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Gonzague Pinieux - One of the best experts on this subject based on the ideXlab platform.
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Molecular Markers of Fibro-Osseous Lesions and Osteosarcomas of the Craniofacial Complex—Current Situation and Recent Advances
Current Oral Health Reports, 2016Co-Authors: Flore Tabareau-delalande, Gonzague PinieuxAbstract:Fibro-osseous lesions share clinical, radiological, and pathological features, particularly in the craniofacial complex, a location where diagnosing these lesions is challenging. Some molecular markers involved in the pathogenesis of these lesions offer significant diagnostic support. Guanine nucleotide-binding protein/alpha subunit ( GNAS ) mutations are specific to fibrous dysplasias and are not encountered in ossifying Fibromas (including juvenile variants), or in low-grade and high-grade osteosarcomas of the jaw. Low-grade and dedifferentiated osteosarcomas show murine double-minute 2 ( MDM2 ) amplification, with overexpression of MDM2, abnormalities not encountered in fibrous dysplasia, or in ossifying Fibroma. No recurrent cytogenetic or molecular abnormality has been reported to date in conventional ossifying Fibromas. The juvenile variants of ossifying Fibroma exhibit MDM2/ RAS protein activator like-1 ( RASAL1 ) co-amplification, without MDM2 overexpression, abnormalities also observed in certain aggressive osteosarcomas of the jaw, which may derive from juvenile ossifying Fibroma. MDM2/RASAL1 co-amplification may constitute an early molecular marker of aggressive juvenile ossifying Fibroma and may indicate a need for closer follow-up and more radical treatment.
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chromosome 12 long arm rearrangement covering mdm2 and rasal1 is associated with aggressive craniofacial juvenile ossifying Fibroma and extracranial psammomatoid fibro osseous lesions
Modern Pathology, 2015Co-Authors: Flore Tabareaudelalande, Christine Collin, Anne Gomezbrouchet, Corinne Bouvier, Annevalerie Decouvelaere, Anne De Muret, Jeanchristophe Pages, Gonzague PinieuxAbstract:To evaluate the diagnostic value of MDM2 status in craniofacial fibro-osseous lesions, we investigated MDM2 expression by immunohistochemistry and analyzed MDM2 amplification by qPCR in 30 cases of ossifying Fibroma (including 13 cases of the juvenile variant) and 17 cases of fibrous dysplasia. Two cases of uncommon extragnathic psammomatoid fibrous dysplasia and a mixed control group of 15 cases of low-grade osteosarcoma and 15 cases of well-differentiated/dedifferentiated liposarcoma were included. MDM2 amplification was found in 33% of ossifying Fibromas (peak of 69% for the juvenile variant) and in 12% of fibrous dysplasia, in none of which was MDM2 overexpressed. All control cases exhibited MDM2 amplification and overexpression. To investigate possible polysomy of chromosome 12, we studied RASAL1 amplification, a gene telomeric to MDM2 on the long arm of chromosome 12. RASAL1 amplification was reported in all benign fibro-osseous lesions exhibiting MDM2 amplification but not in controls. Simultaneous amplification of these two genes was significantly higher in juvenile ossifying Fibromas compared with fibrous dysplasia (P=0.004), non-juvenile ossifying Fibromas (P=0.001), and all other benign craniofacial fibro-osseous lesions combined (P=0.0001). Of the nine cases of juvenile ossifying Fibroma exhibiting amplification, three were locally invasive and four were recurrent, suggesting aggressive disease. The two cases of extragnathic psammomatoid fibrous dysplasia also showed MDM2 and RASAL1 amplification with no MDM2 overexpression. This large chromosome 12 rearrangement, spanning MDM2 and RASAL1, is the first recurrent molecular abnormality to be reported in juvenile ossifying Fibroma. It may represent both a molecular diagnostic marker and a characteristic of more aggressive forms with a higher risk of recurrence. Finally, the presence of this rearrangement in extragnathic psammomatoid fibro-osseous lesions mimicking ossifying Fibromas might reflect a common molecular pathway in their pathogenesis and calls into question the classification of such lesions within fibrous dysplasia.
Hiroshi Kijima - One of the best experts on this subject based on the ideXlab platform.
