Biological Pathway Reviews

AKT (protein kinase B) is a serine threonine kinase that plays a pivotal role in regulating many cell processes, including survival, proliferation, invasion, apoptosis, and angiogenesis.¹ Disruptions in the AKT pathway are associated with cancer, diabetes, cardiovascular and neurological diseases.² In breast cancer, AKT is disrupted in up to 70% of cases, making it a valua

Bruton's tyrosine kinase (BTK), a non-receptor tyrosine kinase, plays an important role in B-cell receptor activation.¹ BCR activation results in translocation and phosphorylation of BTK.

CD19 antigen is a type I transmembrane glycoprotein that is expressed in normal and malignant B cells.¹ It plays a role in B cell development and maturation by modulating B-cell receptor signaling during lymphopoiesis.^2,3 CD19 deficiency leads to an impaired humoral response, resulting

The cell-cycle regulatory proteins CDK4 and CDK6 drive progression through the G₁–S phase transition, a checkpoint in preventing abnormal cell proliferaition.^1,2 Uncontrolled cell division caused by the dysregulated activation of CDK4/6 is common in cancer.Gene deletion, muta

Carcinoembryonic antigen-related cell adhesion molecule 5 (CEACAM5) is a cell surface glycoprotein that is a member of the carcinoembryonic antigen family, which contains 12 glycoproteins. It is used as a clinical biomarker for many different cancers.

The growth-factor-receptor tyrosine kinase family includes EGFR (ErbB1, HER1), ErbB2 (HER2, neu in rodents), ErbB3 (HER3), and ErbB4 (HER4).¹ Receptor overexpression and ligand-dependent and ligand-independent mechanisms can cause abnormal EGFR activation.

By modulating critical gene expression, EZH2 promotes cell cycle progression, cell proliferation, differentiation, and apoptosis.¹

Fibroblast growth factor receptors (FGFR) are a gene family of receptor tyrosine kinases that are differentially expressed in a tissue-specific manner throughout development and into adulthood.

FLT-3 is a receptor tyrosine kinase that activates pathways leading to the proliferation, differentiation, and apoptosis of hematopoietic cells.^1,2 FLT3-ITD mutations and FLT3-TKD mutations can lead to the production of FLT-3 ligands resulting in the activation of FLT-3 and subsequently triggers P