OnCo

Nutrient competition

Tumour and immune cells eat from the same plate. Cancer hoards glucose, dumps lactate and acid, and burns tryptophan and arginine into by-products that paralyse T cells. Fixing the food fight is part of making immunotherapy work.

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.

Light up a product:+20 more via the Connected tab
Glycolytic tumour cell activates Glucose, glutamine depletedGlycolytic tumour cell activates Lactate, acidity (MCT4)Glycolytic tumour cell activates IDO1 → kynurenineHypoxia activates CD39 → CD73 → adenosineHypoxia activates Glycolytic tumour cellGlucose, glutamine depleted inhibits T-cell / NK dysfunctionLactate, acidity (MCT4) inhibits T-cell / NK dysfunctionLactate, acidity (MCT4) activates M2 macrophage polarisationCD39 → CD73 → adenosine inhibits T-cell / NK dysfunctionIDO1 → kynurenine inhibits T-cell / NK dysfunctionArginase (MDSC, TAM) inhibits T-cell / NK dysfunctionGlycolytic tumour cellGlycolytic tumour cellGlucose, glutamine depletedGlucose, glutamine deplet…Lactate, acidity (MCT4)Lactate, acidity (MCT4)CD39 → CD73 → adenosine: CD73 is an enzyme on tumour and immune cells that converts AMP into adenosine, which switches off T and natural killer cells through A2A and A2B receptors.CD39 → CD73 → adenosineIDO1 → kynurenineIDO1 → kynurenineArginase (MDSC, TAM): The receptor that macrophages depend on; blocking it shrinks tenosynovial giant cell tumour (a CSF1-driven tumour) and depletes tumour-supporting macrophages, though the latter has not yet helped patients with common…Arginase (MDSC, TAM)T-cell / NK dysfunction: PD-1 is a brake on T cells. Blocking it releases the immune system against the tumour and has cured some previously incurable cancers.T-cell / NK dysfunctionM2 macrophage polarisationM2 macrophage polarisationHypoxia: A master switch that kidney cancer cells leave permanently on when they lose the VHL gene; belzutifan blocks it.Hypoxiaactivatesinhibitsdruggable target (click)hit by selected productescape route
Nutrient competition & metabolic immunosuppressionTumours and immune cells eat from the same plate. Cancer cells hoard glucose and glutamine, dump lactate and acid, and burn tryptophan and arginine into by-products that paralyse T cells. The tumour wins the food fight, and the immune system loses before it has fired a shot.

A buffet where the tumour arrives first, eats the protein, and leaves the table sticky with lactate. The immune guests arrive hungry and find nothing but by-products that make them drowsy.

What happens

In plain words, then the glossary entries the stage rests on. Chapter 5, Feeding the tumour: A tumour is a construction site that never stops.

Tumour and immune cells eat from the same plate. Cancer hoards glucose, dumps lactate and acid, and burns tryptophan and arginine into by-products that paralyse T cells. Fixing the food fight is part of making immunotherapy work.

Nutrient competition & metabolic immunosuppression. Tumours and immune cells eat from the same plate. Cancer cells hoard glucose and glutamine, dump lactate and acid, and burn tryptophan and arginine into by-products that paralyse T cells. The tumour wins the food fight, and the immune system loses before it has fired a shot.

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.

  • PD-1 is a brake on T cells. Blocking it releases the immune system against the tumour and has cured some previously incurable cancers.

  • CD73 is an enzyme on tumour and immune cells that converts AMP into adenosine, which switches off T and natural killer cells through A2A and A2B receptors. Oleclumab (anti-CD73) with durvalumab slowed progression in a phase 2 lung cancer trial and quemliclustat is in phase 3 in pancreatic cancer, but A2A blockers gave only modest signals and several were dropped.

  • The receptor that macrophages depend on; blocking it shrinks tenosynovial giant cell tumour (a CSF1-driven tumour) and depletes tumour-supporting macrophages, though the latter has not yet helped patients with common cancers.

  • A master switch that kidney cancer cells leave permanently on when they lose the VHL gene; belzutifan blocks it.

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.

AtCD73 / adenosine axisnode CD39 → CD73 → adenosine in Nutrient competition & metabolic immunosuppression2 products
AtCSF1Rnode Arginase (MDSC, TAM) in Nutrient competition & metabolic immunosuppression4 products
AtHIF-2αnode Hypoxia in Nutrient competition & metabolic immunosuppression1 product
Listed at this stage without a drawn target1 product

How tumours escape

Records tied to this stage that describe resistance, evasion or tolerance. The resistance atlas lists the routes class by class.

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.

  • After IDO1 failed, which metabolic checkpoint (adenosine, arginase, lactate) is worth a phase 3?
  • Can CAR-T cells be engineered to thrive in a nutrient-poor, acidic tumour?
Ideas 48 linked ideas

38 more ideas are linked to this stage's pathways, targets and terms; see the rankings →

Key evidence

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

34 more papers in the key-papers index →

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 5.6 of 56.