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[Title] Homozygous P86S mutation of the human glucagon receptor is associated with hyperglucagonemia, alpha cell hyperplasia, and islet cell tumor.

OBJECTIVE: The goal of the study was to investigate the genetic and molecular basis of a novel syndrome of marked hyperglucagonemia and pancreatic alpha cell hyperplasia without glucagonoma syndrome.

METHODS: The glucagon receptor (GCGR) gene and the glucagon gene were sequenced in a patient with hyperglucagonemia and pancreatic alpha cell hyperplasia without glucagonoma syndrome.

Enhanced green fluorescent protein-conjugated wild type (WT) and mutant GCGR were used to characterize the functions of the mutant GCGR.

RESULTS: The glucagon gene sequence was normal, but the GCGR sequencing uncovered a homozygous missense mutation, c.256C>T, p.P86S in the extracellular domain of GCGR.

When expressed in human embryonic kidney 293 cells, GCGR P86S localized to the plasma membrane but bound 96% less radiolabeled glucagon than WT GCGR.

The median effective concentration of glucagon-induced cyclic adenosine monophosphate production was 24 nmol/L for GCGR P86S but 2.4 nmol/L for WT GCGR.

The patient's alpha cells also express glucagonlike peptide 1 and pancreatic polypeptide.

CONCLUSIONS: We hereby report the first homozygous missense mutation in the human GCGR, which is associated with alpha cell hyperplasia and hyperglucagonemia.

This mutation lowers the receptor's affinity to glucagon and decreases cyclic adenosine monophosphate production with physiological concentrations of glucagon.

Thus, the P86S mutation in GCGR likely causes alpha cell hyperplasia and hyperglucagonemia.

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(PMID = 19657311.001).

[ISSN] 1536-4828

[Journal-full-title] Pancreas

[ISO-abbreviation] Pancreas

[Language] ENG

[Grant] United States / NIDDK NIH HHS / DK / DK071870-04; United States / NIDDK NIH HHS / DK / K08 DK071870; United States / NIDDK NIH HHS / DK / DK071870; United States / NIDDK NIH HHS / DK / K08 DK071870-04

[Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Receptors, Glucagon; 147336-22-9 / Green Fluorescent Proteins; 9007-92-5 / Glucagon

[Other-IDs] NLM/ NIHMS139678; NLM/ PMC2767399

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] PIK3CA mutations in intraductal papillary mucinous neoplasm/carcinoma of the pancreas.

PURPOSE: Recent studies have reported high frequencies of somatic mutations in the phosphoinositide-3-kinase catalytic-alpha (PIK3CA) gene in various human solid tumors.

The mutational status of PIK3CA in intraductal papillary mucinous neoplasm/carcinoma (IPMN/IPMC) has not been evaluated previously.

RESULTS: We identified four missense mutations in the nine screened exons of PIK3CA from 36 IPMN/IPMC specimens (11%).

One of the four mutations, H1047R, has been previously reported as a hot-spot mutation.

CONCLUSION: This is the first report of PIK3CA mutation in pancreatic cancer.

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(PMID = 16778113.001).

[ISSN] 1078-0432

[Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research

[ISO-abbreviation] Clin. Cancer Res.

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / K01 CA095434; United States / NCI NIH HHS / CA / R01 CA109525; United States / NCI NIH HHS / CA / CA95434

[Publication-type] Journal Article; Research Support, N.I.H., Extramural

[Publication-country] United States

[Chemical-registry-number] EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.1.137 / PIK3CA protein, human

[Other-IDs] NLM/ NIHMS11634; NLM/ PMC1780026

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Preservation of beta-cell function during immune-mediated, B7-1-dependent alpha-cell destruction.

Type 1 diabetes (T1D) is an autoimmune disease in which the pancreatic beta-cells are destroyed in an immune-mediated process.

In one mouse model of T1D, the co-expression of the costimulatory molecule, B7-1, and the pro-inflammatory cytokine, tumor necrosis factor (TNF)-alpha, on the beta-cells leads to massive insulitis and loss of beta-cells, resulting in T1D.

Here, we have investigated whether the specific loss of beta-cells is due to an intrinsic defect in the beta-cells or is a direct consequence of B7-1 expression.

We show that transgenic mice expressing TNF-alpha on the beta-cells and B7-1 on the alpha-cells are resistant to the development of diabetes despite B7-1-dependent loss of alpha-cells and a massive islet inflammation consisting of T cells, B cells, macrophages and dendritic cells.

Furthermore, islets with alpha-cell expression of B7-1 develop alpha-cell destruction and heavy infiltration, but maintain functional beta-cells when they are engrafted into diabetic mice that co-express TNF-alpha and B7-1 on the beta-cells.

