OnCo

Tissue architecture and the basement membrane

Organs are built like walled towns. Lining cells sit on a dense protein sheet, the basement membrane, and hold hands through junctions. A growth that stays above the sheet is 'in situ' and almost always curable; the disease becomes cancer proper when it cuts through.

Diagram

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.

Polarised epithelium activates E-cadherin junctionsIntegrins / hemidesmosomes activates Basement membraneE-cadherin junctions inhibits Carcinoma in situBasement membrane inhibits Invasive carcinomaMyoepithelial layer inhibits Invasive carcinomaCarcinoma in situ activates MMPs, uPA, invadopodiaMMPs, uPA, invadopodia inhibits Basement membraneMMPs, uPA, invadopodia activates Stroma, vesselsStroma, vessels activates Invasive carcinomaCarcinoma in situ activates Invasive carcinomaPolarised epitheliumPolarised epitheliumE-cadherin junctionsE-cadherin junctionsBasement membraneBasement membraneIntegrins / hemidesmosomesIntegrins / hemidesmosomesCarcinoma in situCarcinoma in situMMPs, uPA, invadopodiaMMPs, uPA, invadopodiaStroma, vesselsStroma, vesselsInvasive carcinomaInvasive carcinomaMyoepithelial layerMyoepithelial layeractivatesinhibitsdruggable target (click)hit by selected productescape route
Basement membrane & tissue barriersEvery organ keeps its lining cells behind a thin, dense sheet of protein called the basement membrane. A tumour that has not crossed it is 'in situ' and essentially curable; crossing it is the moment cancer becomes invasive.

A shop floor with a locked glass floor beneath it. Staff (epithelial cells) can be unruly upstairs and it is still contained; the emergency begins when someone cuts through the glass into the building services below, where the plumbing (blood and lymph vessels) runs.

Contact, stiffness, GPCRs activates MST1/2 → LATS1/2NF2 (Merlin) activates MST1/2 → LATS1/2MST1/2 → LATS1/2 inhibits YAP/TAZYAP/TAZ activates TEAD transcriptionTEAD transcription activates Growth, EMT, drug toleranceContact, stiffness, GPCRsContact, stiffness, GPCRsNF2 (Merlin): NF2 (Merlin) is a gene whose normal job is to hold cell growth in check. The public catalogues list it as a drug target, an oncogene driver, a tumour suppressor and a biomarker, and clinical evidence ties its variants…NF2 (Merlin)MST1/2 → LATS1/2MST1/2 → LATS1/2YAP/TAZYAP/TAZTEAD transcriptionTEAD transcriptionGrowth, EMT, drug toleranceGrowth, EMT, drug toleran…activatesinhibitsdruggable target (click)hit by selected productescape route
Hippo-YAP/TAZThe pathway that tells organs when to stop growing. Cancers disable it so YAP and TAZ stay in the nucleus driving growth; in mesothelioma, NF2 loss does exactly that, and the first drugs against the YAP-TEAD switch are in trials.

A building inspector (Hippo) who checks that the block is full and stops new floors. Cancers fire the inspector, and the architect (YAP/TAZ) keeps adding storeys.

What happens

In plain words, then the glossary entries the stage rests on. Chapter 1, The body's defences: Cancer is not the default.

Organs are built like walled towns. Lining cells sit on a dense protein sheet, the basement membrane, and hold hands through junctions. A growth that stays above the sheet is 'in situ' and almost always curable; the disease becomes cancer proper when it cuts through.

Basement membrane & tissue barriers. Every organ keeps its lining cells behind a thin, dense sheet of protein called the basement membrane. A tumour that has not crossed it is 'in situ' and essentially curable; crossing it is the moment cancer becomes invasive.

Hippo-YAP/TAZ. The pathway that tells organs when to stop growing. Cancers disable it so YAP and TAZ stay in the nucleus driving growth; in mesothelioma, NF2 loss does exactly that, and the first drugs against the YAP-TEAD switch are in trials.

The molecular players

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.

No target record is listed at this stage or drawn in its diagrams; the pathways above carry the mechanism.

Where medicines act

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.

Measured by

Biomarkers, tests and assays in the corpus that read this stage in a patient.

Open questions

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.

  • Which in situ lesions will never progress, so that screening stops over-treating?
  • Can the breach itself be imaged or detected in blood before it happens?
Ideas 10 linked ideas

Key evidence

Papers in the corpus tied to this stage's pathways, targets and terms, newest first.

How this page is built: the stage is one entry in a curated atlas (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 1.1 of 56.