphatase catalytic 2, Relaxin 3 receptor 1, Insulin-like growth factor binding protein 2, RAS-like family 11 member B, and ELK4.
  • After treatment (T15d), when each lung cancer patient's results were compared to their own before treatment results (T0), there was an increase in the expression of: Bcl2, myosin light polypeptide 4; interferon alpha-inducible protein 27; interferon gamma receptor 1; RASSF5, ARHGEF6, IGFBP5, tumor protein p53 inducible nuclear protein 1, peroxisome proliferative activated receptor gamma.
  • A validation of these results and the analysis of the genes that identify patients who will respond positively to erlotinib treatment is being carried out.

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  • (PMID = 27962211.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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19. Wagner AJ, Von Hoff DH, LoRusso PM, Tibes R, Mazina KE, Ware JA, Yan Y, Derynck MK, Demetri GD: A first-in-human phase I study to evaluate the pan-PI3K inhibitor GDC-0941 administered QD or BID in patients with advanced solid tumors. J Clin Oncol; 2009 May 20;27(15_suppl):3501

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A first-in-human phase I study to evaluate the pan-PI3K inhibitor GDC-0941 administered QD or BID in patients with advanced solid tumors.
  • GDC-0941 is a potent and selective oral inhibitor of the class I PI3K with 3 nM IC50 for the p110-alpha subunit in vitro and 28 nM IC50 in a cell-based pAKT assay and demonstrates broad activity in breast, ovarian, lung, and prostate cancer models.
  • METHODS: A Phase I dose escalation study using a 3+3 design was initiated in patients (pts) with solid tumors.
  • RESULTS: Nineteen pts have been enrolled in 5 successive dose-escalation cohorts in the qd arm with dose levels up to 80 mg daily.
  • Potential signs of anti-tumor activity have been observed with a soft tissue sarcoma pt on-study for >176 days with stable disease (30 mg qd), an ovarian cancer pt with an on-study 2.8-fold decrease in CA-125 response to normal levels (30 mg bid) and a pt with endometrial cancer with a decrease in tumor FDG-PET uptake (80 mg qd).
  • CONCLUSIONS: GDC-0941 is generally well-tolerated with potential signs of anti-tumor activity.

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  • (PMID = 27961289.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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20. Overgaard J Sr, Hoff CM, Hansen HS, Specht L, Overgaard M, Grau C, Andersen E, Johansen J, Andersen LJ, Evensen JF, Danish Head and Neck Cancer Group (DAHANCA): Randomized study of darbepoetin alfa as modifier of radiotherapy in patients with primary squamous cell carcinoma of the head and neck (HNSCC): Final outcome of the DAHANCA 10 trial. J Clin Oncol; 2009 May 20;27(15_suppl):6007

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Randomized study of darbepoetin alfa as modifier of radiotherapy in patients with primary squamous cell carcinoma of the head and neck (HNSCC): Final outcome of the DAHANCA 10 trial.
  • : 6007 Background: The study aimed to evaluate if correction of low hemoglobin (Hb) levels by means of the erythropoietin stimulating agent: darbepoetin alpha (Aranesp) during radiotherapy (RT) improves outcome in patients with HNSCC.
  • METHODS: Pts with HNSCC eligible for primary RT alone and with Hb values below 14.0 g/dl were randomized to receive Aranesp together with accelerated fractionated RT. Pts. were stratified according to gender, T and N staging, tumor site, and institution.
  • RESULTS: In total, 522 patients (of a planned intake of 600) were included at the time of the interim analysis.
  • The patients were evenly distributed according to the stratification parameters (gender, T and N staging, tumor site, institution).Aranesp resulted in the expected increase in Hb in more than 81% of the patients.
  • Overall, the results showed a poorer outcome in 5-year loco-regional control (59% vs. 68% (p = 0.04, RR: 1.47 [1.14-1.94]) for the Aranesp vs. control arm.
  • This was also seen for the endpoint of disease-free survival (37% vs. 47%, p = 0.02, RR: 1.32 [1.04-1.68]), whereas there was no significant difference in overall survival (40% vs. 51%, p = 0.16, RR: 1.20 [0.93-1.55]).
  • CONCLUSIONS: Correction of the Hb level with Aranesp in patients with HNSCC resulted in a significantly poorer tumor control after radiotherapy.

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  • (PMID = 27962413.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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21. Rini BI, Halabi S, Rosenberg J, Stadler WM, Vaena DA, Atkins JN, Picus J, Czaykowski P, Dutcher J, Small EJ: Bevacizumab plus interferon-alpha versus interferon-alpha monotherapy in patients with metastatic renal cell carcinoma: Results of overall survival for CALGB 90206. J Clin Oncol; 2009 May 20;27(15_suppl):LBA5019

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Bevacizumab plus interferon-alpha versus interferon-alpha monotherapy in patients with metastatic renal cell carcinoma: Results of overall survival for CALGB 90206.
  • : LBA5019 The full, final text of this abstract will be available in Part II of the 2009 ASCO Annual Meeting Proceedings, distributed onsite at the Meeting on May 30, 2009, and as a supplement to the June 20, 2009, issue of the Journal of Clinical Oncology.

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  • (PMID = 27961198.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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22. Queirolo P, Laurent S, Boitano M, Carrega P, Saverino D, Alviano F, Caielli A, Camoriano M, Ferlazzo G, Pistillo MP: Targeting ctla-4 directly on melanoma cells: A possible novel perspective in the immunotherapy of cutaneous melanoma. J Clin Oncol; 2009 May 20;27(15_suppl):e22138

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Targeting ctla-4 directly on melanoma cells: A possible novel perspective in the immunotherapy of cutaneous melanoma.
  • : e22138 Background: CTLA-4 (CD152) is an omodimeric membrane glycoprotein which behaves as the major negative regulator of T cell-mediated immune response.
  • CTLA-4 inhibitory function in T cells mainly occurs upon engagement with the B7 ligands expressed on antigen presenting cells, resulting in inhibition of cytokine production and T cell proliferation.
  • CTLA-4 expression has also been documented in established human melanoma cell lines and primary melanoma tumours.
  • METHODS: Seven primary cultures were derived from melanoma samples by mechanical tissue dissociation, enzymatic digestion and filtration of single cell suspensions.
  • Flow cytometry (FACS) with an anti-melanoma (MCSP) mAb was used to assess the growth of melanoma cells.
  • Cytokine secretion and apoptotic cells were evaluated by Elisa and Annexin V/PI staining after treatment with an agonistic anti-CTLA-4 mAb (3D5).
  • The angiogenic property of melanoma culture supernatants was evaluated on mesenchimal stromal cells (msc) isolated from human thoracic aortas.
  • RESULTS: Constitutive CTLA-4 expression was found on all melanoma cultures with variable intensity at both the protein and transcript levels.
  • CTLA-4 expressed by these cells is functional as its ligation, with an anti-CTLA-4 agonistic mAb, is able to induce inhibition of cell proliferation, due to apoptosis induction, and of IL-8, TNF-alpha and VEGF cytokine secretion.
  • CONCLUSIONS: Given the physiologic inhibitory function of CTLA-4, our results suggest its possible role in the functional biology of melanoma and open up the possibility of an anti-melanoma immunotherapy based on targeting CTLA-4 directly on tumour cells as this might allow inhibition of tumour cell growth and angiogenesis.

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  • (PMID = 27963585.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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23. Pollak MN, Blouin M, Zakikhani M, Zhao Y, Algire C: Dependence of malignant proliferation associated with loss of PTEN on glucose concentration in the hyperglycemic range: Relevance to population studies linking hyperglycemia to unfavorable cancer prognosis. J Clin Oncol; 2009 May 20;27(15_suppl):11113

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Dependence of malignant proliferation associated with loss of PTEN on glucose concentration in the hyperglycemic range: Relevance to population studies linking hyperglycemia to unfavorable cancer prognosis.
  • : 11113 Background: Loss of function of the tumor suppressor PTEN enhances malignant proliferation, but effects on cellular energy metabolism are less well characterized.
  • Population studies show that the metabolic syndrome (characterized by hyperglycemia, hyperinsulinism, and obesity) is increasingly prevalent in affluent societies and is associated with adverse outcome of many cancers, but the molecular basis for this is poorly understood.
  • METHODS: We used a tetracycline-inducible PTEN expression vector in the PTEN-null U251 glioma cell line to characterize effects of PTEN on cellular energy metabolism.
  • RESULTS: Forced expression of PTEN led to decreased phospho-AKT<sup>Ser473</sup>, decreased hexokinase II and HIF-1 alpha levels, and increased p53 levels.
  • While proliferation of PTEN-positive cells was insensitive to variation in glucose concentration at levels higher than 2.5 mM, PTEN-null cells significantly increased proliferation with increasing glucose concentration across normal physiologic range to ∼10 mM.
  • PTEN-null cells consumed more glucose than PTEN-positive cells (17.2 ± 2.0 vs. 8.8 ± 1.5 mM/million cells/48 hrs) and produced more lactate (35.9 ± 4.8 vs. 10.7 ± 2.3 mM/million cells/48 hrs).
  • When cells were incubated in presence of 2-deoxy-glucose (2-DG), growth inhibition was greater for PTEN-null cells (47.4% inhibition relative to control without 2-DG) compared with PTEN-positive cells (10.8% inhibition relative to control without 2-DG).
  • The data also suggest that PTEN status is relevant to selection of tumors likely to respond to experimental therapies that exploit glucose dependency.

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  • (PMID = 27963493.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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24. Seto T, Yamanaka T, Masuda N, Eguchi K, Takiguchi Y, Okamoto H, Ogura T, Yokoyama A, Ichinose Y, Watanabe K, Thoracic Oncology Research Group: Topoisomerase II, carbonyl reductase I, and chemosensitivity for amrubicin in the treatment of patients with small-cell lung cancer. J Clin Oncol; 2009 May 20;27(15_suppl):8104

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Topoisomerase II, carbonyl reductase I, and chemosensitivity for amrubicin in the treatment of patients with small-cell lung cancer.
  • : 8104 Background: Amrubicin (AMR) has been suggested to provide a new effective therapeutic option for small-cell lung cancer (SCLC).
  • We previously reported the promising result of a prospective phase II trial for AMR monotherapy in patients with second-line SCLC (Thoracic Oncology Research Group Study 0301).
  • Quantification of target cDNA (Top-II alpha, CBR-I and beta-actin gene) was conducted using an ABI PRISM 7700 Sequence Detection System (Applied Biosystems Inc.).
  • RESULTS: The trial registered a total of 60 patients, of which 40 blood samples were available.
  • Nineteen patients achieved a CR or PR to AMR according to the RECIST assessment and 21 did not.
  • Patients with tumor response had a significantly lower Topo-II level than those without (p=0.0465, Wilcoxon test), although there was no association between tumor response and the level of CBR-I (p=0.3229, Wilcoxon test).

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  • (PMID = 27964278.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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25. Massard C, Huguet H, Kramar A, Beyer J, Hartmann JT, Lorch A, Pico J, Rosti G, Droz J, Fizazi K: Cross-validation of a new prognostic index integrating tumor marker decline in patients with relapsed disseminated germ cell tumors. J Clin Oncol; 2009 May 20;27(15_suppl):5086

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cross-validation of a new prognostic index integrating tumor marker decline in patients with relapsed disseminated germ cell tumors.
  • : 5086 Background: Early serum tumor marker decline during chemotherapy was previously shown to be prognostic for progression-free survival (PFS) and overall survival (OS) in patients with relapsed GCT in an analysis of the IT94 phase III trial, which compared conventional chemotherapy versus high dose chemotherapy (Massard C, ASCO 2008.
  • METHODS: Data on tumor site, response to first line chemotherapy, serum tumor markers at baseline and after two cycles of chemotherapy were obtained from 235 patients accrued in the IT94 trial (training set) and from 181 patients included in phase III prospective trials of high-dose chemotherapy conducted by the German GCT group (Lorch et al, J Clin Oncol.
  • The change from baseline of serum alpha-fetoprotein (AFP) and human chorionic gonadotropin (hCG) was assessed and classified into 'favorable marker decline' and 'unfavorable marker decline' group, as previously described (ASCO 2008.
  • RESULTS: In both series, favourable serum AFP decline was significantly associated with a better 2-year PFS (46% vs 24%; p < 0.0001) and OS (62% vs 34%; p = 0.0013) while serum hCG decline did not affect outcome.
  • In multivariate analysis of the IT94 trial, an unfavorable AFP decline and a mediastinal primary site were adverse prognostic factors for both PFS and OS, and this was confirmed in the validation set.
  • Among patients from the good prognostic group (favorable AFP decline and non-mediastinal primary site), those who were treated with high-dose chemotherapy had a better PFS (2-year PFS rate: 54% vs 37%; HR = 0.62; p = 0.017), and a trend for a better OS (2-year OS rate: 68% vs. 58%; HR = 0.77; p = 0.29) as compared to patients who were treated with conventional chemotherapy.
  • CONCLUSIONS: AFP decline during the first 6 weeks of salvage chemotherapy and a mediastinal primary tumor site predict for PFS and OS in patients with relapsed disseminated GCT.

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  • (PMID = 27964274.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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26. Schwandt A, Garcia JA, Elson P, Wyckhouse J, Finke JH, Ireland J, Triozzi P, Zhou M, Dreicer R, Rini BI: A translational phase II trial of celecoxib plus interferon-alpha (IFN-α2b) in metastatic renal cell carcinoma (RCC) patients (pts) with 3+ COX-2 tumor immunostaining. J Clin Oncol; 2009 May 20;27(15_suppl):5116

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A translational phase II trial of celecoxib plus interferon-alpha (IFN-α2b) in metastatic renal cell carcinoma (RCC) patients (pts) with 3+ COX-2 tumor immunostaining.
  • : 5116 Background: Cyclooxygenase-2 (COX-2) has been correlated with RCC stage and grade, and overexpression can lead to dysregulation of dendritic cells (DC) and CD4+/CD25+/FOXP3+ regulatory T cells (Treg).
  • A previous trial of celecoxib in combination with IFNα2b in RCC (Rini et al, Cancer.
  • 2006) demonstrated an association between more intense COX-2 RCC tumor staining and clinical response.
  • METHODS: Pts with cytokine-naïve mRCC with at least 10% maximal COX-2 tumor staining received IFNα2b MU five times/week plus celecoxib 400 mg BID continuously.
  • Baseline tumor tissue was stained for COX-2, CD4+ and CD8+ T cells, Treg and DC (s100 and CD208).
  • Peripheral blood prostaglandin E2 (PGE2), DC and Treg number/function and intracellular T cell cytokine production were measured at baseline, at the end of cycles 2 and 4 and at end of treatment.
  • The trial tested a null hypothesis of ORR <20% vs. alternative hypothesis of ORR >40%; beta = 0.8 and alpha = 0.05 (n = 34).
  • Immune parameters were analyzed using non-parametric methods.
  • RESULTS: Fourteen pts have been enrolled; 79% male, median age 62 (range, 43-74) and 64% ECOG performance status 0.
  • The ORR was 21% and 69% of pts experienced tumor shrinkage.
  • Baseline 3+ COX-2 staining was associated with elevated peripheral blood PGE2 levels (p = 0.02), reduced DC IL-12 expression (p = 0.04) and reduction in IFN gamma-producing CD3+CD4+ T-cells (p = 0.04) compared to a control group of RCC pts with <10% 3+ COX-2 staining (n = 21).
  • No significant changes in immunomodulatory cells were observed with therapy.
  • COX-2 RCC tumor expression promotes an immunosuppressive phenotype.

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  • (PMID = 27964389.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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27. Kuhberg M Sr, Skowronek P, Chen F, Oskay-Oezcelik G, Oskay-Oezcelik G, Lichtenegger W, Lichtenegger W, Sehouli J: Prediction of nutritional status and intestinal tumor involvement in patients with primary or recurrent ovarian cancer: Results of a prospective study. J Clin Oncol; 2009 May 20;27(15_suppl):5570

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prediction of nutritional status and intestinal tumor involvement in patients with primary or recurrent ovarian cancer: Results of a prospective study.
  • 79 (52%) of them had primary and 73 (48%) recurrent disease.
  • At the time of admission for surgical therapy, the body composition was analysed with Bioelectrical Impedance Analysis (BIA) using phase angle alpha and ratio of extra-cellular mass and body cell mass (ECM/BCM).
  • During operation a standardised and validated tumor documentation tool (IMO) was performed.
  • RESULTS: The median age of patients was 56 years (range 48-66) with median BMI 24.4 kg/m<sup>2</sup> (range 21.8-27.3).
  • FIGO stage and NRS correlated negatively with phase angle alpha and positively with ECM/BCM in patients with primary diagnosis (p < 0.05).
  • Patients with primary or recurrent disease who required surgical resection of small or large intestine, phase angle alpha and serum albumin level were significantly lower than in patients with no intestinal involvement (p < 0.05).
  • CONCLUSIONS: Independent of tumor stage, the preoperative evaluation of BIA, especially phase angle α, is a valid method to predict surgical outcome in patients with ovarian and peritoneal cancer.

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  • (PMID = 27962572.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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28. Kamai T, Tomosugi N, Abe H, Yoshida K: Protein profiling of tumor tissues by surface-enhanced laser desorption/ionization time-of-flight mass spectrometry to discriminate between localized and metastatic renal cell carcinoma. J Clin Oncol; 2009 May 20;27(15_suppl):e16098

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Protein profiling of tumor tissues by surface-enhanced laser desorption/ionization time-of-flight mass spectrometry to discriminate between localized and metastatic renal cell carcinoma.
  • : e16098 Background: We previously reported that mRNA of interferon-alpha receptor type 2 (IFNAR2) was upregulated in metastatic and IFN-a resistant renal cell carcinoma (RCC) in comparison to localized RCC or metastatic tumors with good response to IFN-a (BMC Cancer, 2007).
  • Protein profiling using human tumor tissues may give insight into cellular pathways leading to carcinogenesis and metastasis in RCC.
  • METHODS: We examined mRNAs expression for IFNAR2 in paired tumor and non-tumor samples from the surgical specimens of Japanese patients with RCC using a real-time reverse transcription polymerase chain reaction.
  • Then we selected representative five IFNAR2 upregulated clear cell carcinomas cases with metastatic tumor, five IFNAR2 upregulated metastatic sarcomatoid carcinomas, and five normal expression clear cell carcinomas with localized tumor.
  • We investigated protein profiling in the tumor tissues of above three groups using surface-enhanced laser desorption/ionization time-of-flight mass spectrometry (SELDI-TOF MS) coupled with IMAC-Cu chips.
  • RESULTS: For hierarchical clustering analysis, we used the 25 peaks which revealed significant differences in single-marker analysis in the range from 1,500 to 10,000 m/z.
  • The heat map analysis based on the clustering distinguished completely metastatic tumors with IFNAR2 upregulated groups from localized tumors with IFNAR2 normal expression group.
  • Furthermore, the heat map discriminated metastatic sarcomatoid carcinomas from metastatic clear cell carcinomas with a sensitivity of 100% and a specificity of 80%.
  • CONCLUSIONS: SELDI-TOF MS profiling of tumor tissues can be applied to differentiate patients with three types of RCCs.
  • Our findings may reflect different molecular mechanism between localized and metastatic carcinomas, and the different response to immunotherapy with IFN-α.

