Rafael Torres Neto e Renée Laufer Amorim participaram do Encontro anual do American College of Veterinary Pathology (ACVP) em Seattle, Washington, EUA em Dezembro de 2012.
Além das palestras e apresentação de trabalhos, nossos patologistas participaram de Workshops sobre Patologia Reprodutiva (C.L. Davis Foundation Workshop, Birds Do It...Bees Do It.... A Primer on Diagnostic Reproductive) ministradas por pesquisadores renomados da área (Sarah L. Hale, Robert Foster, Dalen W. Agnew, Dianne Creasy) e sobre Imuno-Histoquímica (Immunohistochemistry in Canine and Feline Cancer Diagnosis and Prognosis) com o Professor Matti Kiupel.
Resumos dos Trabalhos apresentados
Torres Neto, R, Laufer Amorim, R, Ferioli, RB, Fonseca-Alves, CE Malagoli, R, Rogatto, SR. EXPRESSION OF IGF-1, M-TOR, SCFAND C-KIT RECEPTOR IN CANINE CUTANEOUS MAST CELL TUMORS IN TISSUE MICROARRAY SLIDES. Wecarried out thestudyevaluatingtheproteinexpressionof SCF, IGF-1, m-TORand c-KIT by immunohistochemical technique in canine cutaneous mast cell tumor (MTC) searching new prognostic factors. We analyzed the relationships between these four proteins with prognostic factors such as histological grade, mitotic index, cell proliferation (Ki67 index), as well as epidemiological data such as age, gender, animal size and location of the mass. 133 samples of MTC were used in a tissue microarray. Statistical association was observed between SCF protein expression and histological grade according to Kiupel et al. (2011), mitotic index, cell proliferation by (Ki-67 index), Iesion location, age, c-KIT pattern and IGF-1. IGF-1 expression was related to mitotic index, the animal size and them-TOR expression. The SCF expression was related to the cytoplasmic c-KIT pattern. The association between the IGF-1 expression and the animal size was observed, and seems to interact withm-TOR co-expression. We can conclude that IGF-1, m-TOR, SCF and c-KIT proteins interacts on the development of canine MTCs, and large and giant-sized animals show higher expression of IGF-1, confirming increased incidence of MTCs on these animals.
Laufer Amorim, R, Busso, A.F, Silveira, S.M, Fonseca-Alves, C.E, Rodrigues, M.M.P, Rogatto, S.R. GENOMIC COPY NUMBER VARIATION IN PROLIFERATIVE, PRE NEOPLASTIC AND NEOPLASTIC PROSTATE LESIONS OF THE DOG.
The dog can spontaneously develop prostate cancer and consequently can be used as an experimental model for prostatic diseases associated with aging, including benign prostate hyperplasia (BPH) and prostate carcinoma (PCa). DNA copy number variations (CNVs) have been used to identify genes associated with cancer development and progression. DNA microarray based comparative genomic hybridization (aCGH) is a technique that allows to identify copy number of thousands of genes throughout the genome. aCGH was used to identify genomic regions with significantly different DNA copy number in three benign prostatic hyperplasia (BPH), four proliferative inflammatory atrophy (PIA), and 14 canine prostate carcinoma (PCa). Five histologically normal prostate tissue were used as reference. Genomic DNA was extracted from formalin fixed and paraffin embedded samples and CNVs data was evaluated in Canine Genome CGH Microarray 4x44K (G2519F, Design ID021193, Agilent). Data analysis was performed using Genomic Workbench Standard Edition 5.0.14 (Agilent). PCa showed higher number of altered genes related to canonical diseases process, cellular functions and molecular pathways as well as greater inter-relationship between genes, compared with PIA and BPH. In conclusion, PCashowed a more complex genotype, be in glosses the most frequent genomic changes. Some discrepancies between genomic alterations in human and canine carcinomas may indicate the different clinical behavior of these tumors in these two species. In addition, it was observed was an ascending pattern of genomic complexity in BPH, PIA and CA consistent with a model of multistep tumor progression.
Laufer Amorim, R, Fonseca-Alves, C.E, Rodrigues, MMP, De Moura, VMBD, Rogatto, S.R. IMMUNOHISTOCHEMICAL EVALUATION OF C-MYC, NKX3.1 AND E-CADHERIN IN CANINE PROSTATIC LESIONS.
The dog is the only species besides humans that develop spontaneous and naturally prostate cancer (PCa). PCa in men presents C-MYC oncogene mutation and reduced CDH1 and NKX3.1protein expression. In this context our objective was to evaluate NKX3, C-MYC and E-cadherin expression in hyperplastic (BPH), pre-neoplastic (prostatic inflammatory atrophy – PIA) and neoplastic prostatic lesions in dogs and verify the role of these proteins in the progression to prostate cancer. A tissue microarray slide was constructed and immunohistochemistry with antibodies C-MYC, NKX3.1, E-cadherin and p63 was performed. Chi-squareor Fisher exact test were used to determine the association between the categorical variables. The evaluation of the C-MYC oncogene showed higher cytoplasmic positivity in PCa and PIA compared to BPH (p= 0.0068). We observed a decrease of NKX3.1 expression in 94.75% of PCa, 100% of PIA and 18.50% of BPH (p=0.0022). Immunohistochemistry p63 positive basal cells were more frequent in PCa and PIA when compared to BPH (p=0.0002). E-cadherin expression was higher in BPH and PIA in comparison to PCa, with no statistical difference.The carcinogenesis process of canine prostatic lesion may be related to basal cells proliferation, gain of C-MYC andlossof NKX3.1.
Apoio: Fapesp