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hypoxia is important in f 18 fdg accumulation in thecoma Fibroma tumors on f 18 fdg pet ct scans
Molecular Medicine Reports, 2016Co-Authors: Hiroko Seino, Shuichi Ono, Hiroyuki Miura, Satoko Morohashi, Fumiyasu Tsushima, Yoshihiro Takai, Hiroshi KijimaAbstract:Several studies have noted benign thecoma‑Fibroma tumors with positive F‑18 fluorodeoxyglucose (FDG) accumulation mimicking malignant ovarian tumors following F‑18 FDG positron emission tomography (PET). The present study analyzed four cases with false‑positive F‑18 FDG PET/computed tomography (CT) diagnoses of thecoma‑Fibroma tumors as malignant tumors due to F‑18 FDG accumulation, compared with eight cases of FDG‑positive ovarian cancers and two cases of FDG‑negative Fibromas. Hypoxia inducible factor (HIF)‑1α expression was examined in the six thecoma‑Fibroma tumors using reverse transcription‑polymerase chain reaction (RT‑PCR). The four F‑18 FDG‑positive cases exhibited higher cellularity, maximum standard uptake and signal intensity on T2‑weighted imaging, and gadolinium (Gd) enhancement using magnetic resonance imaging than the two FDG-negative Fibroma cases. In the F‑18 FDG‑positive thecoma‑Fibroma group, Ki‑67 expression was low and LAT1 expression was not identified, ruling out the diagnosis and potential for malignancy. However, considerable glucose transporter 1, HIF‑1α, and vascular endothelial growth factor expression was observed. HIF‑1α expression was elevated in all four false‑positive cases by RT‑PCR. From these results, it was hypothesized that hypoxia due to elevated cellularity may stimulate HIF‑1α expression and be associated with F‑18 FDG accumulation in F‑18‑positive thecoma‑Fibroma tumors.
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Hypoxia is important in F‑18 FDG accumulation in thecoma‑Fibroma tumors on F‑18 FDG PET/CT scans.
Molecular medicine reports, 2016Co-Authors: Hiroko Seino, Shuichi Ono, Hiroyuki Miura, Satoko Morohashi, Fumiyasu Tsushima, Yoshihiro Takai, Hiroshi KijimaAbstract:Several studies have noted benign thecoma‑Fibroma tumors with positive F‑18 fluorodeoxyglucose (FDG) accumulation mimicking malignant ovarian tumors following F‑18 FDG positron emission tomography (PET). The present study analyzed four cases with false‑positive F‑18 FDG PET/computed tomography (CT) diagnoses of thecoma‑Fibroma tumors as malignant tumors due to F‑18 FDG accumulation, compared with eight cases of FDG‑positive ovarian cancers and two cases of FDG‑negative Fibromas. Hypoxia inducible factor (HIF)‑1α expression was examined in the six thecoma‑Fibroma tumors using reverse transcription‑polymerase chain reaction (RT‑PCR). The four F‑18 FDG‑positive cases exhibited higher cellularity, maximum standard uptake and signal intensity on T2‑weighted imaging, and gadolinium (Gd) enhancement using magnetic resonance imaging than the two FDG-negative Fibroma cases. In the F‑18 FDG‑positive thecoma‑Fibroma group, Ki‑67 expression was low and LAT1 expression was not identified, ruling out the diagnosis and potential for malignancy. However, considerable glucose transporter 1, HIF‑1α, and vascular endothelial growth factor expression was observed. HIF‑1α expression was elevated in all four false‑positive cases by RT‑PCR. From these results, it was hypothesized that hypoxia due to elevated cellularity may stimulate HIF‑1α expression and be associated with F‑18 FDG accumulation in F‑18‑positive thecoma‑Fibroma tumors.
Hiroko Seino - One of the best experts on this subject based on the ideXlab platform.
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hypoxia is important in f 18 fdg accumulation in thecoma Fibroma tumors on f 18 fdg pet ct scans
Molecular Medicine Reports, 2016Co-Authors: Hiroko Seino, Shuichi Ono, Hiroyuki Miura, Satoko Morohashi, Fumiyasu Tsushima, Yoshihiro Takai, Hiroshi KijimaAbstract:Several studies have noted benign thecoma‑Fibroma tumors with positive F‑18 fluorodeoxyglucose (FDG) accumulation mimicking malignant ovarian tumors following F‑18 FDG positron emission tomography (PET). The present study analyzed four cases with false‑positive F‑18 FDG PET/computed tomography (CT) diagnoses of thecoma‑Fibroma tumors as malignant tumors due to F‑18 FDG accumulation, compared with eight cases of FDG‑positive ovarian cancers and two cases of FDG‑negative Fibromas. Hypoxia inducible factor (HIF)‑1α expression was examined in the six thecoma‑Fibroma tumors using reverse transcription‑polymerase chain reaction (RT‑PCR). The four F‑18 FDG‑positive cases exhibited higher cellularity, maximum standard uptake and signal intensity on T2‑weighted imaging, and gadolinium (Gd) enhancement using magnetic resonance imaging than the two FDG-negative Fibroma cases. In the F‑18 FDG‑positive thecoma‑Fibroma group, Ki‑67 expression was low and LAT1 expression was not identified, ruling out the diagnosis and potential for malignancy. However, considerable glucose transporter 1, HIF‑1α, and vascular endothelial growth factor expression was observed. HIF‑1α expression was elevated in all four false‑positive cases by RT‑PCR. From these results, it was hypothesized that hypoxia due to elevated cellularity may stimulate HIF‑1α expression and be associated with F‑18 FDG accumulation in F‑18‑positive thecoma‑Fibroma tumors.
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Hypoxia is important in F‑18 FDG accumulation in thecoma‑Fibroma tumors on F‑18 FDG PET/CT scans.