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  • (PMID = 27963090.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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29. Lopez R, Gallardo E, Ruibal A, Leon L, Sanchez-Salmon A, Abdulkader I, Gude F, Curiel T, Barandela J, Gayoso L: HIF expression and Max-SUV-18F-FDG-PET in non-small cell lung cancer (NSCLC) patients. J Clin Oncol; 2009 May 20;27(15_suppl):e22010

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  • [Title] HIF expression and Max-SUV-18F-FDG-PET in non-small cell lung cancer (NSCLC) patients.
  • : e22010 Background: Tumor hipoxia induces the up-regulation of several genes via the hipoxia-inducible transcription factors (HIF) 1 and 2.
  • HIF-2 alpha (HIF-2 α) and HIF-1 alpha (HIF-1α) are associated with the prognosis of operable NSCLC patients.
  • We studied the immunohistochemical expression of HIF-1α and HIF-2 α in patients with NSCLC and the possible correlation with the maximum standardised uptake value (max SUV) of 18F-FDG as well as other biological parameters.
  • Sections were scored as positive if >10% of cells stained positively.
  • RESULTS: HIF- 1α expression was observed in 84/96 patients (34/39 adenocarcinomas and 50/57 squamous cell carcinomas), however it did not correlate with clinical stage (I-II: 41/45 vs III-IV: 44/51).
  • The maxSUV values of 18F-FDG-PET were higher (p:0,039) in HIF-1α -positive (17,1±8,6) than in negative tumors (11,8±4,4).
  • HIF-2 α expression was observed in 60/103 cases (27/42 adenocarcinomas and 33/61 squamous cell carcinomas) and it did not correlate with clinical stage ((I-II: 28/45 vs III-IV: 32/57).

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  • (PMID = 27963184.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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30. Heinrich MC, Carden R, Griffith D, Liang C, Marino-Enriquez A, McKinley A, Presnell A, Fletcher JA: In vitro activity of sorafenib against imatinib- and sunitinib-resistant kinase mutations associated with drug-resistant GI stromal tumors. J Clin Oncol; 2009 May 20;27(15_suppl):10500

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  • [Title] In vitro activity of sorafenib against imatinib- and sunitinib-resistant kinase mutations associated with drug-resistant GI stromal tumors.
  • : 10500 Background: Most gastrointestinal stromal tumors (GISTs) harbor mutant KIT or platelet-derived growth factor receptor alpha (PDGFRA) kinases, which are targets of imatinib (front-line therapy) or sunitinib (second-line therapy).
  • METHODS: Kinase mutants were biochemically profiled for SOR, SU, and IM sensitivity by measuring inhibition of kinase phosphorylation after drug treatment in mutant-expressing CHO cells.
  • We also tested the biochemical and cellular activity of SOR and IM against GIST cells derived from IM-resistant tumor clones.
  • RESULTS: SOR had superior potency to IM against IM-resistant KIT secondary mutations involving the ATP binding pocket (V654A, T670I) and the activation loop (D816H, D820A/G, N822K, Y823D).
  • To confirm these observations in a GIST cellular context, we tested the relative potency of IM and SU against two previously described IM-resistant GIST cell lines (GIST430: exon 11 + V654A, GIST48: exon 11 + D820A).
  • SOR was significantly more potent than IM against KIT in these cell lines.
  • Based on these results, we hypothesize that SOR might have superior clinical activity to SU in the setting of imatinib-resistant GIST and should be further evaluated for clinical efficacy in the second-line setting.

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  • (PMID = 27963686.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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36. Yoshida A, Sen C, Asa SL, Rosenblum MK: Composite pituitary adenoma and craniopharyngioma?: an unusual sellar neoplasm with divergent differentiation. Am J Surg Pathol; 2008 Nov;32(11):1736-41
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  • [Title] Composite pituitary adenoma and craniopharyngioma?: an unusual sellar neoplasm with divergent differentiation.
  • We report a young man who presented with atrial fibrillation and was subsequently found to have a markedly elevated serum thyroid stimulating hormone level and a solid, noncalcified intrasellar mass on imaging.
  • The patient was treated with thyroid radioablation and hormone replacement and followed for 7 years, during which time the tumor grew to 4.6 cm.
  • At transsphenoidal surgery, a tumor consisting of a pituitary adenoma and adamantinomatous craniopharyngiomalike components was resected.
  • Both components were closely intermingled, but there was no evidence of an intermediate morphologic phenotype.
  • Immunohistochemically, the adenoma was not only positive for beta-thyroid stimulating hormone, alpha subunit, and pituitary transcription factor 1, but also stained for beta-follicle stimulating hormone, steroidogenic factor-1, adrenocorticotropic hormone, and pituitary-restricted transcription factor (Tpit), exhibiting an unusual plurihormonal profile.
  • This lesion may represent an unusual composite tumor attributable to divergent differentiation of a common precursor.
  • Alternatively, it may be viewed as a pituitary adenoma showing metaplastic change analogous to the development of squamous cell nests of the pars tuberalis from adenohypophyseal endocrine cells.
  • [MeSH-major] Adenoma / pathology. Craniopharyngioma / pathology. Neoplasms, Multiple Primary / pathology. Pituitary Neoplasms / pathology

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  • (PMID = 18769335.001).
  • [ISSN] 1532-0979
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 9002-71-5 / Thyrotropin
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37. McCluggage WG, Aydin NE, Wong NA, Cooper K: Low-grade epithelial-myoepithelial carcinoma of bartholin gland: report of 2 cases of a distinctive neoplasm arising in the vulvovaginal region. Int J Gynecol Pathol; 2009 May;28(3):286-91
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  • [Title] Low-grade epithelial-myoepithelial carcinoma of bartholin gland: report of 2 cases of a distinctive neoplasm arising in the vulvovaginal region.
  • We report 2 cases of a distinctive neoplasm arising from Bartholin gland and presenting as a vulval or vaginal mass.
  • The tumors occurred in patients aged 44 and 51 years and were 2 and 3 cm in maximum dimension.
  • The neoplasms were unencapsulated and largely well circumscribed but with a focally infiltrative edge.
  • They were composed of tubular, trabecular, or insular arrangements with a double layer of inner cuboidal cells with round nuclei and outer cells with ovoid nuclei and clear cytoplasm, corresponding to epithelial and myoepithelial cells, respectively.
  • In both cases, a minor proportion of the neoplasm consisted of cribriform arrangements, creating an appearance reminiscent of adenoid cystic carcinoma, although the overall morphology was not typical of that lesion.
  • Immunohistochemically, the inner cells were positive with epithelial markers, including broad-spectrum cytokeratins and epithelial membrane antigen, and the outer cell layer was positive with myoepithelial markers p63, calponin, and alpha-smooth muscle actin.
  • Both neoplasms exhibited diffuse strong immunoreactivity of the epithelial cells with c-kit.
  • Activating mutations in KIT exons 9, 11, 13, and 17 and in platelet-derived growth factor receptor alpha exons 12, 14, and 18 were searched for by polymerase chain reaction and direct sequencing but were not identified.
  • We believe this represents a low-grade carcinoma arising from Bartholin gland composed of a dual population of epithelial and myoepithelial cells and closely resembling the salivary gland neoplasm termed epithelial-myoepithelial carcinoma.
  • [MeSH-major] Bartholin's Glands / pathology. Carcinoma / pathology. Vulvar Neoplasms / pathology

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  • (PMID = 19620948.001).
  • [ISSN] 1538-7151
  • [Journal-full-title] International journal of gynecological pathology : official journal of the International Society of Gynecological Pathologists
  • [ISO-abbreviation] Int. J. Gynecol. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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38. Pilichowska ME, Fleming MD, Pinkus JL, Pinkus GS: CD4+/CD56+ hematodermic neoplasm ("blastic natural killer cell lymphoma"): neoplastic cells express the immature dendritic cell marker BDCA-2 and produce interferon. Am J Clin Pathol; 2007 Sep;128(3):445-53
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  • [Title] CD4+/CD56+ hematodermic neoplasm ("blastic natural killer cell lymphoma"): neoplastic cells express the immature dendritic cell marker BDCA-2 and produce interferon.
  • CD4+/CD56+ hematodermic neoplasm ("blastic natural killer [NK]-cell lymphoma") is a rare highly aggressive neoplasm associated with cutaneous manifestations followed by dissemination to blood, bone marrow, and other tissues.
  • Neoplastic cells exhibit a lineage-negative CD4+/CD56+/CD43+/HLA-DR+ immunophenotype, initially suggesting an NK-cell derivation.
  • The recent discovery of CD123 antigen expression by tumor cells has provided evidence for a relationship to immature dendritic cells (DCs), a group of myeloid and lymphoid early-committed progenitors capable of differentiating into antigen-presenting DCs.
  • Based on flow cytometric analysis, myeloid DCs represent the majority of human peripheral blood DCs and are positive for blood dendritic cell antigen (BDCA)-1 (or CD1c), CD13, CD11c(high), CD33, and CD123(low).
  • Plasmacytoid DCs are BDCA-2+/ CD123(high)+/CD13-/CD33- and produce interferon (IFN)-alpha when triggered by antigens.
  • IFN-alpha production may be detected in tissue sections using antibodies for myxovirus A (MxA) protein, a surrogate marker.
  • This report describes the clinical, histologic, immunophenotypic, cytogenetic, and molecular genetic findings for 3 cases of CD4+/CD56+ hematodermic neoplasms.
  • In all cases, neoplastic cells were reactive for CD123, BDCA-2, and MxA protein, providing strong evidence for an immature plasmacytoid DC derivation for this rare neoplasm.
  • [MeSH-major] Antigens, CD4 / metabolism. Antigens, CD56 / metabolism. Lectins, C-Type / metabolism. Lymphoma, Non-Hodgkin / diagnosis. Membrane Glycoproteins / metabolism. Receptors, Immunologic / metabolism
  • [MeSH-minor] Adolescent. Aged. Dendritic Cells / metabolism. Female. GTP-Binding Proteins / analysis. Humans. Immunophenotyping. Male. Middle Aged. Myxovirus Resistance Proteins

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  • (PMID = 17709319.001).
  • [ISSN] 0002-9173
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD4; 0 / Antigens, CD56; 0 / CLEC4C protein, human; 0 / Lectins, C-Type; 0 / MX1 protein, human; 0 / Membrane Glycoproteins; 0 / Myxovirus Resistance Proteins; 0 / Receptors, Immunologic; EC 3.6.1.- / GTP-Binding Proteins
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39. Ding L, Chen XP, Zhang ZW, Wang H, Cao B, Wang ZH, Li CL: [Synergistic effect of bromocriptine combining tumor necrosis factor-alpha on reversing multidrug resistance in a nude mouse model of liver neoplasm]. Zhonghua Wai Ke Za Zhi; 2005 Oct 1;43(19):1248-53
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  • [Title] [Synergistic effect of bromocriptine combining tumor necrosis factor-alpha on reversing multidrug resistance in a nude mouse model of liver neoplasm].
  • OBJECTIVE: To investigate synergistic effect of bromocriptine (BCT) combining tumor necrosis factor-alpha (TNF-alpha) on reversing multidrug resistance in a nude mouse model of liver neoplasm.
  • METHODS: Human hepatocarcinoma cell line HepG(2) (HepG(2) group), drug resistant hepatocarcinoma cell line HepG(2)/adriamycin (HepG(2)/ADM group) and hepatocarcinoma cell line transfected with TNF-alpha gene HepG(2)/ADM/TNF (TNF group and BCT group) were injected into the liver of nude mice via orthotopic implantation to establish multidrug resistance model of liver neoplasm in vivo.
  • Size and weight of the tumor were measured.
  • Furthermore tumor histological character and growth of the nude mice was observed and its chemosensitivity was tested.
  • MDR associated genes and proteins (MRP, LRP) of implanted tumors were detected by immunohistochemical staining and reverse transcriptive polymerase chain reaction (RT-PCR), and apoptosis rate of hepatocarcinoma cells was detected by TUNEL assay.
  • RESULTS: The nude mouse model of each cell line was all inoculated successfully.
  • The tumor growth rate and weight were significantly different among groups (P < 0.05).
  • After chemotherapy tumor growth inhibition rate was higher in BCT group (67%) compared to ADM and TNF groups (P < 0.01), and similar to HepG(2) group (54%).
  • MDR1 and LRP mRNA could be detected in all groups, but TNF-alpha was detected only in TNF-alpha and BCT groups.
  • Furthermore, MDR1 and LRP protein expression of tumors in TNF-alpha and BCT groups was low similar to HepG(2) group.
  • The apoptosis rate of hepatocarcinoma cells was much higher in BCT group than in other groups (P < 0.05) with TUNEL assay.
  • CONCLUSIONS: TNF-alpha gene can down-regulate the MDR associated genes and proteins expression for example MDR1, LRP, and lower its tumorgenesis.
  • Moreover, bromocriptine can enhance the susceptibility of HepG(2)/ADM cells to cytotoxic drugs.
  • [MeSH-major] Bromocriptine / pharmacology. Drug Resistance, Multiple / drug effects. Drug Resistance, Neoplasm / drug effects. Liver Neoplasms, Experimental / therapy. Tumor Necrosis Factor-alpha / pharmacology
  • [MeSH-minor] Animals. Cell Line, Tumor. Drug Synergism. Female. Humans. Male. Mice. Mice, Nude. Multidrug Resistance-Associated Proteins / biosynthesis. Multidrug Resistance-Associated Proteins / genetics. Neoplasm Transplantation. Transfection. Vault Ribonucleoprotein Particles / biosynthesis. Vault Ribonucleoprotein Particles / genetics

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  • (PMID = 16271222.001).
  • [ISSN] 0529-5815
  • [Journal-full-title] Zhonghua wai ke za zhi [Chinese journal of surgery]
  • [ISO-abbreviation] Zhonghua Wai Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Multidrug Resistance-Associated Proteins; 0 / Tumor Necrosis Factor-alpha; 0 / Vault Ribonucleoprotein Particles; 0 / major vault protein; 3A64E3G5ZO / Bromocriptine
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40. Judson K, Argani P: Intraductal spread by metastatic islet cell tumor (well-differentiated pancreatic endocrine neoplasm) involving the breast of a child, mimicking a primary mammary carcinoma. Am J Surg Pathol; 2006 Jul;30(7):912-8
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  • [Title] Intraductal spread by metastatic islet cell tumor (well-differentiated pancreatic endocrine neoplasm) involving the breast of a child, mimicking a primary mammary carcinoma.
  • Metastases to the breast are rare, accounting for an estimated 1% to 2% of malignant breast neoplasms.
  • The key histopathologic features supporting a metastasis to the breast have been stated to be the absence of elastosis, presence of a pushing border (circumscribed lesion), multiple satellite foci, lymphatic emboli, and, most importantly, the absence of an in situ carcinoma component.
  • We report a unique case of a pancreatic islet cell tumor metastatic to the breast of an 18-year-old girl.
  • However, review of slides from the prior pancreatic neoplasm, review of slides from the subsequent mastectomy, and use of immunohistochemistry allowed recognition of the lesion as a metastasis, which proved to be the first clinical manifestation of a systemic relapse.
  • To our knowledge, this is the second case of islet cell tumor reported to metastasize to the breast, and the first report of a metastasis proven to have grown within existing ducts of the breast by immunohistochemistry.
  • [MeSH-major] Breast Neoplasms / secondary. Carcinoma in Situ / pathology. Carcinoma, Ductal, Breast / pathology. Carcinoma, Islet Cell / secondary. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Adolescent. Biomarkers, Tumor / analysis. Diagnosis, Differential. Female. Humans. Treatment Outcome

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  • (PMID = 16819337.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 88843
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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41. Miettinen M, Makhlouf HR, Sobin LH, Lasota J: Plexiform fibromyxoma: a distinctive benign gastric antral neoplasm not to be confused with a myxoid GIST. Am J Surg Pathol; 2009 Nov;33(11):1624-32
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  • [Title] Plexiform fibromyxoma: a distinctive benign gastric antral neoplasm not to be confused with a myxoid GIST.
  • A great majority of gastric mesenchymal tumors are gastrointestinal stromal tumor (GIST).
  • A rare group of non-GISTs include myxoid mesenchymal neoplasms.
  • In this report, we describe 12 cases of a distinctive gastric tumor, named here as plexiform fibromyxoma.
  • These tumors occurred in 5 men and 7 women of ages 7 to 75 years (median, 41 y).
  • All tumors were located in the gastric antrum and 6 of them also extended into extragastric soft tissues or into the duodenal bulb.
  • The tumors measured from 3 to 15 cm (median, 5.5 cm).
  • Histologically typical was a plexiform intramural growth with multiple micronodules containing paucicellular to moderately cellular myxoid to collagenous and fibromyxoid neoplastic elements.
  • Extramural components included subserosal nodules, and sometimes more cellular, solid nonplexiform spindle cell proliferation.
  • The tumor cells varied from oval to spindled and had limited atypia and mitotic activity < 5/50 high-power fields.
  • Frequent ulceration, mucosal invasion, and vascular invasion (4 cases) had no adverse significance in these tumors.
  • Immunohistochemically, the tumor cells were positive for alpha smooth muscle actin, and variably for CD10, and were consistently negative for KIT, DOG1, CD34, desmin, and S100 protein.
  • No KIT or platelet-derived growth factor receptor alpha mutations were present in the 3 examined cases.
  • Additional 3 patients survived 14 to 25 years with unknown tumor status.
  • Review of large numbers of mesenchymal tumors in the esophagus and intestines did not reveal similar tumors.
  • Plexiform fibromyxoma is a distinctive benign gastric antral neoplasm that should be separated from GIST, nerve sheath tumors, and other fibromyxoid neoplasms.
  • [MeSH-major] Fibroma / diagnosis. Gastrointestinal Stromal Tumors / diagnosis. Pyloric Antrum / pathology. Stomach Neoplasms / diagnosis
  • [MeSH-minor] Adolescent. Adult. Aged. Biomarkers, Tumor / analysis. Child. Diagnosis, Differential. Disease-Free Survival. Female. Humans. Immunohistochemistry. Male. Middle Aged. Neoplasm Invasiveness. Young Adult

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  • (PMID = 19675452.001).
  • [ISSN] 1532-0979
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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42. Piña-Oviedo S, Herrera-Medina H, Coronado H, Del Valle L, Ortiz-Hidalgo C: CD4+/CD56+ hematodermic neoplasm: presentation of 2 cases and review of the concept of an uncommon tumor originated in plasmacytoid dendritic cells expressing CD123 (IL-3 receptor alpha). Appl Immunohistochem Mol Morphol; 2007 Dec;15(4):481-6
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  • [Title] CD4+/CD56+ hematodermic neoplasm: presentation of 2 cases and review of the concept of an uncommon tumor originated in plasmacytoid dendritic cells expressing CD123 (IL-3 receptor alpha).
  • CD4/CD56 hematodermic neoplasm is a rare neoplasm presenting with cutaneous nodules, lymphadenopathy, bone marrow infiltration, and an aggressive clinical course.
  • Recently, the plasmacytoid dendritic cell origin of this neoplasm has been demonstrated.
  • Plasmacytoid dendritic cell is a hematopoietic-derived cell implicated in the regulation of innate and adaptive cell immunity and in the production of certain regulatory cytokines.
  • Recently it has been demonstrated that these cells express cell surface markers such as IL-3 receptor alpha (CD123).
  • In the present report, we describe the clinical, histologic, and immunohistochemical characteristics of 2 cases of CD4/CD56 hematodermic neoplasm.
  • Clinical findings were limited to the skin and consisted of multiple cutaneous nodules located in the thorax and extremities, some of them ulcerated.
  • Histologically, the tumors were characterized by a nonepidermotropic, dermal and subdermal infiltration of homogeneous medium-sized cells resembling lymphoblasts or myeloblasts.
  • Immunohistochemical characterization of the tumors showed expression of CD4, CD56, CD43, and CD123, whereas CD8, CD20, and MPO were negative.
  • This characteristic profile in addition to the expression of CD123, which was detected in both cases, can be used as valuable tools in the diagnosis of this rare neoplasm.

