Michele Gassen Kellermann
State University of Campinas
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Featured researches published by Michele Gassen Kellermann.
Histopathology | 2007
Michele Gassen Kellermann; Lays M. Sobral; S. D. Da Silva; Karina G. Zecchin; Edgard Graner; M.A. Lopes; Inês Nobuko Nishimoto; L.P. Kowalski; Ricardo D. Coletta
with lupus panniculitis. The core biopsy specimen, taken from the recurrent mass in 2003, demonstrated lymphoplasmacytic infiltrates similar to those seen in the previous excision specimen. Surgical intervention was deemed unnecessary and a conservative approach was employed. Lupus mastitis is a rare presentation of lupus profundus, usually following the clinical manifestations of SLE or chronic discoid lupus erythematosus (DLE). In some cases involvement of the fat precedes SLE for months. To our knowledge, only about 16 cases of lupus mastitis have been reported, occurring mainly in association with chronic DLE. The typical presentation of the elementary lesion is a deep subcutaneous nodule or swelling. The overlying skin can be normal or show typical features of discoid lupus. In the breast, fat necrosis commonly mimics malignancy clinically. A history of trauma is absent in most cases at this site. However, fat necrosis caused by trauma is common in the breast and differs from lupus profundus, as the latter process is centred around blood vessels and connective tissue, associated with heavy perivascular and periadnexal lymphocytic infiltrates and hyaline sclerosis of the dermal collagen. It is this feature which is responsible for the hard ‘carcinoma’like feel to lupus mastitis and its dense opacity on mammography. Fat necrosis in the breast is seen in other connective tissue disorders and relevant clinical information is essential when lupus profundus presents at this site. Our case illustrates the importance of providing relevant clinical information to histopathologists to make a diagnosis of lupus mastitis. Lupus mastitis should be suspected in a patient with SLE presenting with a recurrent painful mass in the breast. Equally, acknowledging the increased incidence of breast carcinoma in SLE patients and thus obtaining biopsy confirmation is essential. Lymphocytic vasculitis, sclerosis and hyaline panniculitis in the biopsy specimen would confirm the diagnosis of lupus mastitis and avoid unnecessary excisions which, in these patients, have been reported to lead to atrophic scarring or chronic ulcers. E Nigar K Contractor H Singhal R N Matin Departments of Pathology and Surgery and Dermatology, Northwick Park Hospital, North West London Hospitals NHS Trust, Harrow, UK 1. Irgang S. Lupus erythematosus profundus: report of an example with clinical resemblance to Darier-Roussy sarcoid. Arch. Derm. Syphilol. 1940; 42; 97–108. 2. Holland NW, McKnight K, Challa VR, Agudelo CA. Lupus panniculitis (profundus) involving the breast: report of two cases and review of the literature. J. Rheumatol. 1995; 22; 344–346. 3. Georgian-Smith D, Lawton TJ, Moe RE, Couser WG. Lupus mastitis: radiologic and pathologic features. AJR Am. J. Roentgenol. 2002; 178; 1233–1235. 4. Cernea SS, Kihara M, Sotto MN, Vilela Ma. Lupus mastitis. J. Am. Acad. Dermatol. 1993; 29; 343–346. 5. De Bandt M, Meyer O, Grossin M, Khan MF. Lupus mastitis heralding systemic lupus erythematosus with antiphospholipid syndrome. J. Rheumatol. 1993; 20; 1217–1220. 6. Ujiie H, Shimizu T, Ito M, Arita K, Shimizu H. Lupus erythematosus profundus successfully treated with dapsone: review of the literature. Arch. Dermatol. 2006; 142; 399–401. 7. Cerveira I, Costa Matos L, Garrido A et al. Lupus mastitis. Breast 2006; 15; 670–672. 8. Bernatsky S, Ramsey-Goldman R, Boivin JF et al. Do traditional Gail model risk factors account for increased breast cancer in women with lupus? J. Rheumatol. 2003; 30; 1505–1507.
