Biological Pathway Reviews

ALK is a tyrosine kinase receptor that resides on chromosome 2p23. Chromosomal rearrangements resulting in fusion genes leads to ALK tyrosine kinase that promote cell survival by activating a signaling pathway or by inhibition of apoptosis, which leads to cell proliferation.¹

PIK3CA (phosphatidylinositol 3-kinase catalytic subunit) is an oncogene that encodes one piece (a subunit) of an enzyme called phosphatidylinositol 3-kinase (PI3-Kinase).¹ PIK3CA plays a role in the control of cell growth, cell survival, and cell migration.

Tumor cells have many characteristics, including genomic instability and oncogene activation, which should lead to apoptosis.¹ In a bid to survive, tumor cells may become dependent on the BCL-2 protein.² Certain cancer cells will overexpress BCL-2, which in turn impedes apoptosis and facilitates tumor growth and resistance to chemotherapy.³ These mal

NRG1 stands for Neuregulin 1, a gene that encodes ligands for ERBB family receptors, particularly ERBB3 and ERBB4.

BCMA is a member of the tumor necrosis factor receptor family that is expressed on plasma cells and on late stage normal and malignant B-cells.¹ BCMA binds to BAFF, activating the NF-kB and MAPK8/JNK signaling pathways, which leads to the prolif

Oncogenic mutations in BRAF genes activate the RAF/MEK/ERK pathway, resulting in increased cell proliferation and resistance to apoptosis.¹ BRAF mutations have been identified in 7% to 8% of all cancers.² V600E is the most common activating mutations in BRAF and is associated with more

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