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A dam (the mitochondrial membrane) held by guards (BCL-2, MCL-1, BCL-XL) against demolition crews (BAX, BAK). Cancer hires extra guards; venetoclax fires the BCL-2 guards. Immune killing uses the same dam from the outside.
Pick a product above a diagram to see the nodes it hits and the escape routes below the block. Hover or tap any node or arrow for what it is; every node opens its target, glossary entry or the pathway page. Violet boxes are druggable targets.
A dam (mitochondrial membrane) held by guards (BCL-2, MCL-1) against demolition crews (BAX/BAK). Cancer hires extra guards. Venetoclax fires the BCL-2 guards, and the dam breaks.
A doorbell wired to a self-destruct switch: immune cells ring it. Some tumours rip out the doorbell (FAS loss), some stuff the wiring with insulation (c-FLIP), and some install a second doorbell that rings nowhere (decoy receptors).
In plain words, then the glossary entries the stage rests on. Chapter 4, Evading death and repair: To survive the damage they generate and the treatments thrown at them, cancer cells rewire death and repair.
A dam (the mitochondrial membrane) held by guards (BCL-2, MCL-1, BCL-XL) against demolition crews (BAX, BAK). Cancer hires extra guards; venetoclax fires the BCL-2 guards. Immune killing uses the same dam from the outside.
Intrinsic apoptosis (BCL-2 family). Intrinsic apoptosis is the cell's self-destruct switch. BCL-2 holds it shut; BAX and BAK pull it open. Venetoclax pries BCL-2 off so the switch can fire.
Extrinsic apoptosis (death receptors). Immune cells kill by touch: they present FAS ligand or TRAIL to a target cell, whose death receptors then trigger self-destruction from the outside in. Tumours cut this wire by deleting the receptors or over-producing decoys and blockers.
The proteins and genes at this stage, with their role and how many products act on each. Listed players come from the atlas; drawn players sit as nodes in the diagrams above.
A protein that stops cells from self-destructing. Venetoclax removes that protection and has transformed leukaemia treatment.
CD3 is the switch on every T cell. Bispecific drugs grab it with one arm and the tumour with the other, forcing the T cell to attack.
Products grouped by the node they hit, most advanced first, with the cancers an approved product is linked to. Pick one above the diagram to see it light up.
Records tied to this stage that describe resistance, evasion or tolerance. Resistance: how tumours escape each drug class lists the routes class by class.
If destroying BTK works when every inhibitor has failed, using it first might stop resistance from ever emerging.
Treatment leaves behind damaged cells that stop dividing but do not die, and they release signals that help surviving cancer cells regrow. Removing them could reduce relapse.
Chemotherapy leaves behind senescent cells that inflame tissues and help tumours relapse. A short course of senolytic drugs afterwards might reduce relapse and long-term side effects at once.
Biomarkers, tests and assays in the corpus that read this stage in a patient.
What is not known at this stage: the atlas's own questions, the bottlenecks it bears on, and the ideas in the corpus that try to answer them.
Three genetic classifications of the commonest aggressive lymphoma exist and none of them yet decides anyone's treatment. The trial that would change that has not been run.
Small-cell lung cancer is at least four diseases under the microscope's uniform appearance. Treat each by its transcription-factor subtype.
Papers in the corpus tied to this stage's pathways, targets and terms, newest first.
src/data/mechanics-atlas.ts). Players, medicines, escape routes, tests, ideas and papers are resolved from the knowledge graph at build time through the stage's pathways, targets and terms, so every item here has its own page and sources. Where a section is missing, the corpus has no record tied to the stage yet. Nothing here is medical advice; see about and methodology. Stage 4.1 of 56.