* **p53 Tumor Suppressor Pathway** — featuring p53, MDM2, p21, BAX, and PUMA, it is central to genome surveillance and anticancer defense by enforcing DNA-damage–induced cell cycle arrest, senescence, or apoptosis in genetically compromised cells.
* **DNA Damage Response (ATM/ATR–CHK1/CHK2) Pathway** — using ATM, ATR, BRCA1/2, RAD51, and checkpoint kinases, it prevents oncogenic mutation accumulation by coordinating DNA repair with cell-cycle checkpoints and apoptosis.
* **Intrinsic Apoptosis (Mitochondrial) Pathway** — driven by BCL-2 family proteins, cytochrome-c, APAF-1, and caspases, it eliminates transformed cells by activating programmed cell death in response to irreparable stress signals.
* **Extrinsic Apoptosis (Death Receptor) Pathway** — mediated by FAS, TRAIL receptors, FADD, and caspase-8, it enables immune surveillance to induce cancer-cell apoptosis through ligand-triggered death signaling.
* **Cellular Senescence Pathway** — involving p16^INK4a, RB, p21, and p53, it is anticancer by permanently halting proliferation of at-risk cells despite continued metabolic activity.
* **Autophagy (Tumor-Suppressive Phase)** — centered on AMPK, ULK1, Beclin-1, and LC3, it limits tumor initiation by removing damaged mitochondria and proteins that produce genomic instability and oxidative stress.
* **AMPK–mTOR Metabolic Checkpoint Pathway** — integrating AMPK, LKB1, TSC1/2, and mTORC1, it suppresses cancer by restraining anabolic metabolism and proliferation under low-energy conditions.
* **Hippo Tumor-Suppressor Pathway** — involving MST1/2, LATS1/2, and YAP/TAZ, it curtails oncogenic transcription by phosphorylating and sequestering growth-promoting cofactors from the nucleus.
* **Wnt/β-Catenin Inhibitory Regulation Network** — via APC, GSK3β, Axin, and CK1, it prevents malignant transformation by degrading β-catenin and restricting uncontrolled proliferation signaling.
* **TGF-β Tumor Suppressor Signaling** — mediated by SMAD2/3/4 complexes, it exerts cytostatic and pro-apoptotic effects in early tumorigenesis by controlling differentiation and cell-cycle arrest programs.
* **Immune Checkpoint Surveillance Pathways** — using PD-1/PD-L1, CTLA-4, and cytotoxic T-cell machinery, they provide anticancer activity by enabling immune recognition and elimination of transformed cells when inhibitory brakes are lifted.
* **Oxidative Stress Response (Nrf2-Keap1 Axis)** — involving Nrf2, glutathione synthesis enzymes, and ROS-detox systems, it suppresses early oncogenesis by preventing DNA damage caused by chronic oxidative stress.
* **Ferroptosis Pathway** — driven by iron metabolism, lipid peroxidation processes, GPX4, and system x_c^- transporters, it eliminates cancer cells through regulated oxidative membrane damage distinct from classical apoptosis.
* **Pyruvate Dehydrogenase (PDH) Metabolic Gatekeeping Pathway** — regulated by PDH, PDKs, and mitochondrial oxidative phosphorylation control, it suppresses tumor metabolism by opposing the Warburg shift toward aerobic glycolysis.
* **Unfolded Protein Response–Induced Apoptosis** — utilizing PERK, ATF4, CHOP, and IRE1 signaling, it limits tumor survival by converting prolonged endoplasmic-reticulum stress into apoptotic death programs.