Mitochondrial Dynamics in Non-Small Cell Lung Cancer.

In lung cancer patients, two complementary abnormalities were found that can cause disruption of the mitochondrial network: increased fusion and impaired fission, manifested by reduced levels of FIS1, a mitochondrial division regulator, and increased expression of MFN1, a mitochondrial fusion mediator. Immunoexpression studies of MFN1 and FIS1 proteins were performed in serum samples obtained from 47 patients with non-small cell lung cancer (NSCLC) and 21 controls. In the NSCLC patients, the immunoexpression of the MFN1 protein was significantly higher, and the FIS1 protein level was significantly lower than in the control group (p < 0.01; p < 0.001; UMW test). Patients with early, operable lung cancer had significantly lower levels of MFN1 immunoexpression compared to patients with advanced, metastatic lung cancer (p < 0.05; UMW test). This suggests that early stages of the disease are characterized by greater fragmentation of damaged mitochondria and apoptosis. In contrast, lower FIS1 protein levels were associated with a worse prognosis. Increased mitochondrial fusion in the blood of lung cancer patients may suggest an increase in protective and repair mechanisms. This opens up questions about why these mechanisms fail in the context of existing advanced cancer disease and is a starting point for further research into why protective mechanisms fail in lung cancer patients.

When the same treatment has different response: The role of pharmacogenomics in statin therapy.

Statins, also known as HMG-CoA reductase inhibitors, are one of the most potently prescribed and thoroughly researched medications, predominantly utilized for managing cardiovascular diseases by modulating serum cholesterol levels. Despite the well-documented efficacy of statins in reducing overall mortality via attenuating the risk of cardiovascular diseases, notable interindividual variability in therapeutic responses persists as such variability could compromise the lipid-lowering efficacy of the drug, potentially increasing susceptibility to adverse effects or attenuating therapeutic outcomes.This phenomenon has catalysed a growing interest in the scientific community to explore common genetic polymorphisms within genes that encode for pivotal enzymes within the pharmacokinetic pathways of statins. In our review, we focus to provide insight into potentially clinically relevant polymorphisms associated with statins' pharmacokinetic participants and assess their consequent implications on modulating the therapeutic outcomes of statins among distinct genetic carrier.