Cancer-related survival and proliferation pathways

"Cancer-related survival and proliferation pathways" refers collectively to the intricate molecular networks that regulate *tumor cell growth, cell cycle progression, and evasion of cell death*. These include the Ras/Raf/MEK/ERK (MAPK), PI3K/AKT, JNK, and various transcriptional and cell cycle control pathways. Dysregulation occurs via mutation, amplification, or suppression of key enzymes, transcription factors (such as MYC, AP-1), growth factor receptors (EGFR, FGFR), cyclins, CDKs, and tumor suppressors (p53, Rb, PTEN)[1][2][3][4]. The combined activity of these pathways enables cancer cells to survive in hostile environments, resist apoptosis, and proliferate unchecked. Targeting these pathways forms the backbone of many modern cancer therapies and biomarker-guided patient selection strategies; however, redundancy and pathway cross-talk pose major challenges to effective and lasting treatment[2][3][4].

Other names

Survival pathways in cancerProliferation pathways in cancerCancer signaling networksOncogenic signaling pathways

Inhibition of kinase activity (e.g., Raf, MEK, EGFR inhibitors); Blocking transcription factor activation (e.g., c-Myc, AP-1); Cell cycle arrest (via CDK inhibition or p53 reactivation); Pro-apoptotic induction; Antiproliferative effects