Target intelligence / Profile preview

Oncogenic driver pathways

Molecular classification
Other
01

Overview

Oncogenic driver pathways are complex networks of biochemical reactions that transmit signals from the cell surface to the nucleus, regulating essential processes such as growth, division, and survival. In oncology, these pathways become pathologically activated through genetic alterations like mutations, amplifications, or fusions, which provide a selective growth advantage to cancer cells (Sanchez-Vega et al., 2018, Cell). Key examples include the Mitogen-Activated Protein Kinase (MAPK), Phosphoinositide 3-kinase (PI3K), and Notch signaling pathways (NCI Dictionary of Cancer Terms). Therapeutic strategies often involve the use of targeted inhibitors designed to block specific enzymes or receptors within these pathways to halt tumor progression. However, the clinical utility of these drugs is frequently limited by the emergence of resistance mechanisms and the potential for systemic toxicity due to the pathways' roles in normal cellular homeostasis (Sever & Brugge, 2015, Cold Spring Harbor Perspectives in Biology). Understanding the crosstalk between different oncogenic driver pathways is crucial for developing effective combination therapies in precision medicine.

Other names
Oncogenic signaling pathwaysCancer driver pathwaysOncogenic cascadesTumorigenic signaling pathways
02

Mechanism of action

Inhibition of specific signaling nodes such as tyrosine kinases, serine/threonine kinases, or cell surface receptors to disrupt constitutive downstream signaling (Sever & Brugge, 2015, Cold Spring Harbor Perspectives in Biology).

03

Biological functions

Cell proliferationCell survivalApoptosis regulationMetabolismAngiogenesisCell cycle progressionDifferentiation
04

Disease associations

Cancer
05

Safety considerations

Acquired drug resistanceOn-target toxicity in healthy tissuesFeedback loop activationPathway crosstalkDose-limiting toxicities
06

Interacting drugs

7 more in the full profile.

07

Biomarkers

EGFR mutationKRAS mutationBRAF V600EALK rearrangementPIK3CA mutationHER2 amplificationPTEN loss

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