ABSTRACT
New ways of exploiting the immune system for cancer treatment have been tested for decades with moderate outcomes. Based on previous immunotherapy knowledge, agents targeting immune checkpoints seem to be remarkably effective in a wide range of tumors. Immune checkpoint inhibitors in metastatic non-small cell lung cancer (NSCLC) provide longlasting responses in specific patients. Nevertheless, with overall response rates ≤ 20%, combinational protocols for various patient subgroups are needed. A good partner treatment to immunotherapy could be chemotherapy, as it successfully modulates the immune response either by controlling or enhancing the antitumor immune activity. Primary research provides promising results in metastatic NSCLC patients using this approach, but further large-scale trials are needed. The implementation of immunotherapy in nonmetastatic cases is also appealing. We review the potential clinical benefits of immunotherapy alone or in concert with chemotherapy in NSCLC.
ABSTRACT
The communication between the gastrointestinal tract and the central nervous system (CNS) allows for certain peptide hormones to influence neurocognitive function. Ghrelin, also known as the 'hunger hormone,' has the unique ability to enter the CNS and interact with the growth hormone secretagogue receptor (GHS-R) within the hippocampus. Upon interaction with ghrelin, a conformational change in the receptor causes an increase in transcription factors to foster a wide array of physiologic changes in response to caloric deprivation. With the GHS-R in a relatively high concentration within the hippocampus, ghrelin can promote memory, spatial, learning, and behavioral effects. In fact, ghrelin appears to also have a neuroprotective and neuromodulatory response once active within the hippocampal dentate gyrus. Through the GHS-R, higher levels of ghrelin may alter cognitive circuitry and offer a possible link to the treatment of some pathologies implicated in neurological dysfunction. Alzheimer's disease (AD) is already becoming a significant target for ghrelin neuroreceptor therapy. In such experimental models, ghrelin has been shown to combat this degenerative process by eliciting an ameliorative and regenerative response. Although trials and research are still ongoing, further studies are indicated as early research into this adjuvant therapy is promising. The research team explored the effects of ghrelin by reviewing the downstream signaling modifications of ghrelin's interaction with a specific CNS receptor, the GHS-R. Although the GHS-R is found in multiple locations within the CNS, the team investigated the role of the GHS-R within the hippocampus to focus solely on the neurocognitive implications of ghrelin. The team noted which signaling pathways in particular that ghrelin initiated and used this approach to determine whether ghrelin may have any therapeutic benefits. The team explored the possible therapeutic indications of ghrelin by looking at studies conducted with a specific neurodegenerative disease known to target the hippocampus.
ABSTRACT
The role of vitamin D in the development of autism spectrum disorder (ASD) is of intensified interest in medical science in recent years. Vitamin D has a significant role in neurogenesis, neuroprotection, and neurodevelopment. Due to the close association of vitamin D with the brain, it has been found that in the pathophysiology of several neuropsychiatric disorders vitamin D receptor (VDR) polymorphism plays a significant role. In this review article, we looked for a relation between VDR polymorphism and ASD. We systemically reviewed all the potential articles on the relation between VDR polymorphism and ASD. We found that several VDR variants FokI, BsmI, and TaqI polymorphisms are related to ASD. Even paternal VDR polymorphism can be a causative factor for ASD in the offspring. The relation between FokI (ff) genotype polymorphism and increased level of serum 1,25(OH)D3 in ASD patients is a very significant finding. Variation of ASD-related genotypes in different ethnic population raises a big question on whether the environmental factors also can do changes in human genotypes leading to ASD.
