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๐Ÿ“ฐ Latest breakthroughs
๐Ÿ—บ๏ธ Disease Atlas ยท Genetic, familial or congenital disease

hereditary nonpolyposis colon cancer

A cancer-predisposing condition characterized by the development of colorectal cancer not associated with colorectal polyposis, endometrial cancer, and various other cancers (such as malignant epithelial tumor of ovary, gastric, biliary tract, small bowel, and urinary tract cancer) that are frequently diagnosed at an early age.

๐Ÿ”” Follow weekly
๐Ÿงฌ841genes / proteins with evidence
๐Ÿ’Š0drugs and clinical candidates
๐Ÿงช12+recruiting trials worldwide
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Understand hereditary nonpolyposis colon cancer

Cancer ยท Cells that grow out of control
๐ŸŽ“ Learn more

What it is

A cancer-predisposing condition characterized by the development of colorectal cancer not associated with colorectal polyposis, endometrial cancer, and various other cancers (such as malignant epithelial tumor of ovary, gastric, biliary tract, small bowel, and urinary tract cancer) that are frequently diagnosed at an early age.

From the Open Targets disease record โ†—

๐Ÿงฌ Cancer: Cancer is a group of diseases in which some of the body's cells grow and divide without control, and can spread to other parts of the body.

โ“ Why it happens

  • Changes (mutations) build up in the genes that tell a cell when to grow, divide and die.
  • Most of these changes happen during life: tobacco, too much sun, alcohol, some infections (such as HPV and hepatitis B and C), radiation, obesity and ageing all raise the risk.
  • Some people inherit a faulty gene that raises their risk, such as BRCA1 or BRCA2.

๐Ÿซ€ What it does to the body

  • Cancer cells form a lump (tumour) that can press on or invade nearby organs.
  • They can travel through the blood or lymph to start new tumours elsewhere (metastasis).
  • Blood cancers crowd out healthy blood cells in the bone marrow.

๐Ÿงฑ Why it is hard to cure

  • Every cancer is different, even between two people with the same type - and inside one tumour.
  • Cancer cells keep changing, so they can learn to resist a medicine that worked at first.
  • Cancer cells are the body's own cells, so killing them without harming healthy cells is hard.
  • Many cancers cause no symptoms until they have spread, and a new medicine often takes more than ten years to go from the lab to patients.

๐Ÿš€ What research is trying now

  • Targeted medicines against the exact gene change in a tumour (for example EGFR, ALK or KRAS).
  • Immunotherapy that helps the immune system recognise cancer, including CAR-T cell therapy.
  • Personalised cancer vaccines built from each tumour's mutations, now in late trials.
  • Blood tests that look for tumour DNA to find cancer earlier, and AI to read scans and slides.

General information about cancer, reviewed by people; it does not describe any one person. Below: the evidence for hereditary nonpolyposis colon cancer itself.

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AI briefing

Where the science on hereditary nonpolyposis colon cancer stands, from the evidence on this page

AI reads the targets, drugs, trials and papers below and writes where the science stands โ€” every claim cited. It is shared with everyone who opens hereditary nonpolyposis colon cancer.

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Top targets

Genes and proteins ranked by Open Targets evidence (0-1)
MSH2 mutS homolog 2PROTACsmall molecule๐ŸงŠ AlphaFold structure โ†— 0.90
MSH6 mutS homolog 6PROTACsmall molecule๐ŸงŠ AlphaFold structure โ†— 0.88
MLH1 mutL homolog 1PROTACsmall molecule๐ŸงŠ AlphaFold structure โ†— 0.87
PMS2 PMS1 homolog 2, mismatch repair system componentPROTACsmall molecule๐ŸงŠ AlphaFold structure โ†— 0.87
EPCAM epithelial cell adhesion moleculePROTACantibodyothersmall molecule๐ŸงŠ AlphaFold structure โ†— 0.78
FBXO11 F-box protein 11PROTAC๐ŸงŠ AlphaFold structure โ†— 0.73
LRRFIP2 LRR binding FLII interacting protein 2PROTACantibody๐ŸงŠ AlphaFold structure โ†— 0.72
ATM ATM serine/threonine kinasePROTACsmall molecule๐ŸงŠ AlphaFold structure โ†— 0.65
CHEK2 checkpoint kinase 2PROTACsmall molecule๐ŸงŠ AlphaFold structure โ†— 0.63
MLH3 mutL homolog 3PROTAC๐ŸงŠ AlphaFold structure โ†— 0.57
TGFBR2 transforming growth factor beta receptor 2PROTACantibodysmall molecule๐ŸงŠ AlphaFold structure โ†— 0.56
BRCA2 BRCA2 DNA repair associatedPROTACsmall molecule๐ŸงŠ AlphaFold structure โ†— 0.56
C11orf65 chromosome 11 open reading frame 65๐ŸงŠ AlphaFold structure โ†— 0.53
POLE DNA polymerase epsilon, catalytic subunitPROTACantibodysmall molecule๐ŸงŠ AlphaFold structure โ†— 0.51
MUTYH mutY DNA glycosylasePROTACsmall molecule๐ŸงŠ AlphaFold structure โ†— 0.50

Green labels: what the target is known to be druggable by. The score combines genetics, somatic mutations, drugs, expression and literature.

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Drugs and candidates

Every medicine linked to hereditary nonpolyposis colon cancer, by how far it has got

No drugs recorded yet.

๐Ÿ›ก๏ธ

AI Cure shows public evidence (Open Targets, ClinicalTrials.gov, PubMed, openFDA, DepMap, AlphaFold) with its source, and AI summaries that cite it โ€” not medical advice and not a cure. Treatment decisions belong with your doctor. Research ideas are shared only with approved researchers and labs, who can test them. In an emergency call your local emergency number (112 in India and Europe, 911 in the US). AI Cure Terms of Use ยท Privacy