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  • (PMID = 18091395.001).
  • [ISSN] 1541-2016
  • [Journal-full-title] Applied immunohistochemistry & molecular morphology : AIMM
  • [ISO-abbreviation] Appl. Immunohistochem. Mol. Morphol.
  • [Language] ENG
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD4; 0 / Antigens, CD56; 0 / Interleukin-3 Receptor alpha Subunit
  • [Number-of-references] 50
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43. Verma M, Joseph G, McCluggage WG: Uterine composite tumor composed of leiomyosarcoma and embryonal rhabdomyosarcoma with immature cartilage. Int J Gynecol Pathol; 2009 Jul;28(4):338-42
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  • [Title] Uterine composite tumor composed of leiomyosarcoma and embryonal rhabdomyosarcoma with immature cartilage.
  • SUMMARY: We report a rare composite uterine mesenchymal neoplasm in a 66-year-old woman composed of approximately equal amounts of leiomyosarcoma and embryonal rhabdomyosarcoma, the latter containing foci of immature cartilage.
  • The leiomyosarcomatous element was positive with alpha smooth muscle actin and h-caldesmon and the rhabdomyosarcomatous component with myogenin and myo-D1.
  • In a review of the literature, we have identified only a single example of a similar case.
  • This is likely to represent rhabdomyosarcomatous differentiation in a leiomyomatous neoplasm or alternatively bidirectional differentiation from an uncommitted mesenchymal stem cell.
  • [MeSH-major] Leiomyosarcoma / pathology. Neoplasms, Multiple Primary / pathology. Rhabdomyosarcoma, Embryonal / pathology. Uterine Neoplasms / pathology

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  • (PMID = 19483631.001).
  • [ISSN] 1538-7151
  • [Journal-full-title] International journal of gynecological pathology : official journal of the International Society of Gynecological Pathologists
  • [ISO-abbreviation] Int. J. Gynecol. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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44. Siegel R, Linse R, Rau B: [The question of surgical therapy for necrolytic migratory erythema, a cutaneous disease]. Chirurg; 2006 Jun;77(6):535-8
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  • [Title] [The question of surgical therapy for necrolytic migratory erythema, a cutaneous disease].
  • Its underlying cause is usually a pancreatic islet cell tumour with marked glucagon secretion.
  • The glucagonoma syndrome is characterised by pancreatic neuroendocrine neoplasm, NME, and diabetes mellitus.
  • We present a case of glucagonoma syndrome in a 58-year-old woman with a history of recurrent cutaneous manifestations who was referred for surgical resection of a pancreatic neoplasm after the NME was finally diagnosed.
  • We discuss diagnostic methods, differential diagnosis, and therapeutic management of this disease.
  • [MeSH-major] Erythema / etiology. Glucagonoma / complications. Pancreatic Neoplasms / complications. Paraneoplastic Syndromes

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  • [Cites] Int J Dermatol. 2004 Jan;43(1):12-8 [14693015.001]
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  • (PMID = 16362349.001).
  • [ISSN] 0009-4722
  • [Journal-full-title] Der Chirurg; Zeitschrift fur alle Gebiete der operativen Medizen
  • [ISO-abbreviation] Chirurg
  • [Language] ger
  • [Publication-type] Case Reports; Comparative Study; Journal Article
  • [Publication-country] Germany
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45. Tejerina González E, Argüelles M, Jiménez-Heffernan JA, Dhimes P, Vicandi B, Pinedo F: Cytologic features of hepatoid carcinoma of the ovary: a case report with immunocytologic evaluation of HepPar1. Acta Cytol; 2008 Jul-Aug;52(4):490-4
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  • BACKGROUND: Hepatoid carcinoma is a rare, primary neoplasm of the ovary characterized by histologic, immunobistochemical and analytical evidence of hepatic differentiation.
  • CASE: A 65-year-old woman presented with an abdominopelvic mass, peritoneal implants and elevated levels of CA-125 and a-fetoprotein (AFP).
  • Cytologic examination of the ascitic fluid revealed cellular samples of polygonal cells in trabecular and papillary groups.
  • Neoplastic cells were predominantly monomorphous, but some groups exhibited marked cellular atypia.
  • Histologically, the neoplasm had evident hepatocellular differentiation, with a solid, trabecular growth of polygonal, eosinophilic cells with well-defined boundaries.
  • The cells were immunoreactive with keratins, AFP and HepPar1.
  • CONCLUSION: As occurs with other hepatocellular neoplasms, the hepatic differentiation that characterizes this unusual neoplasm may not be easily recognizable in effusion samples.
  • However, there are some features that, in addition to an elevated AFP value, may help to suggest the diagnosis.
  • A predominant trabecular arrangement with occasional endothelial rimming and HepPar1 immunoreactivity, consistent with hepatic differentiation, are unusual in common surface epithelial ovarian tumors.
  • [MeSH-major] Carcinoma / pathology. Hepatocytes / pathology. Immunohistochemistry. Ovarian Neoplasms / pathology
  • [MeSH-minor] Aged. Antibodies, Monoclonal. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cell Differentiation. Chemotherapy, Adjuvant. Female. Humans. Hysterectomy. Ovariectomy. Treatment Outcome. alpha-Fetoproteins / analysis

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  • (PMID = 18702372.001).
  • [ISSN] 0001-5547
  • [Journal-full-title] Acta cytologica
  • [ISO-abbreviation] Acta Cytol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AFP protein, human; 0 / Antibodies, Monoclonal; 0 / alpha-Fetoproteins
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46. Valent P, Sperr WR, Akin C: How I treat patients with advanced systemic mastocytosis. Blood; 2010 Dec 23;116(26):5812-7
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  • Advanced systemic mastocytosis (SM) is a rare myeloid neoplasm characterized by uncontrolled accumulation of neoplastic mast cells (MCs) in various organs with consecutive impairment of organ function, drug resistance, and a poor prognosis.
  • Advanced SM may present as smoldering or slowly progressing neoplasm but may also present as rapidly progressing aggressive SM or even as MC leukemia.
  • Approximately half of the patients have an associated hematologic non-MC-lineage disease (SM-AHNMD) or develop an AHNMD over time.
  • Drug resistance may not only result from the KIT mutant D816V that is found in most patients, but also from KIT-independent pro-oncogenic signaling pathways that play a role in disease evolution.
  • By contrast, in rapidly progressing aggressive SM and MC leukemia, even polychemotherapy and hematopoietic stem cell transplantation may fail, which points to the need to develop new drugs and treatment concepts for these patients.
  • In SM-AHNMD, separate treatment plans should be established for the SM component and the AHNMD component of the disease, with recognition that the AHNMD often has to be managed and treated as a secondary and thus a high-risk neoplasm.
  • [MeSH-major] Immunologic Factors / therapeutic use. Interferon-alpha / therapeutic use. Mastocytosis, Systemic / drug therapy. Mutation / genetics. Proto-Oncogene Proteins c-kit / genetics

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  • (PMID = 20855864.001).
  • [ISSN] 1528-0020
  • [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 / Immunologic Factors; 0 / Interferon-alpha; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
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47. Starska K, Łukomski M, Tchórzewski H, Głowacka E: [Production of proinflammatory cytokines by peripheral blood mononuclear cells in cocultures with squamous cell carcinoma of the larynx]. Otolaryngol Pol; 2009 Sep;63(7):35-42
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  • [Title] [Production of proinflammatory cytokines by peripheral blood mononuclear cells in cocultures with squamous cell carcinoma of the larynx].
  • PURPOSE: Antitumor mechanisms of cellular immune response are connected with the cytokines activity secreted by peripheral blood mononuclear cells (PBMC).
  • The aim of this study was estimation of proinflammatory cytokine (IL-6 and TNF- ) concentration in patients with laryngeal squamous cell carcinoma and analysis of directed influence of neoplasm cells to the function of PBMC and modification of cytokine profile.
  • MATERIALS AND METHODS: For analysis of cytokine secretion, the cultures of isolated peripheral blood mononuclear cells (PBMC) with marginal neoplasm cells and noncancerous adjacent mucosa cells from 55 patients with laryngeal squamous cell carcinoma were established.
  • RESULTS: Authors reported the increase of IL-6 and decrease of TNF- concentration in cultures of isolated peripheral blood mononuclear cells (PBMC) with marginal neoplasm cells and non-cancerous adjacent mucosa cells.
  • CONCLUSION: The presence of laryngeal squamous carcinoma cells in PBMC culture can modify immunocompetent cells activity and production of proinflammatory cytokines.
  • [MeSH-major] Carcinoma, Squamous Cell / immunology. Interleukin-6 / blood. Laryngeal Neoplasms / immunology. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 20564898.001).
  • [ISSN] 0030-6657
  • [Journal-full-title] Otolaryngologia polska = The Polish otolaryngology
  • [ISO-abbreviation] Otolaryngol Pol
  • [Language] pol
  • [Publication-type] Comparative Study; English Abstract; Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Interleukin-6; 0 / Tumor Necrosis Factor-alpha
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48. Yu R, Nissen NN, Dhall D, Heaney AP: Nesidioblastosis and hyperplasia of alpha cells, microglucagonoma, and nonfunctioning islet cell tumor of the pancreas: review of the literature. Pancreas; 2008 May;36(4):428-31
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  • [Title] Nesidioblastosis and hyperplasia of alpha cells, microglucagonoma, and nonfunctioning islet cell tumor of the pancreas: review of the literature.
  • We report a rare case of nesidioblastosis and hyperplasia of alpha cells, microglucagonoma, and nonfunctioning islet cell tumor of the pancreas.
  • The patient's clinical presentation, diagnosis, treatment, pancreas pathology, and follow-up are reviewed.
  • A 60-year-old patient was incidentally found to harbor a pancreatic mass with markedly elevated glucagon levels but without glucagonoma syndrome.
  • She was initially diagnosed with glucagonoma, and the tumor was resected.
  • Pathological examination demonstrated that the tumor was a nonfunctioning islet cell tumor and revealed nesidioblastosis and hyperplasia of alpha cells and microglucagonoma in the apparently normal surgical margin.
  • No pancreatic tumors recurred 36 months after surgery.
  • This is the third case of alpha-cell nesidioblastosis reported in the English literature.
  • Nesidioblastosis and hyperplasia of alpha cells should be considered in the differential diagnosis of hyperglucagonemia.
  • Somatostatin analog may be used to suppress glucagon secretion in alpha-cell hyperplasia.
  • [MeSH-major] Adenoma, Islet Cell / pathology. Carcinoma, Islet Cell / pathology. Glucagonoma / pathology. Islets of Langerhans / pathology. Nesidioblastosis / pathology. Pancreatic Neoplasms / pathology

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  • (PMID = 18437091.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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49. Siqueira AS, Carvalho MR, Monteiro AC, Freitas VM, Jaeger RG, Pinheiro JJ: Matrix metalloproteinases, TIMPs and growth factors regulating ameloblastoma behaviour. Histopathology; 2010 Jul;57(1):128-37
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  • [Title] Matrix metalloproteinases, TIMPs and growth factors regulating ameloblastoma behaviour.
  • AIMS: Ameloblastoma is an odontogenic neoplasm with local invasiveness and recurrence.
  • We have previously suggested that growth factors and matrix metalloproteinases (MMPs) influence ameloblastoma invasiveness.
  • The aim was to study expression of MMPs, tissue inhibitor of metalloproteinases (TIMPs) and growth factors in ameloblastoma.
  • METHODS AND RESULTS: Thirteen cases of solid/multicystic ameloblastoma were examined.
  • As a control, calcifying cystic odontogenic tumour (CCOT), a non-invasive odontogenic neoplasm with ameloblastomatous epithelium was also studied.
  • Immunohistochemistry detected MMPs, TIMPs and growth factors in ameloblastoma and CCOT.
  • The LI of epidermal growth factor (EGF), transforming growth factor (TGF)-alpha and epidermal growth factor receptor (EGFR) was also increased in ameloblastoma.
  • This neoplasm showed greater expression of MMPs, TIMPs and growth factors compared with CCOT.
  • We then analysed these molecules in ameloblastoma cells and stroma.
  • Ameloblastoma cells exhibited increased LI of MMP-1, -2 and EGFR.
  • We found a positive correlation between EGF and TIMP-1, and between TGF-alpha and TIMP-2.
  • It is known that signals generated by growth factors are transduced by the ERK pathway.
  • CONCLUSIONS: These results suggest an interplay involving growth factors MMPs and TIMPs that may contribute to ameloblastoma behaviour.
  • [MeSH-major] Ameloblastoma / metabolism. Ameloblastoma / pathology. Intercellular Signaling Peptides and Proteins / metabolism. Jaw Neoplasms / metabolism. Jaw Neoplasms / pathology. Matrix Metalloproteinases / metabolism. Tissue Inhibitor of Metalloproteinases / metabolism
  • [MeSH-minor] Cell Proliferation. Epidermal Growth Factor / metabolism. Humans. Immunohistochemistry. MAP Kinase Signaling System. Matrix Metalloproteinase 1 / metabolism. Matrix Metalloproteinase 9 / metabolism. Odontogenic Cyst, Calcifying / metabolism. Odontogenic Cyst, Calcifying / pathology. Receptor, Epidermal Growth Factor / metabolism. Stromal Cells / metabolism. Stromal Cells / pathology. Tissue Inhibitor of Metalloproteinase-2 / metabolism. Transforming Growth Factor alpha / metabolism

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  • (PMID = 20653784.001).
  • [ISSN] 1365-2559
  • [Journal-full-title] Histopathology
  • [ISO-abbreviation] Histopathology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Intercellular Signaling Peptides and Proteins; 0 / Tissue Inhibitor of Metalloproteinases; 0 / Transforming Growth Factor alpha; 127497-59-0 / Tissue Inhibitor of Metalloproteinase-2; 62229-50-9 / Epidermal Growth Factor; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 3.4.24.- / Matrix Metalloproteinases; EC 3.4.24.35 / Matrix Metalloproteinase 9; EC 3.4.24.7 / MMP1 protein, human; EC 3.4.24.7 / Matrix Metalloproteinase 1
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50. Jegalian AG, Facchetti F, Jaffe ES: Plasmacytoid dendritic cells: physiologic roles and pathologic states. Adv Anat Pathol; 2009 Nov;16(6):392-404
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  • [Title] Plasmacytoid dendritic cells: physiologic roles and pathologic states.
  • Plasmacytoid dendritic cells (PDCs) have perplexed pathologists for decades, undergoing multiple adjustments in nomenclature as their lineage and functions have been characterized.
  • Although PDCs account for less than 0.1% of peripheral blood mononuclear cells, they serve as a principal source of interferon-alpha and are also known as interferon-I producing cells (IPCs).
  • Upon activation in vitro, they can differentiate into dendritic cells, and recent studies have substantiated a potential role in antigen presentation.
  • Thus, PDCs may act as a link between innate and adaptive immunity.
  • Normally found in small quantities in primary and secondary lymphoid organs, PDCs accumulate in a variety of inflammatory conditions, including Kikuchi-Fujimoto lymphadenopathy, hyaline-vascular Castleman disease, and autoimmune diseases, and in certain malignancies such as classical Hodgkin lymphoma and carcinomas.
  • Demonstrating potential for neoplastic transformation reflective of varying stages of maturation, clonal proliferations range from PDC nodules most commonly associated with chronic myelomonocytic leukemia to the rare but highly aggressive malignancy now known as blastic plasmacytoid dendritic cell neoplasm (BPDCN).
  • Formerly called blastic natural killer cell lymphoma or CD4/CD56 hematodermic neoplasm, BPDCN, unlike natural killer cell lymphomas, is not associated with Epstein-Barr virus infection and is generally not curable with treatment regimens for non-Hodgkin lymphomas.
  • In fact, this entity is no longer considered to be a lymphoma and instead represents a unique precursor hematopoietic neoplasm.
  • [MeSH-major] Dendritic Cells / pathology
  • [MeSH-minor] Aged. Aged, 80 and over. Cell Lineage. Child. Child, Preschool. Female. Humans. Leukemia, Myeloid / pathology. Lymphoma, Non-Hodgkin / immunology. Lymphoma, Non-Hodgkin / pathology. Male. Toll-Like Receptors / immunology

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  • (PMID = 19851130.001).
  • [ISSN] 1533-4031
  • [Journal-full-title] Advances in anatomic pathology
  • [ISO-abbreviation] Adv Anat Pathol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Toll-Like Receptors
  • [Number-of-references] 151
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51. Yu JX, Cui L, Zhang QY, Chen H, Ji P, Wei HJ, Ma HY: Expression of NOS and HIF-1alpha in human colorectal carcinoma and implication in tumor angiogenesis. World J Gastroenterol; 2006 Aug 7;12(29):4660-4
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  • [Title] Expression of NOS and HIF-1alpha in human colorectal carcinoma and implication in tumor angiogenesis.
  • AIM: To study CD34, CD105, inducible nitric oxide synthase (iNOS), endogenous nitric oxide synthase (eNOS), and hypoxia-inducible factor 1 (HIF-1) alpha expression in human colorectal carcinomas.
  • METHODS: The tissue microarrays (TMAs) were made up of 80 cases of colorectal carcinoma and 80 cases of non-neoplasm colorectal mucosa.
  • The expression of CD34, CD105, NOS and HIF-1alpha was detected by immunohistochemistry (S-P).
  • RESULTS: iNOS and HIF-1alpha expression in colorectal carcinoma was significantly higher than in non-neoplasm colorectal mucosa (c2 = 43.166, P < 0.01; c2 = 10.4278, P < 0.01); eNOS expression in colorectal carcinoma was significantly lower than in non-neoplasm colorectal mucosa (c2 = 11.354, P < 0.01).
  • [MeSH-major] Adenocarcinoma / metabolism. Colorectal Neoplasms / metabolism. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism. Neovascularization, Pathologic / metabolism. Nitric Oxide Synthase Type II / metabolism. Nitric Oxide Synthase Type III / metabolism
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antigens, CD / genetics. Antigens, CD / metabolism. Antigens, CD34 / genetics. Antigens, CD34 / metabolism. Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry. Microcirculation. Middle Aged. Receptors, Cell Surface / genetics. Receptors, Cell Surface / metabolism. Tissue Array Analysis

