Frequency of venous thromboembolism events during acute inpatient rehabilitation in a comprehensive cancer centre.

OBJECTIVE: To determine the frequency of venous thromboembolism, possible predictors, and the association between venous thromboembolism and Functional Independence Measure (FIM) scores and length of stay among cancer patients admitted to the inpatient rehabilitation unit at a cancer centre. DESIGN: Retrospective analysis of patients admitted to acute inpatient rehabilitation from September 2011 to June 2013. Subject/patients: Cancer patients in the acute inpatient rehabilitation unit within a tertiary cancer centre. METHODS: International Classification of Diseases (ICD-9) codes identified deep vein thrombosis, pulmonary embolism, and inferior vena cava filter. RESULTS: Venous thromboembolism occurred in 32/611 patients (5.2%): 23/611 (3.8%) during the course of hospitalization before admission to rehabilitation, and 9/611 patients (1.5%) during rehabilitation. Patients with lower extremity oedema at admission (p = 0.0218) had a higher chance of subsequently developing venous thromboembolism. Patients with venous thromboembolism during rehabilitation had a significantly lower FIM transfer score at admission to rehabilitation (p = 0.0247), a longer length of stay in rehabilitation (p = 0.0013) and overall hospitalization (p = 0.0580). CONCLUSION: Cancer patients with low FIM transfer scores and lower extremity oedema are at higher risk of venous thromboembolism. Patients with these clinical findings at admission may require measures for more aggressive surveillance for the presence of venous thromboembolism. Patients with venous thromboembolism had an increased length of stay in rehabilitation, but ultimately did not have significant differences in FIM score changes.

NDN is an imprinted tumor suppressor gene that is downregulated in ovarian cancers through genetic and epigenetic mechanisms.

NDN is a maternally imprinted gene consistently expressed in normal ovarian epithelium, is dramatically downregulated in the majority of ovarian cancers. Little or no NDN expression could be detected in 73% of 351 epithelial ovarian cancers. NDN was also downregulated in 10 ovarian cancer cell lines with total loss in 6 of 10. Re-expression of NDN decreased Bcl-2 levels and induced apoptosis, which significantly inhibited ovarian cancer cell growth in cell culture and in xenografts. In addition, re-expression of NDN inhibited cell migration by decreasing actin stress fiber and focal adhesion complex formation through deactivation of Src, FAK and RhoA. Loss of NDN expression in ovarian cancers could be attributed to LOH in 28% of 18 informative cases and to hypermethylation of CpG sites 1 and 2 of NDN promoter in 23% and 30% of 43 ovarian cancers, respectively. Promoter hypermethylation was also found in 5 of 10 ovarian cancer cell lines. Treatment with the demethylating agent 5-aza-2'-deoxycytidine restored NDN expression in 4 of 7 cell lines with enhanced promoter methylation levels. These observations support the conclusion that NDN is an imprinted tumor suppressor gene which affects cancer cell motility, invasion and growth and that its loss of function in ovarian cancer can be caused by both genetic and epigenetic mechanisms.