fig1

Acquired resistance to molecularly targeted therapies for cancer

Figure 1. Schematic representation of parallels between PI3K/Akt and MAPK signal pathways. Both pathways become activated when growth factors bind to their respective RTKs, causing RAS GTPases to relay signals downstream. Activation of these pathways promotes increased cell proliferation and survival. Some of the intricacies in signaling by mTORC1 and mTORC2 are shown leading to some distinct effects on metabolism and cell fate. PI3K: Phosphoinositide 3-kinase; Akt: protein kinase B; MAPK: mitogen activated protein kinase; RTK: receptor tyrosine kinase; RAS: oncogene; PTEN: phosphatase and tensin homolog; PIP2: phosphatidylinositol 4,5-bisphosphate; PIP3: phosphatidylinositol 3,4,5-triphosphate; PDK1: 3-phosphoinositidedependent protein kinase 1; mTORC1: mTOR complex 1; mTORC2: mTOR complex 2; RAF: rapidly accelerated fibrosarcoma; MEK: mitogen-activated extracellular signal-regulated kinase; ERK: extracellular signal-related kinase. Created in BioRender. Purcell, C. (2025) https://BioRender.com/3us5vg.

Cancer Drug Resistance
ISSN 2578-532X (Online)

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