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

familial colorectal cancer type X

Hereditary nonpolyposis colorectal cancer characterized by the absence of germline mutations in DNA mismatch-repair genes.

๐Ÿ”” Follow weekly
๐Ÿงฌ165genes / proteins with evidence
๐Ÿ’Š0drugs and clinical candidates
๐Ÿงช2recruiting trials worldwide
๐Ÿงฌ

Understand familial colorectal cancer type X

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

What it is

Colorectal cancer is cancer that develops in the tissues of the colon or rectum. Your colon and rectum are part of your digestive system:

Your colon is the first and longest part of your large intestine. It absorbs water and some nutrients from foods. It also changes the leftover waste products into stool (poop).

Your rectum is the lower part of your large intestine. It's where your body stores stool.

From MedlinePlus: Colorectal Cancer (US National Library of Medicine) 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 familial colorectal cancer type X itself.

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AI briefing

Where the science on familial colorectal cancer type X 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 familial colorectal cancer type X.

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Top targets

Genes and proteins ranked by Open Targets evidence (0-1)
ATM ATM serine/threonine kinasePROTACsmall molecule๐ŸงŠ AlphaFold structure โ†— 0.64
BRCA2 BRCA2 DNA repair associatedPROTACsmall molecule๐ŸงŠ AlphaFold structure โ†— 0.55
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†— 0.49
BMPR1A bone morphogenetic protein receptor type 1APROTACantibodyothersmall molecule๐ŸงŠ AlphaFold structure โ†— 0.46
POLD1 DNA polymerase delta 1, catalytic subunitPROTACsmall molecule๐ŸงŠ AlphaFold structure โ†— 0.42
CHEK2 checkpoint kinase 2PROTACsmall molecule๐ŸงŠ AlphaFold structure โ†— 0.41
RPS20 ribosomal protein S20PROTACothersmall molecule๐ŸงŠ AlphaFold structure โ†— 0.40
NPAT nuclear protein, coactivator of histone transcriptionPROTAC๐ŸงŠ AlphaFold structure โ†— 0.40
SEMA4A semaphorin 4APROTACantibody๐ŸงŠ AlphaFold structure โ†— 0.37
EXOC4 exocyst complex component 4PROTACantibody๐ŸงŠ AlphaFold structure โ†— 0.16
MYO5A myosin VAPROTACsmall molecule๐ŸงŠ AlphaFold structure โ†— 0.05
ELP2 elongator acetyltransferase complex subunit 2PROTACsmall molecule๐ŸงŠ AlphaFold structure โ†— 0.05
GLRA1 glycine receptor alpha 1PROTACantibodysmall molecule๐ŸงŠ AlphaFold structure โ†— 0.05

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 familial colorectal cancer type X, 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