ABSTRACT
Phosphatase and tensin homolog (PTEN) belongs to the group of gatekeeper tumor suppressor genes and is involved in multiple mechanisms leading to cellular defense against neoplastic transformation and progression. Twenty-four dogs and 17 cats were submitted to a 2-year follow-up study, and clinicopathologic features were recorded and compared with immunohistochemical PTEN staining. PTEN-negative status occurred in 33% of canine and 76% of feline mammary carcinomas. In canine mammary carcinomas, there was a significant (P < .05) correlation between loss of PTEN protein expression and simple carcinoma histotype, lymphatic vessel invasion, lymph node metastases, distant organ metastases, tumor dedifferentiation, tumor recurrence, and shorter overall survival. In feline mammary tumors, a significant correlation between loss of PTEN protein expression and lymphatic vessel invasion was found. Loss of PTEN expression could be a useful prognostic marker in canine mammary carcinomas.
Subject(s)
Carcinoma/veterinary , Cat Diseases/metabolism , Dog Diseases/metabolism , Mammary Neoplasms, Animal/metabolism , PTEN Phosphohydrolase/metabolism , Animals , Carcinoma/metabolism , Carcinoma/pathology , Cat Diseases/pathology , Cats , Dog Diseases/pathology , Dogs , Female , Follow-Up Studies , Immunohistochemistry/veterinary , Kaplan-Meier Estimate , Mammary Neoplasms, Animal/pathology , Neoplasm Recurrence, Local/metabolism , Neovascularization, Pathologic/metabolism , Neovascularization, Pathologic/pathologyABSTRACT
A platelets count was performed on 100 subjects using both the electronic counter and a manual method; the results obtained concerning healthy subjects are overlapping. In subjects with structural alterations regarding platelets and red blood cells, the electronic counter method has overestimated the number, yet making note of it.
Subject(s)
Platelet Count/methods , Evaluation Studies as Topic , Humans , Platelet Count/instrumentation , Predictive Value of TestsABSTRACT
Serum complement levels (UE50, C3, C4, act. C3, C1q) were determined in 75 healthy subjects and 130 cancer patients undergoing treatment. The results were correlated with statistical analysis. The patients were divided into the following groups: a) with local tumor; b) with tumor in complete remission; c) with tumor in incomplete remission; d) stationary. Three blood samples were obtained over a period of about two months. All cancer patients had decreased UE50 levels and increased act. C3 levels compared to normal values, while C3, C4, and C1q were normal. C4 levels were not significant in any group of cancer patients, but act. C3 levels were significantly increased (as compared to those of the healthy subjects). UE50 levels appeared significantly decreased only in the group with complete remission, C3 levels were increased in incomplete remission patients and were variable in stationary patients. C1q values were always increased except in the complete remission group. The variability of complement levels was dependent on the stage of the disease and on the therapy: our results provide considerable support for this hypothesis. We found that complement activity was triggered through classic or alternative means caused by antigen-antibody complexes or inflammatory processes, according to the increase or decrease of the tumor mass.