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1.
Arch Pathol Lab Med ; 137(8): 1117-28, 2013 Aug.
Article in English | MEDLINE | ID: mdl-23899070

ABSTRACT

CONTEXT: Myofibroblastic proliferations of the urinary bladder, which share some similarities with nodular fasciitis, were first reported in 1980. Since then, they have had several designations, the most frequently used being inflammatory myofibroblastic tumor. Based on both histopathologic and prognostic grounds, some authors prefer the term pseudosarcomatous myofibroblastic proliferation, at least for some of the proliferations. These same scientists also assimilate the so-called postoperative spindle cell nodules with the pseudosarcomatous myofibroblastic proliferations. Little is known about these low-grade myofibroblastic proliferations. OBJECTIVES: To review the literature about low-grade myofibroblastic proliferations occurring in the urinary bladder. DATA SOURCES: Textbooks and literature review. We obtained most of the clinicopathologic peculiarities from a patient population composed of the most-relevant, previously reported cases. CONCLUSIONS: The low-grade myofibroblastic proliferations of the urinary bladder are rare lesions affecting males more often than they do females. The most-common signs and symptoms are hematuria and dysuria. Histopathologically, they are spindle cell proliferations in a loose myxoid stroma, even though compact proliferations or hypocellular fibrous patterns can be found. Immunohistochemistry is quite nonspecific, except for ALK-1 positivity (20%-89%). Fluorescence in situ hybridization has demonstrated clonal genetic aberrations involving the ALK gene in 50% to 60% of cases. After surgery, only 6% of patients experience local recurrence, without metastases or deaths from the disease. Malignant transformation has been reported exceptionally. These myofibroblastic proliferations are probably part of a continuum with, at one end, benign pseudosarcomatous proliferations and, at the opposite end, more-aggressive lesions. Because of the frequently indolent clinical course, aggressive treatment would be unjustified.


Subject(s)
Myofibroblasts/pathology , Urinary Bladder/pathology , Anaplastic Lymphoma Kinase , Cell Proliferation , Female , Humans , Immunohistochemistry , Inflammation/metabolism , Inflammation/pathology , Male , Myofibroblasts/metabolism , Neoplasms, Muscle Tissue/enzymology , Neoplasms, Muscle Tissue/genetics , Neoplasms, Muscle Tissue/pathology , Receptor Protein-Tyrosine Kinases/genetics , Receptor Protein-Tyrosine Kinases/metabolism , Urinary Bladder/metabolism , Urinary Bladder Neoplasms/enzymology , Urinary Bladder Neoplasms/genetics , Urinary Bladder Neoplasms/pathology
2.
Nephrol Dial Transplant ; 27(10): 3875-84, 2012 Oct.
Article in English | MEDLINE | ID: mdl-23114905

ABSTRACT

BACKGROUND: Idiopathic retroperitoneal fibrosis (IRF) is a rare fibro-inflammatory disorder characterized by a periaortic tissue which often encases the ureters causing acute renal failure. IRF histology shows fibrosis and a chronic inflammatory infiltrate with frequent tissue eosinophilia. We assessed a panel of molecules promoting eosinophilia and fibrosis in IRF patients and performed an immunogenetic study. METHODS: Serum levels of eotaxin/CCL11, regulated and normal T-cell expressed and secreted (RANTES), granulocyte colony-stimulating factor (G-CSF), interleukin (IL)-5, platelet-derived growth factor (PDGF) and fibroblast growth factor (FGF) were measured using a multiplex assay in 24 newly diagnosed, untreated IRF patients and 14 healthy controls. Retroperitoneal biopsies (available in 8/24 patients) were histologically evaluated to assess eosinophil infiltration, whereas mast cells (MCs) were identified by immunohistochemical analysis for human tryptase. Immunohistochemistry for eotaxin/CCL11 and its receptor CCR3 was also performed. Six single nucleotide polymorphisms (SNPs) within the CCL11 gene (rs6505403, rs1860184, rs4795896, rs17735961, rs16969415 and rs17809012) were investigated in 142 IRF patients and 214 healthy controls. RESULTS: Serum levels of eotaxin/CCL11 were higher in IRF patients than in controls (P = 0.009). Eotaxin/CCL11 drives tissue infiltration of eosinophils and MCs, which can promote fibrosis. Eosinophilic infiltration was prominent (>5 cells/hpf) in five (62.5%) cases, and abundant tryptase-positive MCs were found in all cases; notably, MCs were in a degranulating state. Immunohistochemistry showed that CCL11 was highly produced by infiltrating mononuclear cells and that its receptor CCR3 was expressed by infiltrating eosinophils, MCs, lymphocytes and fibroblasts. None of the tested CCL11 SNPs showed disease association, but the TTCCAT haplotype was significantly associated with IRF (P = 0.0005). CONCLUSIONS: These findings suggest that the eotaxin/CCL11-CCR3 axis is active in IRF and may contribute to its pathogenesis; the TTCCAT haplotype within the CCL11 gene is significantly associated with IRF.


