Genotoxic Treatment Enhances Immune Response in a Genetic Model of Lung Cancer.

Recent advances in immunotherapy have reshaped the clinical management of lung cancer, and immune checkpoint inhibitors (ICIs) are now first-line treatment for advanced lung cancer. However, the majority of patients do not respond to ICIs as single agents, and many develop resistance after initial responses. Therefore, there is urgent need to improve the current ICI strategies.

Regulation of Metabolic Reprogramming by Long Non-Coding RNAs in Cancer.

Metabolic reprogramming is a well described hallmark of cancer. Oncogenic stimuli and the microenvironment shape the metabolic phenotype of cancer cells, causing pathological modifications of carbohydrate, amino acid and lipid metabolism that support the uncontrolled growth and proliferation of cancer cells. Conversely, metabolic alterations in cancer can drive changes in genetic programs affecting cell proliferation and differentiation.

Metabolic Regulation of Epigenetic Modifications and Cell Differentiation in Cancer.

Metabolic reprogramming is a hallmark of cancer, with consistent rewiring of glucose, glutamine, and mitochondrial metabolism. While these metabolic alterations are adequate to meet the metabolic needs of cell growth and proliferation, the changes in critical metabolites have also consequences for the regulation of the cell differentiation state. Cancer evolution is characterized by progression towards a poorly differentiated, stem-like phenotype, and epigenetic modulation of the chromatin structure is an important prerequisite for the maintenance of an undifferentiated state by repression of lineage-specific genes.

Heterogeneity of Glucose Transport in Lung Cancer.

Increased glucose uptake is a known hallmark of cancer. Cancer cells need glucose for energy production via glycolysis and the tricarboxylic acid cycle, and also to fuel the pentose phosphate pathway, the serine biosynthetic pathway, lipogenesis, and the hexosamine pathway. For this reason, glucose transport inhibition is an emerging new treatment for different malignancies, including lung cancer.

Nucleolar organizer regions in a chronic stress and oral cancer model.

This study aimed to examine the role of chronic restraint stress (RS) on oral squamous cell carcinomas induced by 4-nitroquinoline-1-oxide (4-NQO) in CF-1 mouse tongues, measured by the expression of argyrophilic staining of nucleolar organizer regions (AgNOR). Thirty one samples of lingual epithelial tissue of CF-1 mice with a diagnosis of oral squamous cell carcinoma (OSSC) were assigned to two experimental groups: the RS/4-NQO group, where animals received RS and induction of oral chemical carcinogenesis (n=17); and the 4-NQO group, where animals received induction of chemical carcinogenesis without restraint stress (n=14). The mean number and distribution pattern of AgNOR were recorded.