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  • (PMID = 16937436.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD34; 0 / ENG protein, human; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Receptors, Cell Surface; EC 1.14.13.39 / Nitric Oxide Synthase Type II; EC 1.14.13.39 / Nitric Oxide Synthase Type III
  • [Other-IDs] NLM/ PMC4087830
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52. Lobo I, Carvalho A, Amaral C, Machado S, Carvalho R: Glucagonoma syndrome and necrolytic migratory erythema. Int J Dermatol; 2010 Jan;49(1):24-9
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  • [Title] Glucagonoma syndrome and necrolytic migratory erythema.
  • The glucagonoma syndrome is a rare disorder, characterized by necrolytic migratory erythema, elevated serum glucagon levels, abnormal glucose tolerance, weight loss, and anemia in association with a glucagon-secreting alpha-cell tumor of the pancreas.
  • The clinical investigation revealed a pancreatic glucagonoma with resolution of the cutaneous and systemic features after surgical removal.
  • The dermatologic and endocrine approach to this syndrome is discussed here.
  • Early recognition and treatment may prevent metastatic disease and ensure its cure with resolution of the cutaneous and catabolic manifestations.
  • [MeSH-major] Erythema / etiology. Erythema / pathology. Glucagonoma / complications. Pancreatic Neoplasms / complications. Skin / pathology
  • [MeSH-minor] Aged. Biopsy. Glucagon / blood. Humans. Male. Necrosis. Pancreatectomy. Tomography, X-Ray Computed

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  • (PMID = 20465606.001).
  • [ISSN] 1365-4632
  • [Journal-full-title] International journal of dermatology
  • [ISO-abbreviation] Int. J. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 9007-92-5 / Glucagon
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53. De Palma M, Mazzieri R, Politi LS, Pucci F, Zonari E, Sitia G, Mazzoleni S, Moi D, Venneri MA, Indraccolo S, Falini A, Guidotti LG, Galli R, Naldini L: Tumor-targeted interferon-alpha delivery by Tie2-expressing monocytes inhibits tumor growth and metastasis. Cancer Cell; 2008 Oct 07;14(4):299-311
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  • [Title] Tumor-targeted interferon-alpha delivery by Tie2-expressing monocytes inhibits tumor growth and metastasis.
  • The use of type I interferons (IFNs) in cancer therapy has been limited by ineffective dosing and significant toxicity.
  • Here, we exploited the tumor-homing ability of proangiogenic Tie2-expressing monocytes (TEMs) to deliver IFN-alpha to tumors.
  • By transplanting hematopoietic progenitors transduced with a Tie2 promoter/enhancer-driven Ifna1 gene, we turned TEMs into IFN-alpha cell vehicles that efficiently targeted the IFN response to orthotopic human gliomas and spontaneous mouse mammary carcinomas and obtained significant antitumor responses and near complete abrogation of metastasis.
  • TEM-mediated IFN-alpha delivery inhibited tumor angiogenesis and activated innate and adaptive immune cells but did not impair myelopoiesis and wound healing detectably.
  • These results illustrate the therapeutic potential of gene- and cell-based IFN-alpha delivery and should allow the development of IFN treatments that more effectively treat cancer.
  • [MeSH-major] Cell Proliferation. Genetic Therapy / methods. Glioma / therapy. Hematopoietic Stem Cell Transplantation. Hematopoietic Stem Cells / metabolism. Interferon-alpha / metabolism. Mammary Neoplasms, Experimental / prevention & control. Monocytes / metabolism. Receptor, TIE-2 / metabolism
  • [MeSH-minor] Animals. Cell Line, Tumor. Cells, Cultured. Female. Hematopoiesis. Humans. Immunity, Innate. Mice. Mice, Nude. Mice, Transgenic. Neoplasm Metastasis. Neovascularization, Pathologic / immunology. Neovascularization, Pathologic / metabolism. Neovascularization, Pathologic / prevention & control. Promoter Regions, Genetic. Recombinant Fusion Proteins / metabolism. Time Factors. Transduction, Genetic. Wound Healing

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  • (PMID = 18835032.001).
  • [ISSN] 1878-3686
  • [Journal-full-title] Cancer cell
  • [ISO-abbreviation] Cancer Cell
  • [Language] eng
  • [Grant] Italy / Telethon / / TGT06S01
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Interferon-alpha; 0 / Recombinant Fusion Proteins; EC 2.7.10.1 / Receptor, TIE-2
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54. Mendoza-Milla C, Machuca Rodríguez C, Córdova Alarcón E, Estrada Bernal A, Toledo-Cuevas EM, Martínez Martínez E, Zentella Dehesa A: NF-kappaB activation but not PI3K/Akt is required for dexamethasone dependent protection against TNF-alpha cytotoxicity in L929 cells. FEBS Lett; 2005 Jul 18;579(18):3947-52
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  • [Title] NF-kappaB activation but not PI3K/Akt is required for dexamethasone dependent protection against TNF-alpha cytotoxicity in L929 cells.
  • Tumor necrosis factor alpha (TNF-alpha) is one of the best-described cell death promoters.
  • In murine L929 fibroblasts, dexamethasone inhibits TNF-alpha-induced cytotoxicity.
  • Since phosphatidyl inositol 3 kinase (PI3K) and nuclear factor kappa B (NF-kappaB) proteins regulate several survival pathways, we evaluated their participation in dexamethasone protection against TNF-alpha cell death.
  • We interfered with these pathways by overexpressing a negative dominant mutant of PI3K or a non-degradable mutant of inhibitor of NF-kappaB alpha (IkappaBalpha) (the cytoplasmic inhibitor of NF-kappaB) in L929 cells.
  • The loss of dexamethasone protection was associated with a diminished accumulation in XIAP and c-IAP proteins.
  • [MeSH-major] Dexamethasone / pharmacology. NF-kappa B / metabolism. Phosphatidylinositol 3-Kinases / metabolism. Tumor Necrosis Factor-alpha / metabolism
  • [MeSH-minor] Animals. Blotting, Western. Cell Death. Cell Line. Cell Nucleus / metabolism. Cell Proliferation. Cell Survival. Dose-Response Relationship, Drug. Down-Regulation. Fibroblasts / metabolism. Glucocorticoids / pharmacology. Inhibitor of Apoptosis Proteins. Mice. Mutation. Plasmids / metabolism. Proteins / metabolism. Signal Transduction. X-Linked Inhibitor of Apoptosis Protein

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  • (PMID = 16000198.001).
  • [ISSN] 0014-5793
  • [Journal-full-title] FEBS letters
  • [ISO-abbreviation] FEBS Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Glucocorticoids; 0 / Inhibitor of Apoptosis Proteins; 0 / NF-kappa B; 0 / Proteins; 0 / Tumor Necrosis Factor-alpha; 0 / X-Linked Inhibitor of Apoptosis Protein; 7S5I7G3JQL / Dexamethasone; EC 2.7.1.- / Phosphatidylinositol 3-Kinases
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55. Yoshimura H, Kimura N, Nakahira R, Michishita M, Ohkusu-Tsukada K, Takahashi K: Lipid-rich carcinoma in the mammary gland of a Djungarian hamster (Phodopus sungorus). J Vet Diagn Invest; 2010 Mar;22(2):305-9

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Lipid-rich carcinoma in the mammary gland of a Djungarian hamster (Phodopus sungorus).
  • The animal underwent surgery for a primary tumor arising in the mammary gland at the age of 16 months, and also for a recurrent tumor 6 months later.
  • Histologically, the primary neoplasm was composed of 2 different cell populations: nonvacuolated glandular neoplastic cells with moderate atypia, and vacuolated neoplastic cells with marked atypia.
  • Transition from the nonvacuolated glandular cells to the vacuolated cells was frequently seen.
  • The recurrent neoplasm was composed predominantly of vacuolated neoplastic cells that often invaded the surrounding soft tissue.
  • The cytoplasmic vacuoles contained neutral lipids, as confirmed by oil red O and Nile blue staining.
  • The vacuolated neoplastic cells were immunopositive for cytokeratin and negative for vimentin, alpha-smooth muscle actin, p63, estrogen receptor alpha, and androgen receptor.
  • [MeSH-major] Carcinoma / veterinary. Mammary Neoplasms, Animal / pathology

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  • (PMID = 20224099.001).
  • [ISSN] 1040-6387
  • [Journal-full-title] Journal of veterinary diagnostic investigation : official publication of the American Association of Veterinary Laboratory Diagnosticians, Inc
  • [ISO-abbreviation] J. Vet. Diagn. Invest.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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56. Pardanani A, Lim KH, Lasho TL, Finke C, McClure RF, Li CY, Tefferi A: Prognostically relevant breakdown of 123 patients with systemic mastocytosis associated with other myeloid malignancies. Blood; 2009 Oct 29;114(18):3769-72
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  • The prognostic heterogeneity of the World Health Organization category of "systemic mastocytosis with associated clonal hematologic nonmast cell lineage disease" (SM-AHNMD) has not been systematically validated by primary data.
  • Among 138 consecutive cases with SM-AHNMD, 123 (89%) had associated myeloid neoplasm: 55 (45%) myeloproliferative neoplasm (SM-MPN), 36 (29%) chronic myelomonocytic leukemia, 28 (23%) myelodysplastic syndrome (SM-MDS), and 4 (3%) acute leukemia.
  • The presence of eosinophilia, although prevalent (34%), was prognostically neutral, and the overall results were not affected by exclusion of FIP1L1-PDGFRA-positive cases.
  • We conclude that it is clinically more useful to consider specific entities, such as SM-MPN, systemic mastocytosis with chronic myelomonocytic leukemia, SM-MDS, and systemic mastocytosis with-acute leukemia, rather than their broad reference as SM-AHNMD.
  • [MeSH-major] Hematologic Neoplasms / epidemiology. Mastocytosis, Systemic / epidemiology. Neoplasms, Second Primary / epidemiology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Eosinophilia / complications. Eosinophilia / diagnosis. Eosinophilia / epidemiology. Eosinophilia / genetics. Eosinophilia / metabolism. Female. Humans. Male. Middle Aged. Oncogene Proteins, Fusion / genetics. Oncogene Proteins, Fusion / metabolism. Prognosis. Receptor, Platelet-Derived Growth Factor alpha / genetics. Receptor, Platelet-Derived Growth Factor alpha / metabolism. mRNA Cleavage and Polyadenylation Factors / genetics. mRNA Cleavage and Polyadenylation Factors / metabolism

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  • (PMID = 19713463.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / FIP1L1-PDGFRA fusion protein, human; 0 / Oncogene Proteins, Fusion; 0 / mRNA Cleavage and Polyadenylation Factors; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha
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57. Santini D, Poli F, Lega S: Solid-papillary tumors of the pancreas: histopathology. JOP; 2006;7(1):131-6
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  • [Title] Solid-papillary tumors of the pancreas: histopathology.
  • A solid-pseudopapillary tumor is an uncommon and "enigmatic" pancreatic neoplasm, and the term encompasses the two most conspicuous histological features: solid and pseudopapillary areas.
  • Grossly, it appears as a large solid, cystic or solid-cystic mass frequently having necrotic and hemorrhagic zones.
  • Histologically, solid-pseudopapillary tumors are generally characterized by solid areas alternating with a pseudopapillary pattern, and cystic spaces which are the results of degenerative changes occurring in the solid neoplasm.
  • Its immunohistochemical pattern is very distinctive and neoplastic cells are consistently vimentin-, CD10- and CD56-positive.
  • Some cases express focal positivity for alpha-1-antitrypsin, alpha-1-antichymotrypsin, neuron-specific enolase and synaptophysin.
  • Endocrine and pancreatic enzyme markers are absent; the origin of solid-pseudopapillary tumors has not yet been clarified.
  • Many investigators favor the theory that solid-pseudopapillary tumors originate from multipotent primordial cells while others suggest an extra-pancreatic origin from genital ridge angle-related cells.
  • Solid-pseudopapillary tumors appear as a low malignancy tumor and only a small number of cases recur or develop metastases after resection.
  • [MeSH-major] Carcinoma, Papillary / pathology. Pancreas / pathology. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Antigens, CD56 / analysis. Cell Proliferation. Humans. Immunohistochemistry. Neoplasm Invasiveness. Neprilysin / analysis. Receptors, Progesterone / analysis. Vimentin / analysis

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  • (PMID = 16407635.001).
  • [ISSN] 1590-8577
  • [Journal-full-title] JOP : Journal of the pancreas
  • [ISO-abbreviation] JOP
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antigens, CD56; 0 / Receptors, Progesterone; 0 / Vimentin; EC 3.4.24.11 / Neprilysin
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58. Petrakakou E, Grapsa D, Stergiou ME, Mikou P, Tsarpalis D, Polyzos A, Giahnaki A, Ioakim-Liossi A: Ascitic fluid cytology of yolk sac tumor of the ovary: a case report. Acta Cytol; 2009 Nov-Dec;53(6):701-3
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  • [Title] Ascitic fluid cytology of yolk sac tumor of the ovary: a case report.
  • BACKGROUND: Yolk sac tumor (YST) of the ovary is a rare neoplasm typically affecting children and young women.
  • We describe the cytomorphology of this tumor in ascitic fluid and discuss its differential diagnosis from other neoplasms.
  • CASE: Smear preparations of the ascitic fluid showed a predominance of clusters of malignant cells with vacuolated cytoplasm, mimicking a mucinous adenocarcinoma, and fewer syncytial-like and glandular structures.
  • Immunocytochemistry was positive for alpha-fetoprotein.
  • [MeSH-major] Ascitic Fluid / pathology. Endodermal Sinus Tumor / diagnosis. Endodermal Sinus Tumor / pathology. Ovarian Neoplasms / pathology
  • [MeSH-minor] Adult. Cell Aggregation. Female. Humans. Periodic Acid-Schiff Reaction. alpha-Fetoproteins / metabolism

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  • (PMID = 20014563.001).
  • [ISSN] 0001-5547
  • [Journal-full-title] Acta cytologica
  • [ISO-abbreviation] Acta Cytol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / alpha-Fetoproteins
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59. Ichikawa M, Kurokawa M: [Molecular mechanisms in the development of acute myeloid leukemia]. Nihon Rinsho; 2009 Oct;67(10):1889-93
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  • Acute myeloid leukemia (AML) is a malignant hematopoietic neoplasm characterized by clonal proliferation of tumor cells that arise from the hematopoietic stem/progenitor population within the bone marrow.
  • Cytogenetic abnormalities or point mutations of the hematopoiesis-specific genes are frequently found in patients with AML, and these genetic aberrations are closely associated with the pathophysiology of the disease.
  • Molecular pathogenesis of AML has been disclosed through analyses of such gene aberrations, including AML1 and MLL abnormalities, PML-RARA chimeric gene, activating mutations of FLT3, and EVI-1 abnormalities.
  • [MeSH-minor] Adaptor Proteins, Signal Transducing / genetics. Bone Marrow Cells / pathology. Cell Transformation, Neoplastic / pathology. Chimera / genetics. Chromosome Aberrations. Core Binding Factor Alpha 2 Subunit / genetics. DNA-Binding Proteins / genetics. Hematopoiesis / genetics. Hematopoietic Stem Cells / pathology. Histone-Lysine N-Methyltransferase. Humans. Myeloid-Lymphoid Leukemia Protein / genetics. Point Mutation. Proto-Oncogenes / genetics. Transcription Factors / genetics. fms-Like Tyrosine Kinase 3 / genetics

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  • (PMID = 19860185.001).
  • [ISSN] 0047-1852
  • [Journal-full-title] Nihon rinsho. Japanese journal of clinical medicine
  • [ISO-abbreviation] Nippon Rinsho
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Core Binding Factor Alpha 2 Subunit; 0 / DNA-Binding Proteins; 0 / MECOM protein, human; 0 / MLL protein, human; 0 / PRAM1 protein, human; 0 / RUNX1 protein, human; 0 / Transcription Factors; 149025-06-9 / Myeloid-Lymphoid Leukemia Protein; EC 2.1.1.43 / Histone-Lysine N-Methyltransferase; EC 2.7.10.1 / FLT3 protein, human; EC 2.7.10.1 / fms-Like Tyrosine Kinase 3
  • [Number-of-references] 11
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60. Calabrò L, Di Giacomo AM, Altomonte M, Fonsatti E, Mazzei MA, Volterrani L, Miracco C, Maio M: Primary hepatic epithelioid hemangioendothelioma progressively responsive to interferon-alpha: is there room for novel anti-angiogenetic treatments? J Exp Clin Cancer Res; 2007 Mar;26(1):145-50
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  • [Title] Primary hepatic epithelioid hemangioendothelioma progressively responsive to interferon-alpha: is there room for novel anti-angiogenetic treatments?
  • Primary hepatic epithelioid hemangioendothelioma (HEH) is a rare, low-grade malignant neoplasm of endothelial origin, with an unpredictable clinical course and prognosis.
  • No standard therapeutic strategies are still available for HEH, due to the infrequency of the disease and to its variable natural history that limit the identification of the most effective treatment.
  • In the absence of metastatic disease, surgical resection or liver transplantation represent the treatment of choice for HEH, while several antineoplastic agents have been proposed in the presence of metastatic nonresectable disesase.
  • Herein, we describe the biological characterization and the clinical course of a primary HEH progressively responsive to treatment with intermediate doses of interferon-alpha (IFN)-alpha2a.
  • Furthermore, based on the newly-identified expression of endoglin (CD105) on HEH, we discuss the clinical potential of novel anti-angiogenetic approaches to the disease.
  • [MeSH-major] Angiogenesis Inhibitors / therapeutic use. Hemangioendothelioma, Epithelioid / drug therapy. Interferon-alpha / therapeutic use. Liver Neoplasms / drug therapy. Neovascularization, Pathologic / prevention & control
  • [MeSH-minor] Antigens, CD / analysis. Antigens, CD31 / analysis. Antigens, CD34 / analysis. Female. Humans. Immunohistochemistry. Middle Aged. Receptors, Cell Surface / analysis. Recombinant Proteins. Tomography, X-Ray Computed. Treatment Outcome

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  • (PMID = 17550144.001).
  • [ISSN] 0392-9078
  • [Journal-full-title] Journal of experimental & clinical cancer research : CR
  • [ISO-abbreviation] J. Exp. Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antigens, CD; 0 / Antigens, CD31; 0 / Antigens, CD34; 0 / ENG protein, human; 0 / Interferon-alpha; 0 / Receptors, Cell Surface; 0 / Recombinant Proteins; 76543-88-9 / interferon alfa-2a
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61. Bauer R: Cylindroma of the prostate. Am J Surg Pathol; 2007 Aug;31(8):1288-91
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  • A sporadic prostate tumor morphologically and immunophenotypically identical to dermal cylindroma is reported for the first time.
  • Histologically, basaloid epithelial islands with broad rims of basement membrane material and strong immunoreactivity for alpha-smooth muscle actin in peripherally sited cells were the most distinguishing features.
  • The only obvious difference from typical dermal cylindroma was a lack of intratumoral Langerhans cells in the prostate neoplasm.
  • Differentiation from all hitherto known variants of basal cell proliferative lesions of the prostate was straightforward.
  • [MeSH-major] Carcinoma, Adenoid Cystic / pathology. Prostatic Neoplasms / pathology
  • [MeSH-minor] Aged. Biomarkers, Tumor / analysis. Disease-Free Survival. Fluorescent Antibody Technique, Direct. Humans. Male. Transurethral Resection of Prostate. Treatment Outcome