Thus, our results show that the beta-cells are able to survive in a severely inflamed organ where the neighboring alpha-cells are destroyed, suggesting that in this model B7-1 expression on the target cells is the primary determinant for the loss of islet cells.

[MeSH-major] Antigens, CD80 / immunology. Cell Death / immunology. Diabetes Mellitus, Type 1 / immunology. Islets of Langerhans / immunology. Tumor Necrosis Factor-alpha / immunology

[MeSH-minor] Animals. Crosses, Genetic. Glucagon / immunology. Glucagon-Like Peptide 1. Immunohistochemistry. Insulin / immunology. Islets of Langerhans Transplantation. Mice. Mice, Inbred C57BL. Mice, Transgenic. Peptide Fragments / immunology. Protein Precursors / immunology. Reverse Transcriptase Polymerase Chain Reaction. Statistics, Nonparametric

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(PMID = 16078275.001).

[ISSN] 0014-2980

[Journal-full-title] European journal of immunology

[ISO-abbreviation] Eur. J. Immunol.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Germany

[Chemical-registry-number] 0 / Antigens, CD80; 0 / Insulin; 0 / Peptide Fragments; 0 / Protein Precursors; 0 / Tumor Necrosis Factor-alpha; 89750-14-1 / Glucagon-Like Peptide 1; 9007-92-5 / Glucagon

   

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[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

   

[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

   

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Epithelial Protein Lost in Neoplasm alpha (Eplin-alpha) is transcriptionally regulated by G-actin and MAL/MRTF coactivators.

Epithelial Protein Lost in Neoplasm alpha is a novel cytoskeleton-associated tumor suppressor whose expression inversely correlates with cell growth, motility, invasion and cancer mortality.

Here we show that Eplin-alpha transcription is regulated by actin-MAL-SRF signalling.

In a transcriptome analysis with a combination of actin binding drugs which specifically and differentially interfere with the actin-MAL complex (Descot et al., 2009), we identified Eplin to be primarily controlled by monomeric actin.

Further analysis revealed that induction of the Eplin-alpha mRNA and its promoter was sensitive to drugs and mutant actins which stabilise the repressive actin-MAL complex.

Knockdown of MRTFs or dominant negative MAL which inhibits SRF-mediated transcription impaired Eplin-alpha expression.

Conversely, constitutively active mutant actins and MAL induced Eplin-alpha.

MAL and SRF were bound to a consensus SRF binding site of the Eplin-alpha promoter; the recruitment of MAL to this region was enhanced severalfold upon induction.

The tumor suppressor Eplin-alpha is thus a novel cytoskeletal target gene transcriptionally regulated by the actin-MAL-SRF pathway, which supports a role in cancer biology.

[MeSH-minor] Animals. Mice. Mutation / genetics. NIH 3T3 Cells. Promoter Regions, Genetic / genetics. Protein Binding. Serum Response Factor / metabolism. Signal Transduction

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(PMID = 20236507.001).

[ISSN] 1476-4598

[Journal-full-title] Molecular cancer

[ISO-abbreviation] Mol. Cancer

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / Actins; 0 / Cytoskeletal Proteins; 0 / D15Ertd366e protein, mouse; 0 / MKL1 protein, mouse; 0 / Serum Response Factor; 0 / Trans-Activators

[Other-IDs] NLM/ PMC2848193

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] PIK3CA, KRAS, and BRAF mutations in intraductal papillary mucinous neoplasm/carcinoma (IPMN/C) of the pancreas.

BACKGROUND AND AIMS: Recent studies have reported high frequencies of somatic mutations in the phosphoinositide-3-kinase catalytic-alpha (PIK3CA) gene in various human tumors.

The Raf/MEK/ERK (mitogen-activated protein kinase) signal transduction is an important mediator of a number of cellular fates including growth, proliferation, and survival.

The BRAF gene is activated by oncogenic RAS, leading to cooperative effects in cells responding to growth factor signals.

Here we evaluate the mutational status of PIK3CA, KRAS, and BRAF in intraductal papillary mucinous neoplasm/carcinoma (IPMN/IPMNC) of the pancreas.

RESULTS: We identified four somatic missense mutations of PIK3CA within the 36 IPMN/IPMC specimens (11%).

CONCLUSION: This data is the first report of PIK3CA mutation in pancreatic cancer and it appears to be the first oncogene to be mutated in IPMN/IPMC but not in conventional ductal adenocarcinoma of the pancreas.

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(PMID = 18343945.001).

