To identify physical examination and perioperative CBC variables in dogs with splenic hemangiosarcoma (HSA) that could aid in predicting progression-free interval (PFI) and overall survival time (OST) in affected dogs.
70 client-owned dogs with splenic HSA treated with splenectomy and chemotherapy between September 2004 and October 2016.
A retrospective search of the University of Minnesota Veterinary Medical Center medical records database was performed to identify dogs with splenic HSA treated with splenectomy and with evidence in the medical records of intent to treat with chemotherapy. Data collection included dog signalment and body surface area, results from CBCs performed within 6 days before to 2 days after splenectomy, whether dogs had hemoabdomen or received transfusions, and tumor stage. Hematocrit, WBC count, and platelet count were treated as categorical variables (divided into terciles: above, within, or below reference limits) because of variation among reference intervals for the numerous analyzers used. Associations between variables and PFI or OST were investigated with Cox regression analyses, and hazard ratios (HRs) for a shorter PFI or OST were reported. Population Pearson correlation coefficient (ρ) analysis was performed to identify potential associations between variables of interest.
Stage 3 HSA was identified as a negative prognostic indicator of PFI (HR, 6.6) and OST (HR, 4.5). Perioperative thrombocytopenia was similarly associated with shorter PFI (HR, 2.2) and OST (HR, 2.0). Results for Hct correlated (ρ = 0.58) with those for platelet count, and although our findings did not indicate a notable association between anemia and shorter PFI, such could not be ruled out.
CONCLUSIONS AND CLINICAL RELEVANCE
The prognostic value of thrombocytopenia warrants further substantiation to understand causal and mechanistic connections, and the presence of thrombocytopenia ultimately may prove valuable in guiding treatment recommendations for dogs with splenic HSA.
OBJECTIVE To investigate protein kinase CK2 (CK2) expression in squamous cell carcinoma (SCC) of cats and to examine effects of CK2 downregulation on in vitro apoptosis and viability in SCC.
SAMPLE Biopsy specimens of oral mucosa and testis and blood samples from clinically normal cats, biopsy specimens of oral SCC from cats, and feline SCC (SCCF1) and mammary gland carcinoma (K12) cell lines.
PROCEDURES Immunohistochemical labeling for CK2α was performed on biopsy specimens. Sequences of the CK2α subunit gene and CK2α’ subunit gene in feline blood and feline cancer cell lines were determined by use of PCR and reverse-transcription PCR assays followed by direct Sanger sequencing. Specific small interfering RNAs (siRNAs) were developed for feline CK2α and CK2α'. The SCCF1 cells were treated with siRNA and assessed 72 hours later for CK2α and CK2α’ expression and markers of apoptosis (via western blot analysis) and for viability (via 3-[4,5-dimethylthiazol-2-yl]-5-[3-carboxymethoxyphenyl]-2-[4-sulfophenyl]-2H-tetrazolium assays).
RESULTS CK2α was expressed in all feline oral mucosa samples and 7 of 8 oral SCC samples. Expression of CK2α and CK2α’ was successfully downregulated in SCCF1 cells by use of siRNAs, which resulted in decreased viability and induction of apoptosis.
CONCLUSIONS AND CLINICAL RELEVANCE In this study, CK2 appeared to be a promising therapeutic target for SCCs of cats. A possible treatment strategy for SCCs of cats would be RNA interference that targets CK2.
To determine if dogs with neoplasia produce more coated platelets, a subpopulation of activated platelets generated by dual stimulation with thrombin and convulxin, a glycoprotein VI agonist, than healthy control dogs.
Client-owned dogs diagnosed with lymphoma (n = 19) or solid tumors (14) and healthy control dogs (14).
Platelets were stimulated ex vivo with thrombin and convulxin. Flow cytometry was used to quantify the percentage of coated platelets based on high levels of surface fibrinogen. To compare the percentage of coated platelets between the three groups, an ANOVA was performed followed by pairwise 95% confidence intervals (CI) adjusted for multiple comparisons using Tukey’s method.
We observed a greater mean percentage of coated platelets in dogs with solid tumors, compared with healthy control dogs, by 10.9 percentage points (95% CI: −1.0, 22.8), and a mean percentage of coated platelets in dogs with lymphoma that was less than healthy control dogs by 0.3 percentage points (95% CI: −11.4, 10.8).
This study provides the first data-based evidence that dogs with solid tumors may have a greater mean coated platelet percentage when compared with healthy control dogs, although there is overlap between groups. Further studies are needed investigating coated platelets in specific subsets of neoplasia and investigating additional mechanisms of hypercoagulability in dogs with neoplasia.