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  • (PMID = 17667556.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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62. Ferri E, Iaderosa GA, Armato E: Atypical fibroxanthoma of the external ear in a cardiac transplant recipient: case report and the causal role of the immunosuppressive therapy. Auris Nasus Larynx; 2008 Jun;35(2):260-3
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  • Atypical fibroxanthoma (AF) is an unusual cutaneous fibrohistiocytic tumour that is most commonly found in ENT sun-exposed areas of elderly males.
  • Cardiac transplant patients have an increased incidence of multiple cutaneous neoplasms, but the AF is uncommon.
  • Although this neoplasm is benign, it may mimic spindle cell carcinoma, squamous cell carcinoma, melanoma and soft tissue sarcoma on histologic examination.
  • Immunohistochemical stains for cytokeratin, alpha-1-antichymotrypsin, S100 protein and vimentin may be helpful in differential diagnosis.
  • We present a case of a cardiac transplant recipient who developed, after multiple cutaneous squamous tumours, an AF of external ear following the prolonged immunosuppressive treatment with cyclosporin.
  • [MeSH-major] Ear Neoplasms / pathology. Ear, External. Heart Transplantation. Histiocytoma, Benign Fibrous / pathology

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  • (PMID = 17804184.001).
  • [ISSN] 0385-8146
  • [Journal-full-title] Auris, nasus, larynx
  • [ISO-abbreviation] Auris Nasus Larynx
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Cyclosporins; 0 / Immunosuppressive Agents
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63. McCluggage WG, Young RH: Ovarian sertoli-leydig cell tumors with pseudoendometrioid tubules (pseudoendometrioid sertoli-leydig cell tumors). Am J Surg Pathol; 2007 Apr;31(4):592-7
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  • [Title] Ovarian sertoli-leydig cell tumors with pseudoendometrioid tubules (pseudoendometrioid sertoli-leydig cell tumors).
  • The propensity for ovarian endometrioid adenocarcinomas to morphologically mimic Sertoli, Sertoli-Leydig, and granulosa cell tumors, is well known.
  • The converse situation, mimicry of an endometrioid neoplasm by a sex cord-stromal tumor, has not been emphasized.
  • In this report, we describe 9 ovarian Sertoli-Leydig cell tumors (5 well differentiated, 4 of intermediate differentiation) with areas containing hollow, sometimes dilated, tubules which resemble endometrioid glands; we refer to these as pseudoendometrioid tubules.
  • The tumors, all of which were unilateral except for one, ranged from 3.5 to 19 cm and were variously described as tan, pale, yellow, or gold.
  • The proportion of the tumor made up of pseudoendometrioid tubules ranged from 10% to >90%.
  • When widespread, their presence sometimes resulted in consideration of a borderline endometrioid adenofibroma or a well-differentiated endometrioid adenocarcinoma.
  • However, all the neoplasms contained typical Sertoli tubules and one or more of the characteristic patterns of Sertoli-Leydig cell tumors as well as Leydig cells, although the latter cells were inconspicuous in some cases.
  • Immunohistochemistry, performed in 4 cases, showed that the pseudoendometrioid tubules, as well as the more typical Sertoli cell elements, were either positive for alpha inhibin (3 of 4 cases) or calretinin (3 of 4 cases) or both, although sometimes focally so.
  • This report illustrates the potential for ovarian Sertoli-Leydig cell tumors to contain tubules with a pseudoendometrioid appearance which mimic a borderline or malignant endometrioid neoplasm.
  • The presence of more typical Sertoli cell elements and Leydig cells, an absence of squamous elements, endometriosis or associated adenofibroma, and the characteristic immunophenotype assist in diagnosis.
  • [MeSH-major] Ovarian Neoplasms / pathology. Sertoli-Leydig Cell Tumor / pathology
  • [MeSH-minor] Adolescent. Adult. Biomarkers, Tumor / analysis. Carcinoma, Endometrioid / pathology. Diagnosis, Differential. Female. Humans. Immunohistochemistry. Middle Aged

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  • (PMID = 17414107.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
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64. Lan YH, Li YG, Liang ZW, Chen M, Peng ML, Tang L, Hu HD, Ren H: A DNA vaccine against chimeric AFP enhanced by HSP70 suppresses growth of hepatocellular carcinoma. Cancer Immunol Immunother; 2007 Jul;56(7):1009-16

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  • [Title] A DNA vaccine against chimeric AFP enhanced by HSP70 suppresses growth of hepatocellular carcinoma.
  • Alpha-fetoprotein (AFP) is produced principally in fetal liver, gastrointestinal tract and the yolk sac which is temporarily present during embryonic development.
  • AFP is overexpressed in the majority of hepatocellular carcinoma (HCC) and thus offers an attractive target for immunotherapy against this neoplasm.
  • We also demonstrated that this vaccine elicited a marked and highly effective AFP specific CTL response against AFP-positive target cells.
  • This vaccine also induced the prolongation of life span in mice bearing the tumor and the eradication of HCC.
  • [MeSH-major] Cancer Vaccines. Carcinoma, Hepatocellular / therapy. HSP70 Heat-Shock Proteins / genetics. Liver Neoplasms, Experimental / therapy. Vaccines, DNA. alpha-Fetoproteins / genetics
  • [MeSH-minor] Animals. Cell Line, Tumor. Chimera. Cytokines / biosynthesis. Enzyme-Linked Immunosorbent Assay. Immunotherapy / methods. Mice. Mice, Inbred C57BL. Plasmids / genetics. Recombinant Fusion Proteins / immunology. T-Lymphocytes, Cytotoxic / immunology

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  • (PMID = 17186291.001).
  • [ISSN] 0340-7004
  • [Journal-full-title] Cancer immunology, immunotherapy : CII
  • [ISO-abbreviation] Cancer Immunol. Immunother.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Cancer Vaccines; 0 / Cytokines; 0 / HSP70 Heat-Shock Proteins; 0 / Recombinant Fusion Proteins; 0 / Vaccines, DNA; 0 / alpha-Fetoproteins
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65. Lazzareschi I, Furfaro IF, Coccia P, Puma N, Riccardi R: Extragonadal yolk sac tumor outside of the midline of the body: a case report of a child with a yolk sac tumor of the pontocerebellar angle. Tumori; 2009 Nov-Dec;95(6):840-2
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  • [Title] Extragonadal yolk sac tumor outside of the midline of the body: a case report of a child with a yolk sac tumor of the pontocerebellar angle.
  • Yolk sac tumor is a rare germ cell neoplasm occurring mainly in the gonads.
  • Extragonadal yolk sac tumor is a very rare malignancy; its main distribution is along the midline of the body at three principal sites: mediastinum, central nervous system and retroperitoneum.
  • Most yolk sac tumors are diagnosed between seven months and three years of age.
  • We report a case of primary yolk sac tumor in a 13-month-old child.
  • The tumor was located in the pontocerebellar angle, an atypical location that may not have suggested a yolk sac tumor as first diagnosis.
  • We want to highlight the importance of performing tumor marker measurements during the first year of life, also for tumors located away from the midline.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Brain Stem Neoplasms. Cerebellar Neoplasms. Endodermal Sinus Tumor. Pons
  • [MeSH-minor] Disease Progression. Humans. Immunohistochemistry. Infant. Magnetic Resonance Imaging. Male. Tomography, X-Ray Computed. alpha-Fetoproteins / metabolism

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  • (PMID = 20210256.001).
  • [ISSN] 0300-8916
  • [Journal-full-title] Tumori
  • [ISO-abbreviation] Tumori
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / alpha-Fetoproteins
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66. Pozharisskiĭ KM, Leenman EE, Arzumanov AA: [Achievements in morphological diagnosis of prostatic cancer: alpha-methylacyl-coenzyme-A-racemase--a new marker of malignant cell transformation]. Arkh Patol; 2005 Sep-Oct;67(5):15-9
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  • [Title] [Achievements in morphological diagnosis of prostatic cancer: alpha-methylacyl-coenzyme-A-racemase--a new marker of malignant cell transformation].
  • Gene P504S is considered as the most specific for prostatic carcinoma and its protein (alpha-methylacyl coenzyme A racemaze (AMACR/P504S) is higly sensitive and specific marker not only for adenocarcinoma cells but also for preceding changes - prostatic intraepithelial neoplasm (PIN).
  • AMACR/P504S seems to be the first marker of malignant transformation and tumor progression.
  • Use of immunohistochemical method for revealing this marker together with methods of basal prostatic cells observation (cytokeratin of a high molecular weight, cytokeratin 5/6, p63) improves morphological diagnosis of prostatic carcinoma, particularly on the material of needle biopsies.
  • This combination allows one to identify neoplastic nature of some difficult lesions.
  • [MeSH-major] Biomarkers, Tumor / analysis. Cell Transformation, Neoplastic. Prostatic Intraepithelial Neoplasia / diagnosis. Prostatic Neoplasms / diagnosis. Racemases and Epimerases / analysis

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  • (PMID = 16323473.001).
  • [ISSN] 0004-1955
  • [Journal-full-title] Arkhiv patologii
  • [ISO-abbreviation] Arkh. Patol.
  • [Language] rus
  • [Publication-type] Editorial; English Abstract
  • [Publication-country] Russia (Federation)
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 5.1.- / Racemases and Epimerases; EC 5.1.99.4 / alpha-methylacyl-CoA racemase
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67. Armor JF, Fazili J, Toubia N, Kern W, Kamble R, Kharfan-Dabaja MA: Remission of natural-killer cell lymphoma of the liver with anti-hepatitis C therapy. Am J Hematol; 2005 Mar;78(3):212-5
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  • [Title] Remission of natural-killer cell lymphoma of the liver with anti-hepatitis C therapy.
  • Non-Hodgkin lymphomas (NHL) consist of a diverse group of lymphoproliferative neoplasms with unique patterns of biology, behavior, and differing responses to therapy.
  • A rare subtype of malignancy arising from cells of putative natural killer (NK) origin is being recognized as a distinct clinicopathological entity.
  • Viruses including hepatitis C have been reported in association with various types of NHL but not the NK-cell subtype.
  • We hereby report a unique case of a patient with hepatitis C who developed hepatic NK-cell lymphoma and chronic NK-cell leukemia.
  • Interestingly, we observed clinical and radiologic remission of the neoplasm following treatment with anti-hepatitis C therapy.
  • [MeSH-major] Antiviral Agents / therapeutic use. Hepatitis C / drug therapy. Killer Cells, Natural / pathology. Liver Neoplasms / pathology. Lymphoma, Non-Hodgkin / pathology. Tumor Virus Infections / pathology
  • [MeSH-minor] Humans. Interferon-alpha / therapeutic use. Male. Middle Aged. Recombinant Proteins. Remission Induction. Ribavirin / therapeutic use

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  • (PMID = 15726605.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antiviral Agents; 0 / Interferon-alpha; 0 / Recombinant Proteins; 49717AWG6K / Ribavirin; 99210-65-8 / interferon alfa-2b
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68. Ding XL, Sun AJ, Zhou YZ, Tian QJ, Yu Q, He FF, Shen K, Lang JH: [Identification of potential neoplastic risk in gonadal development abnormality with Y chromosome of 79 cases]. Zhonghua Fu Chan Ke Za Zhi; 2008 Jun;43(6):442-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Identification of potential neoplastic risk in gonadal development abnormality with Y chromosome of 79 cases].
  • OBJECTIVE: To identify the potential neoplastic risk in gonadal development abnormality with Y chromosome.
  • RESULTS: Among 41 cases of androgen insensitive syndrome, spermatogenic cell neoplasm occurred in 1 patient, sertoli cell tumor in 2, and interstitial cell hyperplasia in 5.
  • Among 14 cases of 17 alpha-hydroxylase deficiency (XY) syndrome, one was sertoli cell tumor, and one was sertoli cell hyperplasia.
  • One of 16 cases of XO/XY gonadal dysgenesis was spermatogenic cell neoplasm with agenda cell tumor.
  • All of the gonadoblastoma and germ-cell tumor were located in the pelvis.
  • Tumors occurred mostly during 15 years of age to 32 years.
  • CONCLUSIONS: The gonads of XY pure gonadal dysgenesis has high risks of gonadoblastoma and germ-cell tumor.
  • [MeSH-major] Androgen-Insensitivity Syndrome / genetics. Chromosomes, Human, Y / genetics. Gonadal Dysgenesis, 46,XY / genetics. Gonadoblastoma / genetics. Ovarian Neoplasms / genetics

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  • (PMID = 19035140.001).
  • [ISSN] 0529-567X
  • [Journal-full-title] Zhonghua fu chan ke za zhi
  • [ISO-abbreviation] Zhonghua Fu Chan Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
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69. Kaim U, Moritz A, Failing K, Baumgärtner W: The regression of a canine Langerhans cell tumour is associated with increased expression of IL-2, TNF-alpha, IFN-gamma and iNOS mRNA. Immunology; 2006 Aug;118(4):472-82
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  • [Title] The regression of a canine Langerhans cell tumour is associated with increased expression of IL-2, TNF-alpha, IFN-gamma and iNOS mRNA.
  • Canine cutaneous histiocytoma is a benign epidermal neoplasm of Langerhans cell origin, which usually displays spontaneous regression.
  • Based on the degree of lymphocytic infiltration, 30 histiocytomas were classified into four groups representing different stages of tumour regression.
  • To elucidate further the mechanisms of the antitumour immune response CD3+, CD21+, CD4+, CD8+ and myeloid/histiocyte antigen+ inflammatory cells were differentiated by immunohistochemistry and quantified.
  • In addition, the number of apoptotic cells was detected using the TdT-mediated biotin-dUTP nick-end labelling (TUNEL) method.
  • Furthermore, the expression of interleukin- (IL-2), IL-12(p40), tumour necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma), IL-10 and transforming growth factor-beta (TGF-beta) as well as inducible nitric oxid synthase (iNOS) mRNA was determined by reverse transcription-polymerase chain reaction (RT-PCR).
  • Phenotyping of inflammatory cells revealed a significantly increased infiltration of all lymphocyte subsets and myeloid/histiocytic cells with the onset of tumour regression.
  • The latter was significantly correlated to up-regulation of IL-2, TNF-alpha, IFN-gamma and iNOS mRNA expression.
  • Expression of remaining cytokines and percentage of apoptotic cells showed no group-specific changes.
  • The results indicate an initial infiltration of CD4+ T cells followed by increased expression of Th1 cytokines and recruitment of antitumour effector cells as the principal mechanism for tumour regression.
  • Canine cutaneous histiocytoma is a unique example for an effective immune response in a naturally occurring neoplasm derived from epidermal Langerhans cells and might represent a valuable animal model to investigate tumour immunity.
  • [MeSH-major] Cytokines / genetics. Dog Diseases / immunology. Gene Expression Regulation, Neoplastic. Histiocytoma, Benign Fibrous / veterinary. Neoplasm Regression, Spontaneous / immunology. Skin Neoplasms / veterinary
  • [MeSH-minor] Animals. Apoptosis. Biomarkers. Cell Count. Dogs. Female. In Situ Nick-End Labeling. Interferon-gamma / genetics. Interleukin-2 / genetics. Langerhans Cells / immunology. Langerhans Cells / pathology. Macrophages / immunology. Macrophages / pathology. Male. Nitric Oxide Synthase Type II / genetics. RNA, Messenger / analysis. Reverse Transcriptase Polymerase Chain Reaction. Statistics, Nonparametric. Tumor Necrosis Factor-alpha / genetics

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  • (PMID = 16764690.001).
  • [ISSN] 0019-2805
  • [Journal-full-title] Immunology
  • [ISO-abbreviation] Immunology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Cytokines; 0 / Interleukin-2; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; 82115-62-6 / Interferon-gamma; EC 1.14.13.39 / Nitric Oxide Synthase Type II
  • [Other-IDs] NLM/ PMC1782326
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70. Cooper LD, Doss RP, Price R, Peterson K, Oliver JE: Application of Bruchin B to pea pods results in the up-regulation of CYP93C18, a putative isoflavone synthase gene, and an increase in the level of pisatin, an isoflavone phytoalexin. J Exp Bot; 2005 Apr;56(414):1229-37
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  • [Title] Application of Bruchin B to pea pods results in the up-regulation of CYP93C18, a putative isoflavone synthase gene, and an increase in the level of pisatin, an isoflavone phytoalexin.
  • Bruchins, mono and bis (3-hydroxypropanoate) esters of long chain alpha,omega-diols, are a recently discovered class of insect elicitors that stimulate cell division and neoplasm formation when applied to pods of peas and certain other legumes.
  • The corresponding amplification product was cloned and sequenced and a full length cDNA sequence was obtained.
  • This, the first report of induction of phytoalexin biosynthesis by an insect elicitor, suggests that Bruchin B not only stimulates neoplasm formation, but also activates other plant defence responses.

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  • (PMID = 15753113.001).
  • [ISSN] 0022-0957
  • [Journal-full-title] Journal of experimental botany
  • [ISO-abbreviation] J. Exp. Bot.
  • [Language] eng
  • [Databank-accession-numbers] GENBANK/ AF532999
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 9-docosen-1,22-diol bis(3-hydroxypropanoate) ester; 0 / DNA Primers; 0 / Plant Extracts; 0 / Plant Proteins; 0 / Propionates; 0 / Pterocarpans; 0 / Sesquiterpenes; 0 / Terpenes; 20186-22-5 / pisatin; 37297-20-4 / phytoalexins; 9035-51-2 / Cytochrome P-450 Enzyme System; EC 1.13.- / Oxygenases; EC 1.14.13.- / isoflavone synthase
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71. Schrader H, Menge BA, Breuer TG, Ritter PR, Uhl W, Schmidt WE, Holst JJ, Meier JJ: Impaired glucose-induced glucagon suppression after partial pancreatectomy. J Clin Endocrinol Metab; 2009 Aug;94(8):2857-63
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  • [Title] Impaired glucose-induced glucagon suppression after partial pancreatectomy.
  • INTRODUCTION: The glucose-induced decline in glucagon levels is often lost in patients with type 2 diabetes.
  • It is unclear whether this is due to an independent defect in alpha-cell function or secondary to the impairment in insulin secretion.
  • We examined whether a partial pancreatectomy in humans would also impair postchallenge glucagon concentrations and, if so, whether this could be attributed to the reduction in insulin levels.
  • PATIENTS AND METHODS: Thirty-six patients with pancreatic tumours or chronic pancreatitis were studied before and after approximately 50% pancreatectomy with a 240-min oral glucose challenge, and the plasma concentrations of glucose, insulin, C-peptide, and glucagon were determined.
  • RESULTS: Fasting and postchallenge insulin and C-peptide levels were significantly lower after partial pancreatectomy (P < 0.0001).
  • Likewise, fasting glucagon concentrations tended to be lower after the intervention (P = 0.11).
  • Oral glucose ingestion elicited a decline in glucagon concentrations before surgery (P < 0.0001), but this was lost after partial pancreatectomy (P < 0.01 vs. preoperative values).
  • The loss of glucose-induced glucagon suppression was found after both pancreatic head (P < 0.001) and tail (P < 0.05) resection.
  • The glucose-induced changes in glucagon levels were closely correlated to the respective increments in insulin and C-peptide concentrations (P < 0.01).
  • CONCLUSIONS: The glucose-induced suppression in glucagon levels is lost after a 50% partial pancreatectomy in humans.
  • This suggests that impaired alpha-cell function in patients with type 2 diabetes may also be secondary to reduced beta-cell mass.
  • Alterations in glucagon regulation should be considered as a potential side effect of partial pancreatectomies.
  • [MeSH-major] Glucagon / blood. Glucose / pharmacology. Pancreatectomy
  • [MeSH-minor] Adult. Aged. Blood Glucose / analysis. C-Peptide / analysis. Female. Glucagon-Secreting Cells / physiology. Humans. Insulin / secretion. Insulin-Secreting Cells / pathology. Male. Middle Aged

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  • (PMID = 19491219.001).
  • [ISSN] 1945-7197
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Blood Glucose; 0 / C-Peptide; 0 / Insulin; 9007-92-5 / Glucagon; IY9XDZ35W2 / Glucose
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72. Tonetti DA, Zhang Y, Zhao H, Lim SB, Constantinou AI: The effect of the phytoestrogens genistein, daidzein, and equol on the growth of tamoxifen-resistant T47D/PKC alpha. Nutr Cancer; 2007;58(2):222-9
Hazardous Substances Data Bank. GENISTEIN .