International Journal of Pediatric Otorhinolaryngology | 2008
Michelle Agostini; Jorge Esquiche León; Michele Gassen Kellermann; Renato Valiati; Edgard Graner; Oslei Paes de Almeida
We report the case of a 4-month-old Caucasian male baby who presented an uncommon mass in the anterior mandibular ridge. The patient was born with two natal mandibular incisors, which exfoliated some weeks after birth, followed by a growth of nodular lesion in the same region. Based on the clinical and histopathological features, the diagnosis was of myxoid calcified hamartoma. Immunohistochemical and scanning electron microscopic analysis of the lesion were performed. Hamartomas in the mandibular ridges associated with natal teeth are rare, but they must be considered in the differential diagnosis of common lesions, such as congenital granular cell epulis.
Brazilian Oral Research | 2010
Lays M. Sobral; Michele Gassen Kellermann; Edgard Graner; Hercílio Martelli-Júnior; Ricardo D. Coletta
Cyclosporin A (CyA) induces gingival overgrowth via its stimulatory effects on expression of transforming growth factor-beta1 (TGF-beta1) and collagen. It is not known whether CyA has a direct effect on gingival fibroblasts or induces its effect indirectly via stimulation of myofibroblast transdifferentiation. The present study was undertaken to examine the in vivo and in vitro effect of CyA on myofibroblast transdifferentiation. Rats were treated for 60 days with a daily subcutaneous injection of CyA, and the gingival overgrowth tissue was analyzed by immunohistochemistry. In vitro, fibroblasts from normal gingiva (NG) were cultured in the presence of different concentrations of CyA, and subjected to semi-quantitative reverse transcriptase-polymerase chain reaction and western blot. Although CyA treatment stimulated TGF-beta1 expression by NG fibroblasts, it lacked to induce expression and production of isoform alpha of smooth muscle actin (alpha-SMA), the specific myofibroblast marker. The expression levels of connective tissue growth factor (CTGF), which has been considered a key molecule to promote the transdifferentiation of myofibroblasts via TGF-beta1 activation, were unaffected by CyA. Our results demonstrate that CyA-induced gingival overgrowth is not associated with activation of myofibroblast transdifferentiation, since CyA is not capable to increase CTGF expression.
Oral Oncology | 2008
Michele Gassen Kellermann; Lays M. Sobral; Sabrina D. Silva; Karina G. Zecchin; Edgard Graner; Márcio Ajudarte Lopes; L.P. Kowalski; Ricardo D. Coletta
Journal of Clinical Periodontology | 2006
Carolina C. Bitu; Lays M. Sobral; Michele Gassen Kellermann; Hercílio Martelli-Júnior; Karina G. Zecchin; Edgard Graner; Ricardo D. Coletta
Leukemia & Lymphoma | 2012
Renato Nicolás Hopp; Mateus Terribile Marchi; Michele Gassen Kellermann; Victor H. T. Rizo; Márcio Ajudarte Lopes; Jacks Jorge
Oral Surgery, Oral Medicine, Oral Pathology, and Oral Radiology | 2018
Bárbara Soldatelli Ballardin; Mariana Mahler Rost; Michele Gassen Kellermann; Danieli Rosane Dallemole; Joel Henrique Ellwanger; Leo Krather Neto
Oral Surgery, Oral Medicine, Oral Pathology, and Oral Radiology | 2018
Michele Gassen Kellermann; Bárbara Soldatelli Ballardin; Jane Dagmar Pollo Renner; Danieli Rosane Dallemole; Joel Henrique Ellwanger; Leo Kraether Neto
Oral Surgery, Oral Medicine, Oral Pathology, and Oral Radiology | 2018
Bárbara Soldatelli Ballardin; Michele Gassen Kellermann; Danieli Rosane Dallemole; Joel Henrique Ellwanger; Leo Kraether Neto
Oral Surgery, Oral Medicine, Oral Pathology, and Oral Radiology | 2017
Diana Maria Pigatto Cocco; Bárbara Soldatelli Ballardin; Joel Henrique Ellwanger; Michele Gassen Kellermann; Leo Kraether Neto