[ISSN] 1435-2451

[Journal-full-title] Langenbeck's archives of surgery

[ISO-abbreviation] Langenbecks Arch Surg

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / CA095434-05; United States / NCI NIH HHS / CA / R01 CA109525-03; United States / NCI NIH HHS / CA / CA109525-03; United States / NCI NIH HHS / CA / CA109525-04; United States / NCI NIH HHS / CA / R01 CA109525; United States / NCI NIH HHS / CA / R01 CA109525-04; United States / NCI NIH HHS / CA / K01 CA095434; United States / NCI NIH HHS / CA / K01 CA095434-05

[Publication-type] Journal Article

[Publication-country] Germany

[Other-IDs] NLM/ NIHMS235132; NLM/ PMC3915028

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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

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[Copyright] Copyright 2010 AGA Institute. Published by Elsevier Inc. All rights reserved.

(PMID = 20138042.001).

[ISSN] 1528-0012

[Journal-full-title] Gastroenterology

[ISO-abbreviation] Gastroenterology

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Biomarkers; 0 / Insulin; 0 / Men1 protein, mouse; 0 / Proto-Oncogene Proteins; 0 / Transcription Factors; 9007-92-5 / Glucagon

   

[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

   

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Effect of caffeine treatment on low-dose γ- irradiation-induced chromatid-type aberrations in human leukemia cells and human normal fibroblast cells in culture.

We investigated the effects of caffeine on low dose- gamma-radiation-induced chromosomal damage in human T leukemia cells (Jurket T-cells) and two normal human fibroblast cell lines (AG1522 and GM 2149).

METHOD: Jurkat cells were maintained in RPMI 1640 medium and fibroblast in alpha-minimal essential medium (MEM) All cells were incubated at 37o C in a humidified atmosphere of 5% CO2 in air.

Cells from the exponential phase were treated with 1 mg/ml caffeine ( control cells received same amount of solvent) and irradiated with low doses (3, 5, 10, 20 and 40 cGy,), using a 137 Cs-gamma radiation source.

Cells were fixed in methanol: acetic acid solution and stained with Giemsa.

100 irradiated and un-irradiated metaphase- like cells were scored for chromatid-type aberrations.

RESULTS: Low dose gamma-radiation increased the levels of chromatid breaks(dose dependent) in both normal and cancer cells; however, cancer cells appeared to be more sensitive than the normal cells.

Caffeine treatment markedly increased chromatid aberrations in Jurkat T-cells at all radiation doses but not in normal cells.

Previously, we reported that caffeine eliminates gamma-ray-induced G2 delay in other human tumor cells but not normal cells (Jha, et.al., Radiat. Res.

CONCLUSIONS: The mechanisms that may underlie this differential effect of caffeine in cancer and normal cells are unknown, but if one result of a G2 delay is to allow more time for chromosome breakage rejoining processes to occur, then elimination of this delay by caffeine in tumor cells but not normal cells might account for the difference.

To the extent these observations are generally true for tumor vs normal cells, the differential sensitization could have an impact in improving the efficacy of radiation therapy.

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(PMID = 27963510.001).

[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

   

[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

   

[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^Ser473, 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

   

[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_hCG-AFP, 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_hCG-AFP) and to test its prognostic value.

Survival univariate and multivariate analyses tested the prognostic value of AUC_hCG-AFP regarding PFS.

RESULTS: Mono-exponential models best fitted AFP and hCG decreases: C_AFP (t) = 381*e ^{- 0.14 *t} +3.27 and C_hCG (t) = 1230*e - ^{0.25 *t} +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

   

[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

   

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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

   

[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

   

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] A phase II study of early up-front red blood cell transfusion followed by maintenance epoetin-alpha subcutaneously support during chemotherapy.

: e20719 Background: To determine in patients with cancer related anaemia (Hb<11,3 g/d) starting with their chemotherapy the efficacy and safety of up-front red blood cell transfusion and subsequently maintenance epoetin-alpha (Epo) administration.

The study target was the range of low-normal Hb levels of 11,3 to 12,9 g/dL aiming at improving tumor oxygenation.

RESULTS: 18 Patients enrolled in this study from March 30, 2006 to November 11, 2008.

An intention-to-treatment analysis was performed for the primary objectives in 16 patients (8 with breast-, 4 with colorectal-, 1 with ovarian- and 1 with pancreatic cancer) and reported here.

Grade 3/4 adverse events and serious adverse events that occurred were found to be all chemotherapy or progressive disease related.

This was presumably related to the lesser than projected yield of the red blood cell transfusion.

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(PMID = 27962027.001).

[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

   

[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/m² (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

   

[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

   

[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

   

[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

   

[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

   

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] A phase I trial of tumor-associated antigen-pulsed dendritic cell immunotherapy for patients with brain stem glioma and glioblastoma.