Molecular medicine reports, 2016Co-Authors: Hiroko Seino, Shuichi Ono, Hiroyuki Miura, Satoko Morohashi, Fumiyasu Tsushima, Yoshihiro Takai, Hiroshi KijimaAbstract:Several studies have noted benign thecoma‑Fibroma tumors with positive F‑18 fluorodeoxyglucose (FDG) accumulation mimicking malignant ovarian tumors following F‑18 FDG positron emission tomography (PET). The present study analyzed four cases with false‑positive F‑18 FDG PET/computed tomography (CT) diagnoses of thecoma‑Fibroma tumors as malignant tumors due to F‑18 FDG accumulation, compared with eight cases of FDG‑positive ovarian cancers and two cases of FDG‑negative Fibromas. Hypoxia inducible factor (HIF)‑1α expression was examined in the six thecoma‑Fibroma tumors using reverse transcription‑polymerase chain reaction (RT‑PCR). The four F‑18 FDG‑positive cases exhibited higher cellularity, maximum standard uptake and signal intensity on T2‑weighted imaging, and gadolinium (Gd) enhancement using magnetic resonance imaging than the two FDG-negative Fibroma cases. In the F‑18 FDG‑positive thecoma‑Fibroma group, Ki‑67 expression was low and LAT1 expression was not identified, ruling out the diagnosis and potential for malignancy. However, considerable glucose transporter 1, HIF‑1α, and vascular endothelial growth factor expression was observed. HIF‑1α expression was elevated in all four false‑positive cases by RT‑PCR. From these results, it was hypothesized that hypoxia due to elevated cellularity may stimulate HIF‑1α expression and be associated with F‑18 FDG accumulation in F‑18‑positive thecoma‑Fibroma tumors.
David G Gardner - One of the best experts on this subject based on the ideXlab platform.
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central odontogenic Fibroma current concepts
Journal of Oral Pathology & Medicine, 1996Co-Authors: David G GardnerAbstract:The author reviews current knowledge concerning the central odontogenic Fibroma, which at present in incompletely understood, and reaches the following conclusions. 1) The separation of this lesion into simple and WHO types remains valid because they exhibit different histologic features. However, more care should be taken in rendering the diagnosis of the WHO type than in the past; unlike the simple type, it is a fibroblastic lesion. 2) Complex central odontogenic Fibroma is a more appropriate term than the WHO type because the WHO does not use the latter term in its 1992 manual. 3) The microscopic distinction of simple odontogenic Fibroma from desmoplastic Fibroma remains difficult in some cases. 4) The granular cell odontogenic tumor, which has sometimes been referred to as a type of odontogenic Fibroma, is a separate entity, although some simple odontogenic Fibromas exhibit scattered granular cells. 5) The separation of lesions that have been reported recently as odontogenic Fibromas with giant cell reactions from central giant cell granulomas that exhibit foci of odontogenic epithelium requires further study.
Vikram Deshpande - One of the best experts on this subject based on the ideXlab platform.
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Fibroma like pecoma a tuberous sclerosis complex related lesion
The American Journal of Surgical Pathology, 2018Co-Authors: Ana B Larque, Richard L Kradin, Ivan Chebib, Petur G Nielsen, Martin K Selig, Elizabeth A Thiele, Anat Stemmerrachamimov, Miriam A Bredella, Pawel Kurzawa, Vikram DeshpandeAbstract:Perivascular epithelioid cell tumor (PEComa), mesenchymal tumors morphologically characterized by epithelioid cells, coexpress melanocytic and muscle markers. Herein, we describe a heretofore-undescribed tuberous sclerosis complex (TSC)-related neoplasm, morphologically resembling a soft tissue Fibroma-like lesion, but showing an immunophenotype resembling PEComa. We identified 3 soft tissue Fibroma-like lesions in individuals with TSC. We also evaluated 6 TSC-related periungual Fibroma as well as a range of non-TSC Fibroma-like lesions (n=19). Immunohistochemistry for HMB-45, desmin, smooth muscle actin, TFE3, and S100 was performed on the TSC-related Fibromas. Periungual Fibromas and non-TSC Fibroma-like lesions were also stained for HMB-45. All 3 TSC patients were female, ranging in age from 4 to 51 years (mean, 26.7 y). Two tumors were located in extremities and 1 on the chest wall. The tumors showed elongated to stellate spindle-shape cells, prominent collagenous background, and lacked mitotic activity and cytologic atypia. Immunohistochemically, all 3 tumors were positive for HMB-45; smooth muscle actin or desmin was positive in both tumors tested. TFE3 was negative. All patients were alive with no evidence of disease with median follow-up of 55 months (range, 6 to 131 mo). Non-TSC Fibroma-like lesions and oral and periungual Fibromas were negative for HMB-45. Fibroma-like PEComa, a newly recognized soft tissue tumor with a strong association with TSC, mimics soft tissue Fibroma but shows reactivity with melanocytic markers.