Outcome and Metastatic Behavior of Canine Sinonasal Osteosarcoma (2005-2015).

Sinonasal neoplasms in dogs behave locally aggressively, and metastatic disease has not been a common cause of death. The metastatic rate of sinonasal osteosarcoma (OSA) is not well characterized, and reported outcomes of these patients are variable. The purpose of this study is to evaluate the outcome and metastatic behavior of canine sinonasal OSA. Medical records of canine patients diagnosed with sinonasal OSA via histopathology between January 2005 and December 2015 were reviewed. Patients with any form of treatment or no treatment were included. Time to local progression, time to metastasis, and overall survival data were evaluated. Variables that may impact outcome, such as tumor stage and treatment type, were evaluated. Twenty-seven dogs were identified that fit the inclusion criteria. Overall, 30.0% of dogs developed metastasis over the disease course, with a median time to metastasis of 458 days (95% confidence interval [CI] 318-758 days). The median time to local progression was 335 days (95% CI 264-544 days). The overall median survival time was 410 days (95% CI 341-627 days). Regarding metastasis, sinonasal OSA behaves similarly to sinonasal neoplasms of other histologies and dissimilarly to appendicular OSA. The outcome of treated patients appears similar to that of sinonasal tumor patients with other histologies.

Differential response to exercise in claudin-low breast cancer.

Exposure to exercise following a breast cancer diagnosis is associated with reductions in the risk of recurrence. However, it is not known whether breast cancers within the same molecular-intrinsic subtype respond differently to exercise. Syngeneic mouse models of claudin-low breast cancer (i.e., EO771, 4TO7, and C3(1)SV40Tag-p16-luc) were allocated to a uniform endurance exercise treatment dose (forced treadmill exercise) or sham-exercise (stationary treadmill). Compared to sham-controls, endurance exercise treatment differentially affected tumor growth rate: 1- slowed (EO771), 2- accelerated (C3(1)SV40Tag-p16-luc), or 3- was not affected (4TO7). Differential sensitivity of the three tumor lines to exercise was paralleled by effects on intratumoral Ki-67, Hif1-α, and metabolic programming. Inhibition of Hif1-α synthesis by the cardiac glycoside, digoxin, completely abrogated exercise-accelerated tumor growth in C3(1)SV40Tag-p16-luc. These results suggest that intratumoral Hif1-α expression is an important determinant of claudin-low breast cancer adaptation to exercise treatment.