RESUMO
The largest cause of cancer-related fatalities worldwide is lung cancer. In its early stages, lung cancer often exhibits no signs or symptoms. Its signs and symptoms often appear when the condition is advanced. The Kirsten rat sarcoma virus oncogene homolog is one of the most frequently mutated oncogenes found in non-small cell lung cancer. Patients who have these mutations may do worse than those who do not, in terms of survival. To understand the nuances in order to choose the best treatment options for each patient, including combination therapy and potential resistance mechanisms, given the quick development of pharmaceuticals, it is necessary to know the factors that might contribute to this disease. It has been observed that single nucleotide polymorphisms altering let-7 micro-RNA might impact cancer propensity. On the other hand, gefitinib fails to stop the oncogenic protein from directly interacting with phosphoinositide3-kinase, which may explain its resistance towards cancer cells. Additionally, Atorvastatin may be able to overpower gefitinib resistance in these cancer cells that have this mutation regardless of the presence of phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha. De novo lipogenesis is also regulated by this virus. To overcome these effects, several targeted therapies have been proposed. One such therapy is to use inhibitors of focal adhesion kinases. When this is inhibited, viral oncogene mutant cancers are effectively stopped because it functions downstream of the virus. Mutant oncoproteins like epidermal growth factor receptor may depend on Heat Shock protein90 chaperones more frequently than they do on natural counterparts that make it more attractive therapeutic target for this virus. Inhibition of the phosphoinositide 3-kinase pathway is frequent in lung cancer, and fabrication of inhibitors against this pathway can also be an effective therapeutic strategy. Blocking programmed cell death ligand1 is another therapy that may help T cells to recognize and eliminate cancerous cells. This homolog is a challenging therapeutic target due to its complex structural makeup and myriad biological characteristics. Thanks to the unrelenting efforts of medical research, with the use of some inhibitors, immunotherapy, and other combination methods, this problem is currently expected to be overcome.
RESUMO
Traumatic brain injury (TBI) is a common cause of disability and fatality worldwide. Depending on the clinical presentation, it is a type of acquired brain damage that can be mild, moderate, or severe. The degree of patient's discomfort, prognosis, therapeutic approach, survival rates, and recurrence can all be strongly impacted by an accurate diagnosis made early on. The Glasgow Coma Scale (GCS), along with neuroimaging (MRI (Magnetic Resonance Imaging) and CT scan), is a neurological assessment tools used to evaluate and categorize the severity of TBI based on the patient's level of consciousness, eye opening, and motor response. Extracellular vesicles (EVs) are a growing domain, explaining neurological complications in a more detailed manner. EVs, in general, play a role in cellular communication. Its molecular signature such as DNA, RNA, protein, etc. contributes to the status (health or pathological stage) of the parental cell. Brain-derived EVs support more specific screening (diagnostic and prognostic) in TBI research. Therapeutic impact of EVs are more promising for aiding in TBI healing. It is nontoxic, biocompatible, and capable of crossing the blood-brain barrier (BBB) to transport therapeutic molecules. This review has highlighted the relationships between EVs and TBI theranostics, EVs and TBI-related clinical trials, and related research domain-associated challenges and solutions. This review motivates further exploration of associations between EVs and TBI and develops a better approach to TBI management.