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  • [Title] The effect of the phytoestrogens genistein, daidzein, and equol on the growth of tamoxifen-resistant T47D/PKC alpha.
  • We previously described a T47D:A18/protein kinase C (PKC)alpha TAM-resistant tumor model that exhibits autonomous growth and estradiol-induced tumor regression.
  • We compared the estrogenicity of the isoflavones genistein, daidzein, and the daidzein metabolite equol in the parental T47D:A18 and T47D:A18/PKC alpha cell lines in vitro and in vivo.
  • Whereas equol exerts estrogenic effects on T47D:A18 cells in vitro, none of the isoflavones stimulated T47D:A18 tumor growth.
  • T47D:A18/PKC alpha tumor growth was partially stimulated by genistein, yet partially inhibited by daidzein.
  • Interestingly, coadministration of TAM with either daidzein or genistein produced tumors of greater size than with TAM alone.
  • These findings suggest that simultaneous consumption of isoflavone supplements with TAM may not be safe.
  • [MeSH-minor] Animals. Breast Neoplasms / drug therapy. Breast Neoplasms / prevention & control. Cell Division. Cell Line, Tumor. Drug Interactions. Equol. Female. Humans. Mice. Mice, Nude. Random Allocation. Safety. Soybeans / chemistry

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  • (PMID = 17640169.001).
  • [ISSN] 0163-5581
  • [Journal-full-title] Nutrition and cancer
  • [ISO-abbreviation] Nutr Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA96517
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 4',7-dihydroxy-3,4-dihydroisoflavone; 0 / Antineoplastic Agents; 0 / Antineoplastic Agents, Hormonal; 0 / Isoflavones; 094ZI81Y45 / Tamoxifen; 531-95-3 / Equol; 6287WC5J2L / daidzein; DH2M523P0H / Genistein
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73. Shen HC, Ylaya K, Pechhold K, Wilson A, Adem A, Hewitt SM, Libutti SK: Multiple endocrine neoplasia type 1 deletion in pancreatic alpha-cells leads to development of insulinomas in mice. Endocrinology; 2010 Aug;151(8):4024-30
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  • [Title] Multiple endocrine neoplasia type 1 deletion in pancreatic alpha-cells leads to development of insulinomas in mice.
  • The pancreatic alpha- and beta-cells are critical components in regulating blood glucose homeostasis via secretion of glucagon and insulin, respectively.
  • Both cell types are typically localized in the islets of Langerhans.
  • The lack of suitable cell lines to study alpha- and beta-cells interactions have led us to develop an alpha-cell-specific Cre-expressing transgenic line utilizing a glucagon promoter sequence, the Glu-Cre transgenic mouse.
  • Here, we demonstrate that the Glu-Cre could specifically and efficiently excise floxed target genes in adult islet alpha-cells.
  • We further showed that deletion of the tumor suppressor gene, multiple endocrine neoplasia type 1 (Men1), in alpha-cells led to tumorigenesis.
  • However, to our surprise, the lack of Men1 in alpha-cells did not result in glucagonomas but rather beta-cell insulinomas.
  • Because deletion of the Men1 alleles was only present in alpha-cells, our data suggested that cross communication between alpha- and beta-cells contributes to tumorigenesis in the absence of Men1.
  • Together, we believed that the new model systems described here will allow future studies to decipher cellular interactions between islet alpha- and beta-cells in a physiological context.

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  • (PMID = 20555035.001).
  • [ISSN] 1945-7170
  • [Journal-full-title] Endocrinology
  • [ISO-abbreviation] Endocrinology
  • [Language] ENG
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Men1 protein, mouse; 0 / Proto-Oncogene Proteins; 9007-92-5 / Glucagon
  • [Other-IDs] NLM/ PMC2940531
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74. Rallis E, Korfitis C, Stavropoulou E, Papaconstantis M: Onset of palmoplantar pustular psoriasis while on adalimumab for psoriatic arthritis: a 'class effect' of TNF-alpha antagonists or simply an anti-psoriatic treatment adverse reaction? J Dermatolog Treat; 2010 Jan;21(1):3-5
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  • [Title] Onset of palmoplantar pustular psoriasis while on adalimumab for psoriatic arthritis: a 'class effect' of TNF-alpha antagonists or simply an anti-psoriatic treatment adverse reaction?
  • Adalimumab is a human, recombinant IgG1 monoclonal antibody that specifically blocks the interaction of tumour necrosis factor (TNF)-alpha with the p55 and the p75 TNF-alpha cell surface receptors.
  • The development or worsening of psoriatic skin lesions is a known side effect of adalimumab and other TNF-alpha antagonists increasingly reported in the literature.
  • Although it has been reported as a 'class-effect' of TNF-alpha antagonists, we believe that the deterioration or new onset of psoriasis is an adverse reaction seen mainly with drugs used for the treatment of psoriasis and not solely with anti-TNF agents.


75. Chang YH, Hsieh SL, Chao Y, Chou YC, Lin WW: Proinflammatory effects of LIGHT through HVEM and LTbetaR interactions in cultured human umbilical vein endothelial cells. J Biomed Sci; 2005;12(2):363-75
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  • [Title] Proinflammatory effects of LIGHT through HVEM and LTbetaR interactions in cultured human umbilical vein endothelial cells.
  • Members of the tumor necrosis factor (TNF) receptor (TNFR) superfamily are known to be potent mediators of immune responses.
  • LIGHT can induce either cell death and/or NF-kappaB activation via its interaction with LTbetaR and/or HVEM.
  • In this study, we investigated the effects of LIGHT in human umbilical vein endothelial cells (HUVECs).
  • We demonstrated that both LTbetaR and HVEM, but not DcR3, are present in HUVECs, and LIGHT can induce the secretion of chemokines (IL-8 and GRO-alpha), cell surface expression of adhesion molecules (ICAM-1 and VCAM-1), PGI2 release, and COX-2 expression.
  • However, the LIGHT mutein, LIGHT-R228E, which has been shown to exhibit binding specificity to LTbetaR, could not induce the secretion of GRO-alpha, PGI2, or the expression of COX-2.
  • These results indicate that both LTbetaR and HVEM can discriminatively mediate the expression of different genes in HUVECs, and suggest that LIGHT is a proinflammatory cytokine.
  • [MeSH-major] Endothelium, Vascular / cytology. Membrane Proteins / physiology. Receptors, Tumor Necrosis Factor / metabolism. Tumor Necrosis Factor-alpha / metabolism. Umbilical Veins / cytology
  • [MeSH-minor] Cell Adhesion. Cell Death. Cell Line. Cells, Cultured. Chemokine CXCL1. Chemokines, CXC / biosynthesis. Chemokines, CXC / metabolism. Cyclooxygenase 2. Dose-Response Relationship, Drug. Enzyme-Linked Immunosorbent Assay. Epoprostenol / metabolism. Flow Cytometry. Humans. Immunoblotting. Inflammation. Intercellular Adhesion Molecule-1 / biosynthesis. Intercellular Adhesion Molecule-1 / metabolism. Intercellular Signaling Peptides and Proteins / biosynthesis. Intercellular Signaling Peptides and Proteins / metabolism. Interferon-gamma / metabolism. Interleukin-8 / biosynthesis. Interleukin-8 / metabolism. Lymphotoxin beta Receptor. Membrane Glycoproteins / metabolism. Monocytes / metabolism. NF-kappa B / metabolism. Prostaglandin-Endoperoxide Synthases / biosynthesis. Prostaglandin-Endoperoxide Synthases / metabolism. Receptors, Cell Surface / metabolism. Receptors, Tumor Necrosis Factor, Member 14. Receptors, Tumor Necrosis Factor, Member 6b. Receptors, Virus / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Tumor Necrosis Factor Ligand Superfamily Member 14. Up-Regulation. Vascular Cell Adhesion Molecule-1 / biosynthesis. Vascular Cell Adhesion Molecule-1 / metabolism

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  • (PMID = 15917993.001).
  • [ISSN] 1021-7770
  • [Journal-full-title] Journal of biomedical science
  • [ISO-abbreviation] J. Biomed. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / CXCL1 protein, human; 0 / Chemokine CXCL1; 0 / Chemokines, CXC; 0 / Intercellular Signaling Peptides and Proteins; 0 / Interleukin-8; 0 / LTBR protein, human; 0 / Lymphotoxin beta Receptor; 0 / Membrane Glycoproteins; 0 / Membrane Proteins; 0 / NF-kappa B; 0 / Receptors, Cell Surface; 0 / Receptors, Tumor Necrosis Factor; 0 / Receptors, Tumor Necrosis Factor, Member 14; 0 / Receptors, Tumor Necrosis Factor, Member 6b; 0 / Receptors, Virus; 0 / TNFRSF14 protein, human; 0 / TNFRSF6B protein, human; 0 / TNFSF14 protein, human; 0 / Tumor Necrosis Factor Ligand Superfamily Member 14; 0 / Tumor Necrosis Factor-alpha; 0 / Vascular Cell Adhesion Molecule-1; 126547-89-5 / Intercellular Adhesion Molecule-1; 82115-62-6 / Interferon-gamma; DCR9Z582X0 / Epoprostenol; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases
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76. McCluggage WG, McKenna M, McBride HA: CD56 is a sensitive and diagnostically useful immunohistochemical marker of ovarian sex cord-stromal tumors. Int J Gynecol Pathol; 2007 Jul;26(3):322-7
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  • [Title] CD56 is a sensitive and diagnostically useful immunohistochemical marker of ovarian sex cord-stromal tumors.
  • Ovarian sex cord-stromal tumors comprise a heterogeneous group of neoplasms with wide morphological diversity, and they can be mistaken for a variety of other tumors.
  • Some types, including granulosa and Sertoli cell tumor, may be confused with a neuroendocrine neoplasm.
  • CD56 is a widely used neuroendocrine marker with a high sensitivity for neuroendocrine tumors and is commonly used as part of a panel to distinguish between a neuroendocrine neoplasm and other tumors in the differential diagnosis.
  • In this study, we investigate CD56 staining in ovarian sex cord-stromal tumors.
  • CD56 staining has not previously been studied in this group of neoplasms.
  • We stained a large series of ovarian sex cord-stromal neoplasms (n = 85) with CD56.
  • Neoplasms studied were adult granulosa cell tumor (n = 40), juvenile granulosa cell tumor (n = 8), Sertoli cell tumor (n = 1), Sertoli-Leydig cell tumor (n = 14), Leydig cell tumor (n = 2), steroid cell tumor, not otherwise specified (n = 2), sclerosing stromal tumor (n = 1), sex cord tumor with annular tubules (n = 2), and fibroma (n = 15).
  • Three uterine tumors resembling ovarian sex cord tumor were also studied.
  • Nonneoplastic ovaries, including 3 cases of pregnancy-related granulosa or Sertoli cell proliferation, were also included.
  • In nontumorous ovaries, granulosa cells of follicular and corpus luteum cysts were consistently negative.
  • All sex cord-stromal tumors except one were positive with CD56; staining ranged from focal to diffuse but was usually diffuse involving more than 50% of tumor cells.
  • CD56 immunoreactivity is almost universal in ovarian sex cord-stromal tumors of all the major morphological types and is of no value in distinguishing a sex cord-stromal and a neuroendocrine neoplasm.
  • Since CD56 is an extremely sensitive marker of ovarian sex cord-stromal tumors, it may be useful in the diagnosis of this group of neoplasms, especially in cases which are alpha inhibin or calretinin negative, and in distinguishing these from mimics which are CD56 negative.
  • [MeSH-major] Antigens, CD56 / metabolism. Biomarkers, Tumor / metabolism. Ovarian Neoplasms / metabolism. Sex Cord-Gonadal Stromal Tumors / metabolism

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  • (PMID = 17581419.001).
  • [ISSN] 0277-1691
  • [Journal-full-title] International journal of gynecological pathology : official journal of the International Society of Gynecological Pathologists
  • [ISO-abbreviation] Int. J. Gynecol. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD56; 0 / Biomarkers, Tumor
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77. Kutzner H, Kerl H, Pfaltz MC, Kempf W: CD123-positive plasmacytoid dendritic cells in primary cutaneous marginal zone B-cell lymphoma: diagnostic and pathogenetic implications. Am J Surg Pathol; 2009 Sep;33(9):1307-13
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] CD123-positive plasmacytoid dendritic cells in primary cutaneous marginal zone B-cell lymphoma: diagnostic and pathogenetic implications.
  • The histogenesis of primary cutaneous marginal zone B-cell lymphoma (PCMZL) has not yet been clarified.
  • Plasma-cytoid dendritic cells (PDC) play a crucial role in the initiation of immune responses and activation of T-cells and B-cells.
  • We analyzed the presence of PDC by immunohistochemistry in various forms of primary cutaneous B-cell lymphomas and in B-cell pseudolymphomas.
  • Clusters of CD123+PDC were observed in all PCMZL (23 of 23 cases; 100%) and in two-thirds of cutaneous B-cell pseudolymphomas (14 of 22; 64%), but only in a minority of primary cutaneous follicle center lymphoma (4 of 31; 13%) and not in primary cutaneous diffuse large B-cell lymphoma, leg type.
  • CD123+ PDC clusters were found in close proximity to monoclonal plasma cells and T-cells and were already present at high numbers in early lesions and initial recurrences of PCMZL.
  • In conclusion, the detection of larger clusters of PDC in PCMZL provides a useful adjunctive diagnostic marker and suggests a pathogenetically relevant role of these cells in PCMZL.
  • Furthermore, the occurrence of PDC could explain the high number of T-cells typically found in PCMZL.
  • We propose considering PCMZL as a unique and potentially antigen-driven neoplasm with PDC, T-cells, and B-cells as the constitutive tumor components.
  • [MeSH-major] Dendritic Cells / metabolism. Interleukin-3 Receptor alpha Subunit / metabolism. Lymphoma, B-Cell, Marginal Zone / metabolism. Plasma Cells / metabolism. Skin Neoplasms / metabolism
  • [MeSH-minor] Biomarkers, Tumor / metabolism. Clone Cells. Gene Rearrangement, B-Lymphocyte, Light Chain. Humans. Immunoenzyme Techniques. Immunoglobulin Light Chains / metabolism. Lymph Nodes / pathology. Lymphoma, Follicular / genetics. Lymphoma, Follicular / metabolism. Lymphoma, Follicular / pathology. Lymphoma, Large B-Cell, Diffuse / genetics. Lymphoma, Large B-Cell, Diffuse / metabolism. Lymphoma, Large B-Cell, Diffuse / pathology. Polymerase Chain Reaction

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  • (PMID = 19718787.001).
  • [ISSN] 1532-0979
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / IL3RA protein, human; 0 / Immunoglobulin Light Chains; 0 / Interleukin-3 Receptor alpha Subunit
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78. Khoo JJ, Alwi RI, Abd-Rahman I: Myoid hamartoma of breast with chondroid metaplasia: a case report. Malays J Pathol; 2009 Jun;31(1):77-80
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  • Breast hamartoma is an uncommon poorly recognised benign breast neoplasm.
  • The smooth muscle cells showed strong and diffuse immunoreactivity for vimentin, myogloblin, alpha-smooth muscle actin, desmin and CD34 and failed to express pan-cytokeratin or S100 protein.
  • The ducts lined by epithelial cells were reactive to pan-cytokeratin while the myoepithelial cells were reactive to S100 protein.
  • The various immuno-histochemical staining as well as the cyto-histological changes encountered in myoid hamartomas are discussed with clinical, radiological and pathological correlation to differentiate it from other benign and malignant breast lesions.
  • [MeSH-minor] Biomarkers / metabolism. Breast Neoplasms / diagnosis. Cartilage / pathology. Cell Differentiation. Diagnosis, Differential. Female. Fibroadenoma / diagnosis. Humans. Immunohistochemistry. Metaplasia / pathology. Middle Aged

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  • (PMID = 19694319.001).
  • [ISSN] 0126-8635
  • [Journal-full-title] The Malaysian journal of pathology
  • [ISO-abbreviation] Malays J Pathol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Malaysia
  • [Chemical-registry-number] 0 / Biomarkers
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79. Bellezza G, Colella R, Sidoni A, Del Sordo R, Ferri I, Cioccoloni C, Cavaliere A: Immunohistochemical expression of Galectin-3 and HBME-1 in granular cell tumors: a new finding. Histol Histopathol; 2008 09;23(9):1127-30
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  • [Title] Immunohistochemical expression of Galectin-3 and HBME-1 in granular cell tumors: a new finding.
  • Granular cell tumor (GCT) is a relatively rare neoplasm, usually located in the upper aerodigestive tract, skin and soft tissue.
  • Because of its uncertain histogenesis, GCT has been the object of many immunohistochemical and ultrastructural studies that have suggested a Schwann cell origin.
  • Our recent observation of a case of GCT immunoreactive for Galectin-3 and HBME-1 led us to further investigate the immunohistochemical profile of these neoplasms.
  • We evaluated the immunohistochemical expression of the traditional markers for GCT (S-100, CD68) along with new markers (Galectin-3, HBME-1, Calretinina and Inhibin-alpha) in 22 granular cell tumors.
  • Our results showed, in all cases, a constant diffuse positivity for S-100 protein, CD68 and Galectin-3.
  • The present study gives a new immunophenotypic profile for GCT, which could help pathologists in distinguishing morphologically ambiguous granular lesions in unusual sites.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Galectin 3 / metabolism. Granular Cell Tumor / metabolism. Head and Neck Neoplasms / metabolism. Skin Neoplasms / metabolism

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  • (PMID = 18581283.001).
  • [ISSN] 1699-5848
  • [Journal-full-title] Histology and histopathology
  • [ISO-abbreviation] Histol. Histopathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Galectin 3; 0 / HBME-1 antigen
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80. Azevedo Rde S, Pires FR, Della Coletta R, de Almeida OP, Kowalski LP, Lopes MA: Oral myofibromas: report of two cases and review of clinical and histopathologic differential diagnosis. Oral Surg Oral Med Oral Pathol Oral Radiol Endod; 2008 Jun;105(6):e35-40
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  • Myofibroma is a benign mesenchymal neoplasm composed of myofibroblasts which has been described with different synonyms since the first report in 1951.
  • It may show clinical and histologic features that may be misinterpreted as a malignancy.
  • We describe 2 cases of oral myofibromas affecting infants; the first one showed a rapid growth with teeth displacement and ulceration; the second one presented a relatively slow growth with an indolent course.
  • Differential diagnosis included benign and malignant mesenchymal neoplasms, salivary gland tumors, and reactive processes.
  • Microscopic analysis of both lesions revealed a spindle cell tumor with immunoreactivity for vimentin, muscle-specific actin, and specific smooth muscle isoform alpha-actin, rendering the diagnoses of myofibroma.
  • Myofibroma presents a wide range of differential diagnosis, including benign and malignant neoplasms.
  • [MeSH-major] Gingival Neoplasms / pathology. Lip Neoplasms / pathology. Myofibroma / pathology

