No abstract

Venous thrombosis is an underappreciated adverse event associated with cancer immunotherapy. Roopkumar et al. describe the incidence of venous thrombosis in individuals with cancer receiving immunotherapy and suggest that elevated levels of myeloid-derived suppressor cells, interleukin-8, and soluble vascular cell adhesion molecule 1 before immunotherapy correlate with development of venous thrombosis.

Introduction Thromboembolism (TE) is common in patients with non‐small cell lung cancer (NSCLC) and is associated with worse outcomes. Recent advances in the understanding of NSCLC have led to the identification of molecular subtypes such as anaplastic lymphocyte kinase (ALK) and epidermal growth factor receptor (EGFR) mutations. The association of these subtypes with risk of TE has not been fully explored. Methods We conducted a retrospective cohort study of consecutive NSCLC patients seen at the Cleveland Clinic from July 2002 through July 2017 for whom molecular classification and follow‐up were available. TE events included deep vein thrombosis (DVT), pulmonary embolism (PE), visceral vein thrombosis (VVT), and arterial events. TE‐free survival and overall survival rates for each of the molecular subtypes (wild‐type, ALK‐mutant, and EGFR‐mutant) were estimated by the Kaplan‐Meier method. Cox proportional hazard regression analysis was used to identify factors associated with the endpoints TE and overall survival. TE was analyzed as a conditional, time‐dependent covariate to assess its impact with respect to overall survival. Results The study population consisted of 461 patients. Approximately half were females (n = 263, 57%) and 58% (n = 270) were older than 65 years. TE occurred in 98 of 461 patients (21.3%) during a median follow‐up of 33.1 months. The highest cumulative rates of TE were observed in patients with ALK‐mutant NSCLC (N = 20/46, 43.5%) followed by patients with EGFR‐mutant cancers (N = 35/165, 21.2%) and wild‐type cancers (N = 43/250, 17.2%) P < .05. Cumulative incidence of TE at 6 months of follow‐up was 15.7% (95% confidence interval [CI]: 5.0%‐26.4%) for ALK‐mutant cancers, 8.8% (95% CI: 4.4%‐13.2%) for EGFR‐mutant cancers, and 9.2% (95% CI: 5.4%‐12.9%) for wild‐type cancers. Patients who experienced TE had worse overall survival (all patients: hazard ratio = 2.8 95% CI 2.1‐3.6, P < .001). Conclusions Patients with ALK‐mutant advanced lung adenocarcinoma have the highest rate of TE. TE is associated with worse survival across molecular subtypes. These findings should be taken into consideration in decision‐making regarding thromboprophylaxis.

Breast cancer is the most commonly diagnosed cancer in women and is a leading cause of cancer-related mortality worldwide. Overall, 6% of U.S. patients with breast cancer present with synchronous metastasis at the time of diagnosis, and almost 30% of all breast cancers will progress to metastatic disease. 1 Approximately 70% of breast cancers are hormone receptor-positive, 2 and endocrine therapy is the preferred initial treatment. [3][4][5] However, acquired resistance to endocrine therapy occurs in the vast majority of patients with estrogen receptor-positive (ER+) mBC. 6 The role of cell-cycle signaling