Insulin resistance has been studied extensively at systemic, organ, tissue and cellular and molecular levels. Overnutrition plays an essential role in the development of chronic metabolic diseases such as obesity and type 2 diabetes. For subjects without genetic defects, the development of insulin resistance and type 2 diabetes is a graduate process. How the transition from an insulinsensitive state to an insulin-resistant state occurs, and what the roles of nutrients are in the process have not been fully understood. Here, we try to summarize the current understanding of insulin-regulate gene expression in the liver, and describe a phenomenon of hepatic insulin resistance at gene expression (HIRAGE), which may be linked to overnutrition.

With increasing rates of obesity, rates of type 2 diabetes and diabetic complications are expected to rise exponentially over the next few decades (American Diabetic Association). A key feature of type 2 diabetes is a resistance to insulin. Insulin signaling is key to a number of physiological processes, including glucose metabolism, cell growth, general gene expression, and apoptosis.

Inflammation drives prostate cancer (PCa) progression. While inflammation is a cancer hallmark, the underlying mechanisms mediating inflammation-induced PCa are still under investigation. Interleukin-1 (IL-1) is an inflammatory cytokine that promotes cancer progression, including PCa metastasis and castration resistance. We previously found that acute IL-1 exposure represses PCa androgen receptor (AR) expression concomitant with the upregulation of pro-survival proteins, causing de novo accumulation of castration-resistant PCa cells.

Mood disorders represent a major medical need requiring chronic treatment. About one million people die by suicide worldwide each year, both as a consequence of major depression or not. Multiple deficits, including cell atrophy and loss, were described in the brains of mood disorders affected patients and in experimental animal models. Numerous changes in gene expression and activity were described in limbic and cortical brain regions. 

Venetoclax, a small-molecule B-cell lymphoma 2 (BCL-2) inhibitor, selectively eradicates leukemic stem cells (LSCs). While venetoclax has revolutionized the treatment of acute myeloid leukemia (AML), treatment failure and disease relapse are common. Mechanisms underlying venetoclax resistance are surprisingly heterogeneous.