The phospholipase D (PLD) family has a ubiquitous expression in cells. PLD isoforms (PLDs) and their hydrolysate phosphatidic acid (PA) have been demonstrated to engage in multiple stages of cancer progression. Aberrant expression of PLDs, especially PLD1 and PLD2, has been detected in various cancers. Inhibition or elimination of PLDs activity has been shown to reduce tumour growth and metastasis. PLDs and PA also serve as downstream effectors of various cell‐surface receptors, to trigger and regulate propagation of intracellular signals in the process of tumourigenesis and metastasis. Here, we discuss recent advances in understanding the functions of PLDs and PA in discrete stages of cancer progression, including cancer cell growth, invasion and migration, and angiogenesis, with special emphasis on the tumour‐associated signalling pathways mediated by PLDs and PA and the functional importance of PLDs and PA in cancer therapy.
BackgroundThe association between driver genes and the incidence of thromboembolic events (TEs) in patients diagnosed with non-small-cell lung cancer (NSCLC) needs to be quantified to guide clinical management.MethodsWe interrogated PubMed, Embase, Web of Science and Cochrane library databases for terms related to venous thromboembolism (VTE) and arterial thromboembolism (ATE) in patients diagnosed with non-small-cell lung cancer harboring driver genes. This search was conducted for studies published between 1 January, 2000 and 31 December, 2020. A random-effects meta-analysis was performed to analyze the pooled incidence and odds ratios of VTE in patients with different driver genes.ResultsOf the 2,742 citations identified, a total of 25 studies that included 21,156 patients met eligibility criteria. The overall pooled incidence of VTE in patients with driver genes was 23% (95% CI 18-29). Patients with ROS1 rearrangements had the highest incidence of VTE (37%, 95%CI 23-52). ALK rearrangements were associated with increased VTE risks (OR=2.08,95% CI 1.69-2.55), with the second highest incidence of VTE (27%, 95%CI 20-35). Both groups of patients with EGFR and KRAS mutations did not show a significantly increased risk for VTE (OR=1.33, 95% CI 0.75-2.34; OR=1.31, 95% CI 0.40-4.28).ConclusionsALK rearrangements were shown to be associated with increased VTE risks in patients diagnosed with non-small lung cancer, while there was no significant relation observed between VTE risks and EGFR or KRAS mutations in lung cancer patients.
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