Subject(s)
Chemokine CCL11/metabolism , Retroperitoneal Fibrosis/immunology , Becaplermin , Case-Control Studies , Chemokine CCL11/blood , Chemokine CCL11/genetics , Chemokine CCL5/blood , Eosinophils/pathology , Female , Fibroblast Growth Factor 2/blood , Genetic Association Studies , Granulocyte Colony-Stimulating Factor/blood , Haplotypes , Humans , Immunogenetic Phenomena , Interleukin-5/blood , Male , Mast Cells/pathology , Middle Aged , Polymorphism, Single Nucleotide , Proto-Oncogene Proteins c-sis/blood , Receptors, CCR3/metabolism , Retroperitoneal Fibrosis/genetics , Retroperitoneal Fibrosis/pathology
3.
Pathol Oncol Res ; 18(1): 101-6, 2012 Jan.
Article in English | MEDLINE | ID: mdl-21197591

ABSTRACT

The epithelioid variant of malignant peripheral nerve sheath tumours (MPNSTs) is a very rare malignancy. We describe the case of a 30-year-old man complaining of acute pain in his right elbow, mild distal paraesthesias, and some motor deficiencies. He was discovered as having a small fusiform swelling of the median nerve. In view of its very small size, shape, and nonspecific MRI signal, it had initially suggested a benign lesion. The diagnosis of epithelioid MPNST was made only at the histopathological examination. This malignant neoplasm recurred locally fourteen months after surgery. In addition to describe the above very rare case, we have reviewed the literature on epithelioid MPNSTs clearly involving deep major nerve trunks. This case serves as a warning that, even in major nerve trunks, tiny lesions may in reality be early intraneural MPNSTs which, due to their deep location, must be treated adequately with wide margin surgery since the resection margin status represents one of the major parameters influencing the local control of disease and its clinical outcome.


Subject(s)
Nerve Sheath Neoplasms/pathology , Peripheral Nervous System Neoplasms/pathology , Adult , Elbow , Humans , Immunohistochemistry , Magnetic Resonance Imaging , Male , Neoplasm Recurrence, Local/metabolism , Neoplasm Recurrence, Local/pathology , Nerve Sheath Neoplasms/metabolism , Peripheral Nervous System Neoplasms/metabolism
4.
J Cardiovasc Electrophysiol ; 23(3): 271-9, 2012 Mar.
Article in English | MEDLINE | ID: mdl-21954878

ABSTRACT

INTRODUCTION: Atrial fibrillation (AF) in mitral regurgitation (MR) is a complex disease where multiple factors may induce left-atrial structural remodeling (SR). We explored the differential SR of the left-atrial posterior wall (LAPW) of patients affected by MR with or without persistent AF, and the expression of key proteins involved in its pathogenesis. METHODS AND RESULTS: Light microscopy of LAPW samples from 27 patients with MR and persistent AF (group 1), 33 with MR in sinus rhythm (group 2), and 15 autopsy controls (group 3) was used to measure myocyte diameter, percentage of myocytolytic myocytes, interstitial fibrosis, and capillary density; RT-PCR and Western blotting were used to assess the mRNA and protein levels of SOD-1, SOD-2, HO-1, calpain, MMP-2, MMP-9, TIMP-1, TIMP-2, and VEGF; immunofluorescence was used to locate these proteins. Myocyte diameter was similar in groups 1 and 2, but larger than controls. Compared to group 2, group 1 had more myocytolytic myocytes (20.8 ± 5.6% vs 14.7 ± 4.5%; P < 0.0001), increased interstitial fibrosis (10.4 ± 5.1% vs 7.5 ± 4.2%; P < 0.05), and decreased capillary density (923 ± 107 No/mm(2) vs 1,040 ± 100 No/mm(2); P < 0.0001). All of the proteins were more expressed in groups 1 and 2 than in controls. The protein and mRNA levels of SOD-1, SOD-2, MMP-2, and MMP-9 were higher in group 1 than in group 2. CONCLUSIONS: The LAPW of MR patients with or without AF shows considerable SR. The former has more severe histopathological changes and higher levels of proteins involved in SR, thereby reaching a threshold beyond which the sinus impulse cannot normally activate atrial myocardium.


Subject(s)
Atrial Fibrillation/metabolism , Atrial Fibrillation/pathology , Heart Atria/metabolism , Heart Atria/pathology , Mitral Valve Insufficiency/metabolism , Mitral Valve Insufficiency/pathology , Adult , Aged , Aged, 80 and over , Arrhythmia, Sinus/physiopathology , Atrial Fibrillation/complications , Autopsy , Blotting, Western , Calpain/metabolism , DNA, Complementary/biosynthesis , DNA, Complementary/isolation & purification , Female , Fluorescent Antibody Technique , Humans , Immunohistochemistry , Male , Matrix Metalloproteinase 2/metabolism , Microscopy, Confocal , Middle Aged , Mitral Valve Insufficiency/complications , Myocytes, Cardiac/pathology , Platelet Endothelial Cell Adhesion Molecule-1/metabolism , RNA/biosynthesis , RNA/isolation & purification , Real-Time Polymerase Chain Reaction , Superoxide Dismutase/genetics , Superoxide Dismutase-1 , Vascular Endothelial Growth Factor A/metabolism
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