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  • (PMID = 18417385.001).
  • [ISSN] 1528-395X
  • [Journal-full-title] Oral surgery, oral medicine, oral pathology, oral radiology, and endodontics
  • [ISO-abbreviation] Oral Surg Oral Med Oral Pathol Oral Radiol Endod
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Actins; 0 / Vimentin
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81. Campos M, Prior C, Warleta F, Zudaire I, Ruíz-Mora J, Catena R, Calvo A, Gaforio JJ: Phenotypic and genetic characterization of circulating tumor cells by combining immunomagnetic selection and FICTION techniques. J Histochem Cytochem; 2008 Jul;56(7):667-75
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  • [Title] Phenotypic and genetic characterization of circulating tumor cells by combining immunomagnetic selection and FICTION techniques.
  • The presence of circulating tumor cells (CTCs) in breast cancer patients has been proven to have clinical relevance.
  • Cytogenetic characterization of these cells could have crucial relevance for targeted cancer therapies.
  • We developed a method that combines an immunomagnetic selection of CTCs from peripheral blood with the fluorescence immunophenotyping and interphase cytogenetics as a tool for investigation of neoplasm (FICTION) technique.
  • Briefly, peripheral blood (10 ml) from healthy donors was spiked with a predetermined number of human breast cancer cells.
  • Nucleated cells were separated by double density gradient centrifugation of blood samples.
  • Tumor cells (TCs) were immunomagnetically isolated with an anti-cytokeratin antibody and placed onto slides for FICTION analysis.
  • Our results show that TCs can be efficiently isolated from peripheral blood and characterized by FICTION.
  • [MeSH-major] Neoplastic Cells, Circulating / pathology
  • [MeSH-minor] Antigens, Neoplasm / genetics. Cell Line, Tumor. Chromosomes, Human, Pair 17 / genetics. Cytogenetic Analysis. DNA Topoisomerases, Type II / genetics. DNA-Binding Proteins / genetics. Feasibility Studies. Gene Dosage. Humans. Immunomagnetic Separation. Immunophenotyping / methods. Receptor, ErbB-2 / genetics

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  • (PMID = 18413646.001).
  • [ISSN] 0022-1554
  • [Journal-full-title] The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society
  • [ISO-abbreviation] J. Histochem. Cytochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / DNA-Binding Proteins; EC 2.7.10.1 / Receptor, ErbB-2; EC 5.99.1.3 / DNA Topoisomerases, Type II; EC 5.99.1.3 / DNA topoisomerase II alpha
  • [Other-IDs] NLM/ PMC2430160
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82. Kourelis K, Papadas T, Vandoros G, Goumas P, Sotiropoulou-Bonikou G: Glottic versus supraglottic tumors: differential molecular profile. Eur Arch Otorhinolaryngol; 2008 Jan;265(1):79-84
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  • [Title] Glottic versus supraglottic tumors: differential molecular profile.
  • Moreover, squamous cell carcinomas arising from these subsites, differ in terms of epidemiology, risk factors, clinical behaviour and prognosis.
  • We investigated in the two tumor types, the expression of epidermal growth factor receptor (EGFR), nuclear factor-kappaB (NF-kappaB) and retinoid X receptor alpha (RXRalpha), principal signal transducers associated with cancer, as well as cyclooxygenase-2 (COX-2), an enzyme induced in malignant neoplasms.
  • The clinical material includes tumor specimens from 61 patients with laryngeal cancer of glottic or supraglottic origin.
  • Intense EGFR and RXRalpha expression was significantly associated with glottic tumor descent (P = 0.011 and 0.001, respectively).
  • No significant relationship was established between neoplasm location and expressions of NF-kappaB, COX-2.
  • Our results show that tumors emerging from the two laryngeal regions, are different with regard to their molecular constitution.
  • [MeSH-major] Carcinoma, Squamous Cell / chemistry. Glottis. Laryngeal Neoplasms / chemistry
  • [MeSH-minor] Adult. Aged. Cyclooxygenase 2 / analysis. Female. Humans. Immunohistochemistry. Male. Middle Aged. NF-kappa B / analysis. Receptor, Epidermal Growth Factor / analysis. Retinoid X Receptors / analysis

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  • (PMID = 17909831.001).
  • [ISSN] 0937-4477
  • [Journal-full-title] European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery
  • [ISO-abbreviation] Eur Arch Otorhinolaryngol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / NF-kappa B; 0 / Retinoid X Receptors; EC 1.14.99.1 / Cyclooxygenase 2; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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83. Malatesta D, Cuomo A, Marà M, Di Guardo G, Gentile L, Macolino A, Della Salda L: Benign giant cell tumour of tendon sheaths in a European Lynx (Lynx lynx). J Vet Med A Physiol Pathol Clin Med; 2005 Apr;52(3):125-30

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Benign giant cell tumour of tendon sheaths in a European Lynx (Lynx lynx).
  • The histological, histochemical, immunohistochemical and ultrastructural features of a benign giant cell tumour (BGCT) of tendon sheaths in a 12-year-old male European lynx (Lynx lynx) are reported herein.
  • The neoplastic mass involved the subcutaneous and inter-muscular tissues of the first, second, third and fourth digit of the left forelimb, from the phalanxes up to the carpus.
  • The tumour appeared as a grey-whitish tissue mottled with darker areas, along with several scattered foci of orange colour.
  • Histologically, the lesion consisted of a mixed population of numerous, multinucleated giant cells and epithelioid or spindle-shaped mononuclear cells embedded in a loose, highly vascular stroma.
  • Neoplastic cells lined cleft formations and synovial-like projections into cystic spaces.
  • The mononuclear and the giant cells were tartrate-resistant acid phosphatase and periodic acid-Schiff positive, being also immunohistochemically reactive for lysozyme and vimentin, with a few cells showing immunopositivity also for alpha-1-antitrypsin.
  • Ultrastructurally, histiocyte-like cells, fibroblast-like cells and multinucleated giant cells were observed, but no virus-like particles could be detected in any of the above cell types.
  • The BGCT of tendon sheaths, a fairly uncommon neoplasm in animals, has not been previously reported in the lynx.
  • [MeSH-major] Giant Cell Tumors / veterinary. Lynx. Tendons / pathology

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  • (PMID = 15836443.001).
  • [ISSN] 0931-184X
  • [Journal-full-title] Journal of veterinary medicine. A, Physiology, pathology, clinical medicine
  • [ISO-abbreviation] J Vet Med A Physiol Pathol Clin Med
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
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84. Imura J, Tomita S, Ono Y, Inaba F, Yamazaki T, Fukasawa I, Inaba N, Fujimori T: Endometrial adenosquamous carcinoma with osteoclast-like giant cells: immunohistochemistry and histogenesis. APMIS; 2005 Feb;113(2):140-4
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  • [Title] Endometrial adenosquamous carcinoma with osteoclast-like giant cells: immunohistochemistry and histogenesis.
  • Primary extraskeletal epithelial neoplasms containing osteoclast-like giant cells (OGCs) are rare.
  • We herein describe a case of adenosquamous carcinoma that developed in the endometrium together with non-neoplastic OGCs.
  • Histologically, the tumor was found to be an adenosquamous carcinoma containing a large number of OGCs and mononuclear cells (MNCs) that had infiltrated into the stroma.
  • Immunohistochemically, the OGCs and MNCs stained strongly positive for KP-1 and alpha-1-antichymotrypsin, and negative for the epithelial markers epithelial membrane antigen (EMA) and cytokeratins.
  • These findings suggest that the OGCs and MNCs in this patient's tumor originated from monocytes/histiocytes, and most likely developed as part of the stromal reaction to the neoplasm.
  • [MeSH-major] Adenocarcinoma / pathology. Carcinoma, Squamous Cell / pathology. Endometrial Neoplasms / pathology. Giant Cells / pathology. Osteoclasts / pathology
  • [MeSH-minor] Aged. Cell Lineage. Female. Humans. Leukocytes, Mononuclear / metabolism. Leukocytes, Mononuclear / pathology

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  • (PMID = 15723689.001).
  • [ISSN] 0903-4641
  • [Journal-full-title] APMIS : acta pathologica, microbiologica, et immunologica Scandinavica
  • [ISO-abbreviation] APMIS
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Denmark
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85. Wen G, Hong M, Calaf GM, Roy D, Partridge MA, Li B, Hei TK: Phosphoproteomic profiling of arsenite-treated human small airway epithelial cells. Oncol Rep; 2010 Feb;23(2):405-12
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  • [Title] Phosphoproteomic profiling of arsenite-treated human small airway epithelial cells.
  • Arsenic is well documented as a chemotherapeutic agent capable of inducing cell death; however, it is also considered as a human carcinogen.
  • Although it has recently been shown that arsenite exposure can potentiate genotoxicity, little is known about its global effects exerted in cells at the proteome level.
  • Immortalized human small airway epithelial cells exposed to arsenite were used to identify phosphoproteins of two major signaling cascades, such as the human phospho-receptor tyrosine kinase (Phospho-RTK) and the mitogen-activated protein kinases (MAPKs).
  • These two arrays included several phosphoproteins, such as EGFR, ErbB2, ErbB4, InsulinR, Flt-3, extracellular signal-regulated kinases (ERK1/2), intracellular kinases such as AKT, GSK-3, c-Jun N-terminal kinases (JNK1-3) and different p38 isoforms (alpha/beta/delta/gamma).
  • In arsenite-treated cells, phosphorylation of EGFR, InsulinR and Flt3R showed an increase when compared to their non-arsenite treated counterparts.
  • Inhibitors of these proteins further confirmed the involvement of such proteins in the neoplasm transformation of arsenite-treated human small airway epithelial cells as seen in changes in plating efficiency, anchorage-independent growth and proliferation rate.
  • [MeSH-major] Arsenites / pharmacology. Epithelial Cells / drug effects. Phosphoproteins / analysis. Proteome / drug effects. Respiratory Mucosa / drug effects
  • [MeSH-minor] Cell Transformation, Neoplastic / drug effects. Cell Transformation, Neoplastic / metabolism. Cells, Cultured. Enzyme Inhibitors / pharmacology. Humans. Metabolome. Proteomics / methods. Receptor Protein-Tyrosine Kinases / antagonists & inhibitors. Teratogens / pharmacology


86. Lopes LF, Bacchi CE: Imatinib treatment for gastrointestinal stromal tumour (GIST). J Cell Mol Med; 2010 Jan;14(1-2):42-50
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  • [Title] Imatinib treatment for gastrointestinal stromal tumour (GIST).
  • Gastrointestinal stromal tumour (GIST) is the most common mesenchymal neoplasm of the gastrointestinal tract.
  • GISTs are believed to originate from intersticial cells of Cajal (the pacemaker cells of the gastrointestinal tract) or related stem cells, and are characterized by KIT or platelet-derived growth factor receptor alpha (PDGFRA) activating mutations.
  • The use of imatinib has revolutionized the management of GIST and altered its natural history, substantially improving survival time and delaying disease progression in many patients.
  • The neoadjuvant (preoperative) use of imatinib is recommended to facilitate resection and avoid mutilating surgery by decreasing tumour size, and adjuvant therapy is indicated for patients at high risk of recurrence.
  • The molecular characterization (genotyping) of GISTs has become an essential part of the routine management of the disease as KIT and PDGFRA mutation status predicts the likelihood of achieving response to imatinib.
  • However, the vast majority of patients who initially responded to imatinib will develop tumour progression (secondary resistance).
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Gastrointestinal Stromal Tumors / drug therapy. Piperazines / therapeutic use. Pyrimidines / therapeutic use
  • [MeSH-minor] Benzamides. Disease Progression. Drug Resistance, Neoplasm / genetics. Humans. Imatinib Mesylate. Mutation. Protein Kinase Inhibitors / therapeutic use. Protein-Tyrosine Kinases / antagonists & inhibitors. Proto-Oncogene Proteins c-kit / genetics. Proto-Oncogene Proteins c-kit / metabolism. Receptor, Platelet-Derived Growth Factor alpha / genetics. Receptor, Platelet-Derived Growth Factor alpha / metabolism

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  • (PMID = 19968734.001).
  • [ISSN] 1582-4934
  • [Journal-full-title] Journal of cellular and molecular medicine
  • [ISO-abbreviation] J. Cell. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha
  • [Number-of-references] 102
  • [Other-IDs] NLM/ PMC3837608
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87. Fregnani ER, Sobral LM, Alves FA, Soares FA, Kowalski LP, Coletta RD: Presence of myofibroblasts and expression of matrix metalloproteinase-2 (MMP-2) in ameloblastomas correlate with rupture of the osseous cortical. Pathol Oncol Res; 2009 Jun;15(2):231-40
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  • Myofibroblasts are frequent in the stroma of neoplasm and by the expression of proteinases they can influence tumor infiltration and progression.
  • In the present study, presence of myofibroblasts and expression of matrix metalloproteinase-2 (MMP-2) and urokinase plasminogen activator (uPA) were examined in intra-osseous solid multicystic ameloblastomas to determine their roles in the clinicopathological features of the tumors.
  • Fifty seven ameloblastomas were analyzed immunohistochemically with antibodies against the isoform alpha of the smooth muscle actin (alpha-SMA), a specific marker of myofibroblasts, MMP-2 and uPA.
  • Myofibroblasts were found in the stroma, in close contact with neoplastic cell islands, of approximately 58% (n = 33) of the ameloblastomas.
  • MMP-2 and uPA were found in the cytoplasm of both neoplastic and stromal cells.
  • Abundant presence of myofibroblast in the stroma of the tumors and expression of MMP-2 in the neoplastic or stromal cells were significantly correlated with rupture of the osseous cortical, which has been considered an important prognostic marker of ameloblastoma aggressiveness.
  • Ours results suggest that abundant presence of myofibroblasts and expression of MMP-2 in solid ameloblastomas may be associated with a more aggressive infiltrative behavior.
  • [MeSH-major] Ameloblastoma / enzymology. Bone Neoplasms / enzymology. Fibroblasts / pathology. Matrix Metalloproteinase 2 / metabolism
  • [MeSH-minor] Adolescent. Adult. Aged. Biomarkers, Tumor / metabolism. Child. Cytoplasm / metabolism. Disease Progression. Female. Humans. Male. Middle Aged. Muscle, Smooth / enzymology. Prognosis. Stromal Cells / enzymology. Urokinase-Type Plasminogen Activator / metabolism. Young Adult

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  • (PMID = 19096916.001).
  • [ISSN] 1219-4956
  • [Journal-full-title] Pathology oncology research : POR
  • [ISO-abbreviation] Pathol. Oncol. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 3.4.21.73 / Urokinase-Type Plasminogen Activator; EC 3.4.24.24 / Matrix Metalloproteinase 2
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88. Starska K, Lukomski M, Lewy-Trenda I, Stasikowska O, Józefowicz-Korczyńska M, Durko M, Głowacka E: [Production of cytokines by peripheral blood mononuclear cells--correlation with clinicomorphological features in laryngeal carcinoma]. Otolaryngol Pol; 2008;62(4):388-94
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  • [Title] [Production of cytokines by peripheral blood mononuclear cells--correlation with clinicomorphological features in laryngeal carcinoma].
  • INTRODUCTION: In studied analyzed role of the cytokines in pathology of neoplasms of various origin the importance of these proteins in regulation of immunocompetent cells function has been described.
  • The aim of this study was to estimate of cho sen cytokines concentration produced by peripheral blood mononuclear cells and in whole blood in patients with laryngeal carcinoma and to analyze the connection of cytokines profile with clinicopathological features.
  • MATERIALA AND METHODS: 55 patients with squamous cell carcinoma of the larynx treated at ENT Department Medical University of Lodz between 2003-2007 were analyzed.
  • For estimation of cytokine secretion the cultures of isolated peripheral blood mononuclear cells (T lymphocytes) and the whole blood were established.
  • RESULTS: Authors reported statistical correlation between chosen cytokines concentration and clinicomorphological parameters: pT and IL-2, IL-6, IL-8, TNFalpha produced by isolated cells and IL-2, IL-6, TNFa and IFNgamma in whole blood, pN and IL-8, IL-10, IFNgamma; ABL score and IL-6, TNFalpha, IFNgamma produced by isolated cells and IL-2, IL-6, IL-10, TNFalpha, IFNgamma in whole blood.
  • CONCLUSION: Our studied indicated the important influence of proinflammatory and regulatory cytokines produced by immunocompetent cells for course of neoplasm disease, aggressiveness and advance in laryngeal carcinoma.
  • [MeSH-major] Biomarkers, Tumor / blood. Carcinoma, Small Cell / immunology. Carcinoma, Small Cell / pathology. Cytokines / biosynthesis. Interferon-gamma / blood. Laryngeal Neoplasms / immunology. Laryngeal Neoplasms / pathology
  • [MeSH-minor] Adult. Aged. Enzyme-Linked Immunosorbent Assay. Female. Humans. Interleukin-10 / blood. Interleukin-2 / blood. Interleukin-6 / blood. Interleukin-8 / blood. Leukocytes, Mononuclear / immunology. Male. Middle Aged. Neoplasm Staging. Poland. Retrospective Studies. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 18837209.001).
  • [ISSN] 0030-6657
  • [Journal-full-title] Otolaryngologia polska = The Polish otolaryngology
  • [ISO-abbreviation] Otolaryngol Pol
  • [Language] pol
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Cytokines; 0 / Interleukin-2; 0 / Interleukin-6; 0 / Interleukin-8; 0 / Tumor Necrosis Factor-alpha; 130068-27-8 / Interleukin-10; 82115-62-6 / Interferon-gamma
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89. Yamada Y, Cancelas JA: FIP1L1/PDGFR alpha-associated systemic mastocytosis. Int Arch Allergy Immunol; 2010;152 Suppl 1:101-5
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  • [Title] FIP1L1/PDGFR alpha-associated systemic mastocytosis.
  • Since the identification of the FIP1L1/PDGFRA fusion gene as a pathogenic cause of the hypereosinophilic syndrome (HES), the importance of the molecular classification of HES leading to the diagnosis of chronic eosinophilic leukemia (CEL) has been recognized.
  • As a result, a new category, 'myeloid and lymphoid neoplasm with eosinophilia and abnormalities in PDGFRA, PDGFRB or FGFR1', has recently been added to the new WHO criteria for myeloid neoplasms.
  • FIP1L1/PDGFR alpha-positive disorders are characterized by clonal hypereosinophilia, multiple organ dysfunctions due to eosinophil infiltration, systemic mastocytosis (SM) and a dramatic response to treatment with imatinib mesylate.
  • A murine HES/CEL model by the introduction of FIP1L1/PDGFR alpha and IL-5 overexpression also shows SM, representing patients with FIP1L1/PDGFR alpha-positive HES/CEL/SM.
  • The murine model and the in vitro development system of FIP1L1/PDGFR alpha-positive mast cells revealed the interaction between FIP1L1/PDGFR alpha, IL-5 and stem cell factor in the development of HES/CEL/SM.
  • Current findings of FIP1L1/PDGFR alpha-positive HES/CEL are reviewed focusing on aberrant mast cell development leading to SM.