: 2032 Background: Previous immunotherapy trials for malignant glioma (Yu, J.,et al, Cancer Res.

2001;61:842-7 and 2004;64;4973-9) have demonstrated efficacy in generating a tumor specific immune response.

METHODS: The goal of this study is to use tumor associated antigens (TAA) known to be expressed on gliomas and pulse dendritic cells with these antigens in an MHC compatible fashion using epitopes of HER-2, TRP-2, gp100, MAGE-1, IL13R alpha, and AIM-3.

Leukapheresis was used to isolate mononuclear cells which were differentiated into dendritic cells in culture, pulsed with tumor peptide, and then administered intradermally three times at 2-week intervals.

RESULTS: Twenty patients, 15 males and five females, were enrolled between November 2006 and December 2008 with one screen failure.

Our data on 19 patients and 54 courses of dendritic cell vaccines demonstrate zero grade 3 /4 toxicities that were attributable to the vaccination.

Thirteen patients continue to have stable disease (ranging from 15 to 115 weeks), six patients have demonstrated tumor progression.

Of 15 patients tested to date, six patients demonstrated an antigen-specific cytotoxic T-cell response to at least one antigen after vaccination.

Only 17% of CTL responders (1/6) demonstrated tumor progression compared to 56% (5/9) of nonresponders to date.

CONCLUSIONS: This phase I study demonstrated the feasibility, safety, and bioactivity of a TAA-pulsed dendritic cell vaccine for patients with glioblastoma progression free survival correlated with CTL response.

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(PMID = 27964632.001).

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Impact of positron emission tomography (PET) in stage III non-small cell lung cancer (NSCLC): A prospective randomized trial (PET START).

The use of PET-CT rather than conventional imaging (CI) may better identify patients for CMT by enhanced tumor staging and improved definition of RT treatment volumes.

The primary outcome was the proportion of patients who did not receive CMT because their tumor was upstaged to Stage 4 or their intrathoracic tumor was too extensive for radical RT.

Target sample size was 400 patients based on a hazard rate reduction of 30% in OS at 2 years in favor of PET-CT with 2-sided alpha = 0.05 and 80% power.

RESULTS: The trial commenced in August 2004.

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(PMID = 27963324.001).

[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

   

[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

   

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Leiomyomatoid angiomatous neuroendocrine tumor (LANT) of the pituitary: a distinctive biphasic neoplasm with primitive secretory phenotype and smooth muscle-rich stroma.

We describe a hitherto undocumented variant of dimorphic pituitary neoplasm composed of an admixture of neurosecretory cells and profuse leiomyomatous stroma around intratumoral vessels.

Radiologically perceived as a macroadenoma of 3.8 cm in diameter, this pituitary mass developed in an otherwise healthy 43-year-old female.

At the term of a yearlong history of amenorrhea and progressive bitemporal visual loss, subtotal resection was performed via transsphenoidal microsurgery.

Histologically, solid sheets, nests and cords of epithelial-looking, yet cytokeratin-negative cells were seen growing in a richly vascularized stroma of spindle cells.

Staining for S100 protein and GFAP, characteristics of sustentacular cells, as well as bcl-2 and c-kit was absent.

Except for alpha-subunit, anterior pituitary hormones tested negative in tumor cells, as did a panel of peripheral endocrine markers, including serotonin, somatostatin, calcitonin, parathormone and vasoactive intestinal polypeptide.

While assignment of this lesion to any established neoplastic entity is not forthcoming, we propose it is being considered as a low-grade neuroendocrine tumor possibly related to null cell adenoma.

[MeSH-major] Neuroendocrine Tumors / pathology. Pituitary Neoplasms / pathology. Stromal Cells / pathology

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(PMID = 16520966.001).

[ISSN] 0001-6322

[Journal-full-title] Acta neuropathologica

[ISO-abbreviation] Acta Neuropathol.

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] Germany

[Chemical-registry-number] 0 / Actins; 0 / Vimentin

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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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MedlinePlus Health Information. consumer health - Pituitary Tumors.

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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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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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Genetic Alliance. consumer health - Myoepithelial carcinoma.

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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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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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(PMID = 16362349.001).

[ISSN] 0009-4722

[Journal-full-title] Der Chirurg; Zeitschrift für alle Gebiete der operativen Medizen

[ISO-abbreviation] Chirurg

[Language] ger

[Publication-type] Case Reports; Comparative Study; English Abstract; Journal Article

[Publication-country] Germany

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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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[Cites] Acta Oncol. 1998;37(6):567-74 [9860315.001]

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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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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

   

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

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

   

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

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