In these large, randomized trials, the presence of comorbid conditions (CCIS > or = 1), rather than age more than 65 years, was associated with poorer survival.

To cite this article: Lazo-Langner A, Goss GD, Spaans JN, Rodger MA. The effect of low-molecular-weight heparin on cancer survival. A systematic review and meta-analysis of randomized trials. J Thromb Haemost 2007; 5: 729-37.Summary. Background: Low-molecular-weight heparins (LMWH) have an antitumor effect in vitro and in experimental animal models of malignancy. Retrospective data suggest that it might improve survival in cancer patients. Objectives: To evaluate the effect of LMWH compared to placebo or no anticoagulant intervention on the survival of cancer patients. Methods: We conducted a systematic review of randomized trials specifically evaluating the impact of LMWH on the survival of cancer patients. Data sources were: MEDLINE, EMBASE, HealthSTAR, Cochrane library, gray literature and cross-referencing from reference lists. Data extraction was performed by one reviewer, and accuracy was independently verified by a second reviewer. Meta-analysis was conducted using: (i) odds ratio (OR) and relative risk (RR); (ii) survival rates using censored endpoints; and (iii) hazard ratios (HR). Results: The pooled HR in all patients was 0.83 (95% CI 0.70-0.99; P ¼ 0.03), and in patients with advanced disease it was 0.86 (95% CI 0.74-0.99; P ¼ 0.04), both in favor of the LMWH group. The results of the OR, RR and survival metaanalysis consistently favored the LMWH group. Sensitivity analyses according to tumor type were not conducted, because of a lack of information. Conclusions: LMWH improves overall survival in cancer patients, even in those with advanced disease. Additional trials are required to define the tumor types, disease stages and dosing schedules most likely to provide the greatest survival benefit.

Patients with advanced or recurrent invasive vulvar squamous cell carcinoma (VSCC) have limited treatment options and a grave prognosis. Understanding the genomic landscape may facilitate the identification of new therapies and improve clinical outcomes. A retrospective chart review and molecular analysis of patients with VSCC from 2000 to 2016 was performed at the Ottawa Hospital Research Institute. The presence of oncogenic human papillomavirus (HPV) was determined by nested PCR and amplified DNA was sequenced using the Ion AmpliSeq Cancer Hotspot v2 Panel. The patients were divided into two groups according to HPV status (HPV-positive versus HPV-negative) and clinical outcome correlated with mutation status using descriptive statistics. In 43 VSCC patients, there was a high mutation rate in both HPV-positive (73%) and HPV-negative (90%) disease with the two subgroups expressing distinct genetic profiles. HPV-positive tumors were characterized by oncogenic mutations in (27%), (14%), and (9%), whereas HPV-negative tumors were found to have mutations in (57%), (24%), (19%), and (14%). Mutation S249C in occurred in 14% of HPV-positive tumors. While there were notable differences in the occurrence of , and mutations according to HPV status, only the rate of mutations was statistically significant ( = 0.0004). No significant difference in prognosis was found between patients with HPV-positive and HPV-negative VSCC. HPV-positive VSCC is characterized by oncogenic mutations that helps classify this subtype as a separate disease. Inhibitors of FGFR3 merit consideration as a therapeutic strategy in this neglected cancer in women..