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  • [Copyright] (c) 2010 S. Karger AG, Basel.
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  • (PMID = 20523072.001).
  • [ISSN] 1423-0097
  • [Journal-full-title] International archives of allergy and immunology
  • [ISO-abbreviation] Int. Arch. Allergy Immunol.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / R01 HL087159; United States / NHLBI NIH HHS / HL / R42 HL080759; United States / NHLBI NIH HHS / HL / HL080759; United States / NHLBI NIH HHS / HL / HL080759-01A2S1
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / FIP1L1-PDGFRA fusion protein, human; 0 / Oncogene Proteins, Fusion; 0 / mRNA Cleavage and Polyadenylation Factors; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha
  • [Number-of-references] 25
  • [Other-IDs] NLM/ PMC2917731
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90. Wang H, Wang H, Zhu Z, Yang S, Feng S, Li K: Characterization of porcine EPLIN gene revealed distinct expression patterns for the two isoforms. Anim Biotechnol; 2007;18(2):101-8

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  • Epithelial protein lost in neoplasm (EPLIN) is a cytoskeleton-associated protein that is down-regulated in transformed cells.
  • Two EPLIN isoforms (alpha and beta) are generated by alternative promoter usage from a single gene.
  • The temporal expression analysis indicated that they are not coexpressional through muscle development: EPLIN-alpha was detected in developing skeletal muscle, but EPLIN-beta was not.

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  • (PMID = 17453649.001).
  • [ISSN] 1532-2378
  • [Journal-full-title] Animal biotechnology
  • [ISO-abbreviation] Anim. Biotechnol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cytoskeletal Proteins; 0 / Protein Isoforms; 0 / RNA, Messenger
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91. Cooper TK, Ronnett BM, Ruben DS, Zink MC: Uterine myxoid leiomyosarcoma with widespread metastases in a cat. Vet Pathol; 2006 Jul;43(4):552-6
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  • Histologic examination revealed an invasive spindle cell neoplasm with features of malignancy, and extensive hypocellular areas containing an alcian blue-positive myxoid matrix.
  • Tumor cells expressed caldesmon, alpha-smooth muscle actin, and estrogen receptor but were negative for desmin.
  • The animal was euthanized 1 month later because of suspected local tumor recurrence.
  • At necropsy, the abdominal cavity contained 120 ml of mucoid ascites; multiple tumor nodules were present in the abdominal and thoracic cavities.
  • The clinical behavior and gross, microscopic, and immunohistochemical findings established a diagnosis of myxoid leiomyosarcoma.
  • [MeSH-major] Cat Diseases / pathology. Leiomyosarcoma / veterinary. Uterine Neoplasms / veterinary
  • [MeSH-minor] Animals. Cats. Female. Hysterectomy / veterinary. Immunohistochemistry / veterinary. Neoplasm Metastasis. Neoplasm Recurrence, Local / veterinary

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  • (PMID = 16846999.001).
  • [ISSN] 0300-9858
  • [Journal-full-title] Veterinary pathology
  • [ISO-abbreviation] Vet. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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92. Isaac JC, Willmore C, Holden JA, Layfield LJ: A c-kit-negative gastrointestinal stromal tumor with a platelet-derived growth factor receptor alpha mutation. Appl Immunohistochem Mol Morphol; 2006 Mar;14(1):52-6
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  • [Title] A c-kit-negative gastrointestinal stromal tumor with a platelet-derived growth factor receptor alpha mutation.
  • Gastrointestinal stromal tumors (GISTs) are well-recognized mesenchymal neoplasms of the intestinal tract.
  • A diagnosis of GIST is not always possible using IHC techniques for detection of c-kit.
  • Histology showed a predominantly epithelioid neoplasm with focal "spindle cell" areas.
  • The morphologic and immunophenotypic appearance could be compatible with either a smooth muscle tumor or a GIST.
  • Because of the differences in treatment protocols and prognosis between these two entities, molecular studies to detect c-kit or platelet-derived growth factor receptor (PDGFR) activating mutations were performed.
  • This additional molecular study allowed the authors to formulate the precise diagnosis of a c-kit-negative GIST with strong smooth muscle marker expression.

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  • (PMID = 16540731.001).
  • [ISSN] 1541-2016
  • [Journal-full-title] Applied immunohistochemistry & molecular morphology : AIMM
  • [ISO-abbreviation] Appl. Immunohistochem. Mol. Morphol.
  • [Language] ENG
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Desmin; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha
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93. Martínez-Rodríguez M, Ramos D, Soriano P, Subramaniam M, Navarro S, Llombart-Bosch A: Poorly differentiated adenocarcinomas of prostate versus high-grade urothelial carcinoma of the bladder: a diagnostic dilemma with immunohistochemical evaluation of 2 cases. Int J Surg Pathol; 2007 Apr;15(2):213-8
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  • The first is an infiltration of the bladder by a poorly differentiated adenocarcinoma of the prostate, which was clinically suspected as a papillary urothelial neoplasm.
  • The second is a collision tumor composed of prostatic adenocarcinoma and urothelial carcinoma observed on a core needle biopsy of the prostate.
  • In both cases, a large panel of immunohistochemical markers were used and demonstrated positivity for prostate-specific antigen and alpha methyl racemase in the prostatic carcinomas and immunoreactivity for CK7, CK20, Ag 34betaE12, and p53 in the urothelial carcinoma.
  • The differentiating histological and immunohistochemical findings are discussed.
  • [MeSH-major] Adenocarcinoma / pathology. Carcinoma, Transitional Cell / pathology. Prostatic Neoplasms / pathology. Urinary Bladder Neoplasms / pathology
  • [MeSH-minor] Aged. Aged, 80 and over. Biomarkers, Tumor / metabolism. Diagnosis, Differential. Humans. Male. Neoplasms, Multiple Primary. Prostate-Specific Antigen / metabolism. Racemases and Epimerases / metabolism

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  • (PMID = 17478786.001).
  • [ISSN] 1066-8969
  • [Journal-full-title] International journal of surgical pathology
  • [ISO-abbreviation] Int. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 3.4.21.77 / Prostate-Specific Antigen; EC 5.1.- / Racemases and Epimerases; EC 5.1.99.4 / alpha-methylacyl-CoA racemase
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94. Kovács RK, Korom I, Dobozy A, Farkas G, Ormos J, Kemény L: Necrolytic migratory erythema. J Cutan Pathol; 2006 Mar;33(3):242-5
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  • The classical symptoms are associated with alpha-cell pancreatic islet cell tumor or 'glucagonoma'.
  • Generally, extracutaneous hallmarks of this disease include weight loss, diabetes, anaemia and diarrhoea.
  • OBSERVATION: We report a case of a 39-year-old woman with a 3-year history of recalcitrant psoriasiform eruption, who had no other associated symptoms on routine examination.
  • Abdominal computer tomography was performed, which revealed a tumor in the tail of the pancreas.
  • After distal resection of the pancreas her skin symptoms resolved in a few days time.
  • CONCLUSIONS: It is infrequent to have only necrolytic migratory erythema, hyperglucagonaemia and islet-cell tumor but no other extracutaneous symptoms in glucagonoma syndrome.
  • Skin symptoms are important, often they are the clue to the diagnosis of glucagonoma syndrome.
  • [MeSH-major] Erythema / etiology. Erythema / pathology. Glucagonoma / complications. Glucagonoma / pathology. Pancreatic Neoplasms / complications. Pancreatic Neoplasms / pathology

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  • (PMID = 16466513.001).
  • [ISSN] 0303-6987
  • [Journal-full-title] Journal of cutaneous pathology
  • [ISO-abbreviation] J. Cutan. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Denmark
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95. Yokota T, Kouno J, Adachi K, Takahashi H, Teramoto A, Matsumoto K, Sugisaki Y, Onda M, Tsunoda T: Identification of histological markers for malignant glioma by genome-wide expression analysis: dynein, alpha-PIX and sorcin. Acta Neuropathol; 2006 Jan;111(1):29-38
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  • [Title] Identification of histological markers for malignant glioma by genome-wide expression analysis: dynein, alpha-PIX and sorcin.
  • Glioblastoma multiforme (GBM), the most malignant class of glial neoplasm (grade IV in WHO criteria), carries the worst clinical prognosis among primary brain tumors in adults.
  • Semi-quantitative RT-PCR experiments with 6 of those genes confirmed higher expression of DNCH2, ARHGEF6, NPM1 and SRI and lower expression of NRGN and TM4SF2 in GBM tumors.
  • Immunohistochemical staining for 3 of the respective gene products, dynein (product of DNCH2), alpha-PIX (product of ARHGEF6), and sorcin (product of SRI) indicated that this technique might be useful for histological grading of glial tumors.
  • To establish criteria for this diagnostic approach, we scored glial tumor tissues of different histological grades according to the staining results; the scores were significantly higher in anaplastic astrocytomas and GBMs than in diffuse astrocytomas or normal brain tissues.
  • These findings indicated that levels of these three proteins might serve as histological markers for malignant glioma classification.
  • [MeSH-major] Biomarkers, Tumor / genetics. Brain Neoplasms / genetics. Calcium-Binding Proteins / genetics. Cell Cycle Proteins / genetics. Dyneins / genetics. Glioblastoma / genetics. Guanine Nucleotide Exchange Factors / genetics
  • [MeSH-minor] DNA, Neoplasm / analysis. DNA, Neoplasm / genetics. Gene Expression Profiling. Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry. Neoplasm Staging. Oligonucleotide Array Sequence Analysis. Prognosis. Reverse Transcriptase Polymerase Chain Reaction. Rho Guanine Nucleotide Exchange Factors

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  • (PMID = 16320026.001).
  • [ISSN] 0001-6322
  • [Journal-full-title] Acta neuropathologica
  • [ISO-abbreviation] Acta Neuropathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / ARHGEF6 protein, human; 0 / Biomarkers, Tumor; 0 / Calcium-Binding Proteins; 0 / Cell Cycle Proteins; 0 / DNA, Neoplasm; 0 / Guanine Nucleotide Exchange Factors; 0 / Rho Guanine Nucleotide Exchange Factors; 0 / SRI protein, human; EC 3.6.4.2 / Dyneins
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96. Nakabayashi M, Shomori K, Kiya S, Shiomi T, Nosaka K, Ito H: Tubular-trabecular type Basal cell adenoma of the parotid gland: a patient report. Yonago Acta Med; 2010 Sep;53(3):65-9

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  • [Title] Tubular-trabecular type Basal cell adenoma of the parotid gland: a patient report.
  • Basal cell adenoma (BCA) is an uncommon benign salivary gland neoplasm that includes isomorphic basaloid cells.
  • The present patient demonstrated a few tumor nests in the fibrous capsule, and her tumor was larger than usual.
  • Histopathologically, the tumor was characterized by multiple duct-like structures and tubular-trabecular masses composed of small isomorphic cells with hyperchromatic, round nuclei and an eosinophilic cytoplasm.
  • It was difficult to determine whether the ductal structures noted in the tumor capsule were invasive.
  • By immunohistochemistry, tumor cells of the tubular nests were positive for cytokeratin 7 and that the outer cells of tubular nests were positive for alpha smooth muscle actin (αSMA) and calponin.
  • Tumor cells were immuno-negative for S-100 protein and glial fibrillary acidic protein.
  • The Ki-67 labeling scores of the cells were extremely low (< 1%).

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  • (PMID = 24031120.001).
  • [ISSN] 0513-5710
  • [Journal-full-title] Yonago acta medica
  • [ISO-abbreviation] Yonago Acta Med
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Other-IDs] NLM/ PMC3763784
  • [Keywords] NOTNLM ; basal cell adenoma / immunohistochemistry / parotid gland
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97. Sutherland MK, Yu C, Lewis TS, Miyamoto JB, Morris-Tilden CA, Jonas M, Sutherland J, Nesterova A, Gerber HP, Sievers EL, Grewal IS, Law CL: Anti-leukemic activity of lintuzumab (SGN-33) in preclinical models of acute myeloid leukemia. MAbs; 2009 Sep-Oct;1(5):481-90
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  • AML cells express the myeloid marker CD33, making it amenable to CD33-targeted therapy.
  • Thus, the in vitro and in vivo anti-tumor activities of lintuzumab (SGN-33), a humanized monoclonal anti-CD33 antibody undergoing clinical evaluation, were investigated.
  • In vitro assays were used to assess the ability of lintuzumab to mediate effector functions and to decrease the production of growth factors from AML cells.
  • SCID mice models of disseminated AML with the multi-drug resistance (MDR)-negative HL60 and the MDR(+), HEL9217 and TF1-alpha, cell lines were developed and applied to examine the in vivo antitumor activity.
  • In vitro, lintuzumab significantly reduced the production of TNFalpha-induced pro-inflammatory cytokines and chemokines by AML cells.
  • Lintuzumab promoted tumor cell killing through antibody-dependent cellular cytotoxicity (ADCC) and phagocytosis (ADCP) activities against MDR(-) and MDR(+) AML cell lines and primary AML patient samples.
  • At doses from 3 to 30 mg/kg, lintuzumab significantly enhanced survival and reduced tumor burden in vivo, regardless of MDR status.
  • The results suggest that lintuzumab may exert its therapeutic effects by modulating the cytokine milieu in the tumor microenvironment and through effector mediated cell killing.
  • [MeSH-minor] Animals. Antibodies, Monoclonal, Humanized. Antibody-Dependent Cell Cytotoxicity. Cell Line, Tumor. Cytokines / metabolism. Disease Models, Animal. HL-60 Cells. Humans. Mice. Mice, SCID. Phagocytosis. Sialic Acid Binding Ig-like Lectin 3. Treatment Outcome. U937 Cells

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  • (PMID = 20065652.001).
  • [ISSN] 1942-0870
  • [Journal-full-title] mAbs
  • [ISO-abbreviation] MAbs
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antigens, CD; 0 / Antigens, Differentiation, Myelomonocytic; 0 / Antineoplastic Agents; 0 / CD33 protein, human; 0 / Cd33 protein, mouse; 0 / Cytokines; 0 / Sialic Acid Binding Ig-like Lectin 3; 0 / lintuzumab
  • [Other-IDs] NLM/ PMC2759498
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98. Abe K, Takeichi M: EPLIN mediates linkage of the cadherin catenin complex to F-actin and stabilizes the circumferential actin belt. Proc Natl Acad Sci U S A; 2008 Jan 8;105(1):13-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The cadherin-catenin complex is the major machinery for cell-cell adhesion in many animal species.
  • In epithelial cells, the AJ encircles the cells near their apical surface and forms the "zonula adherens" or "adhesion belt."
  • Here, we show that EPLIN (epithelial protein lost in neoplasm; also known as Lima-1), an actin-binding protein, couples with alpha-catenin and, in turn, links the cadherin-catenin complex to F-actin.
  • When EPLIN had been depleted in epithelial cells, the adhesion belt was disorganized and converted into zipper-like junctions in which actin fibers were radially arranged.
  • As EPLIN is known to have the ability to suppress actin depolymerization, our results suggest that EPLIN functions to link the cadherin-catenin complex to F-actin and simultaneously stabilizes this population of actin fibers, resulting in the establishment of the adhesion belt.
  • [MeSH-minor] Adherens Junctions / metabolism. Animals. Cell Adhesion. Cell Communication. Dogs. Humans. Mice. Models, Biological. Plasmids / metabolism. Protein Structure, Tertiary

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  • (PMID = 18093941.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Actins; 0 / Cadherins; 0 / Catenins; 0 / Cytoskeletal Proteins; 0 / D15Ertd366e protein, mouse; 0 / LIMA1 protein, human
  • [Other-IDs] NLM/ PMC2224173
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99. Ren Y, Medeiros LJ, Amin HM, Rytting ME, Jorgensen JL, Chen W: Unusual expression of CD94 on CD8+ TCR-alpha beta T cells in infectious mononucleosis. Ann Diagn Pathol; 2007 Feb;11(1):55-60
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  • [Title] Unusual expression of CD94 on CD8+ TCR-alpha beta T cells in infectious mononucleosis.
  • Infectious mononucleosis, caused by primary Epstein-Barr virus (EBV) infection, is usually a benign, self-limited lymphoproliferative disorder.
  • We report a case of a 21-year-old woman who presented with fever, sore throat, severe neutropenia, and absolute lymphocytosis with atypical lymphocytes.
  • In situ hybridization for EBV-encoded small RNA performed on the marrow aspirate clot specimen demonstrated scattered positive cells.
  • Flow cytometry immunophenotypic studies performed on aspirate material revealed a profoundly expanded population of CD8+ T-cell receptor (TCR)-alphabeta T cells with uniform expression of CD94.
  • No evidence of a monoclonal T-cell population was found as assessed by V(beta) use with flow cytometry and by TCR gamma-chain gene rearrangement using a polymerase chain reaction method.
  • Uniform expression of CD94 in an exuberant reactive proliferation of CD8+ TCR-alphabeta T cells in infectious mononucleosis has not been reported previously, and combined with atypical morphology might be misinterpreted as a malignant neoplasm.
  • [MeSH-major] CD8-Positive T-Lymphocytes / metabolism. Infectious Mononucleosis / immunology. NK Cell Lectin-Like Receptor Subfamily D / metabolism. Receptors, Antigen, T-Cell, alpha-beta / metabolism
  • [MeSH-minor] Adult. Cell Proliferation. Female. Gene Expression Regulation. Humans. Immunophenotyping

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  • (PMID = 17240309.001).
  • [ISSN] 1092-9134
  • [Journal-full-title] Annals of diagnostic pathology
  • [ISO-abbreviation] Ann Diagn Pathol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / NK Cell Lectin-Like Receptor Subfamily D; 0 / Receptors, Antigen, T-Cell, alpha-beta
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100. Kdous M, Hachicha R, Gamoudi A, Boussen H, Benna F, Rahal K: [Juvenile granulosa cell tumor of the ovary. A case report]. Tunis Med; 2006 May;84(5):305-8
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  • [Title] [Juvenile granulosa cell tumor of the ovary. A case report].
  • [Transliterated title] Tumeur juvenile de la granulosa ovarienne. A propos d'une observation.
  • Juvenile granulosa cell tumors of the ovary (JGCTs) are a rare form of neoplasm that makes up less than 5% of ovarians tumors in childhood and adolescence.
  • The authors describe a juvenile granulosa cell tumor expressed by an early pseudopuberty occurring in a 6 year old child.
  • Clinically, an endocrine syndrome was associated with a pelvic mass.
  • Tumor was localized strictly to the ovary, so conservative surgery was applied and proved sufficient to remove all tumor tissue.
  • Histological examination showed typical microscopic aspect of a juvenile granulosa cell tumor.
  • The patient is well, 14 years after surgery with a normal growth and mental developpment.
  • [MeSH-major] Granulosa Cell Tumor / diagnosis. Ovarian Neoplasms / diagnosis
  • [MeSH-minor] Biomarkers, Tumor / blood. Child. Estradiol / blood. Female. Follow-Up Studies. Humans. Ovariectomy. Puberty, Precocious / diagnosis. alpha-Fetoproteins / analysis

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  • (PMID = 16915782.001).
  • [ISSN] 0041-4131
  • [Journal-full-title] La Tunisie médicale
  • [ISO-abbreviation] Tunis Med
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Tunisia
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / alpha-Fetoproteins; 4TI98Z838E / Estradiol
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