Knowledge base
Plain-language explanations first, then the detail, then the evidence the crawler actually found. Blue "In plain language" boxes are written for people who have never read a genetics paper; the sections below them are for when you want the numbers and the sources.
A rare, variable genetic condition caused when a small piece of one copy of chromosome 17 is missing. It commonly affects the kidneys and can cause diabetes and learning or speech differences - but the range of what people experience is wide.
written for humans
10 supporting sources
conf 85%
updated today
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Family organisations, rare-disease portals and the primary clinical references, all of which this crawler tracks.
written for humans
10 supporting sources
conf 75%
updated today
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Machine-assembled summary of 6 insights from 6 supporting sources.
auto-generated
6 supporting sources
conf 97%
updated today
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A chromosomal microarray (or genome/exome with CNV calling) finds it. A standard karyotype can miss it. Prenatal detection is increasingly common. Parental testing comes next.
written for humans
10 supporting sources
conf 85%
updated today
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Family planning & counseling
50% transmission risk if a parent carries it. Cascade testing of relatives is the single most useful next step. Prenatal and preimplantation options exist.
written for humans
10 supporting sources
conf 80%
updated today
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Machine-assembled summary of 3 insights from 3 supporting sources.
auto-generated
3 supporting sources
conf 97%
updated today
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About 15 genes are usually deleted. HNF1B does most of the work. The deletion is autosomal dominant: it can come from a parent (often a parent who is mildly affected and undiagnosed) or arise new in the child.
written for humans
10 supporting sources
conf 85%
updated today
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Machine-assembled summary of 257 insights from 864 supporting sources.
auto-generated
864 supporting sources
conf 97%
updated today
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The most medically actionable part of the condition: structural kidney differences, reduced kidney function, and HNF1B-MODY diabetes. All are screenable, and screening changes outcomes.
written for humans
10 supporting sources
conf 85%
updated today
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There is no treatment for the deletion itself. Care is: screen the kidneys, pancreas and glucose; support development early; treat what shows up; and hand over sensibly at the transition to adult services.
written for humans
813 supporting sources
conf 80%
updated today
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Machine-assembled summary of 4 insights from 803 supporting sources.
auto-generated
803 supporting sources
conf 97%
updated today
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learning, speech and behaviour
Machine-assembled summary of 30 insights from 182 supporting sources.
auto-generated
182 supporting sources
conf 97%
updated today
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learning, speech and behaviour
Speech delay is the most commonly reported early sign. Support needs range from none to intellectual disability; autism traits, ADHD and anxiety are over-represented, and there is a raised risk of psychosis in adulthood.
written for humans
126 supporting sources
conf 78%
updated today
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Many carriers go to school, work and live independently. The main threats to quality of life are untreated kidney disease, mislabelled diabetes, and unsupported speech or learning needs.
written for humans
10 supporting sources
conf 72%
updated today
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Natural-history and genotype-phenotype studies, HNF1B cell and animal models, better breakpoint mapping with long-read sequencing, and registries that recruit families.
written for humans
10 supporting sources
conf 70%
updated today
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Machine-assembled summary of 44 insights from 44 supporting sources.
auto-generated
44 supporting sources
conf 97%
updated today
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Machine-assembled summary of 62 insights from 433 supporting sources.
auto-generated
433 supporting sources
conf 97%
updated today
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Kidneys and urinary tract, pancreas/diabetes, liver enzymes, reproductive anatomy, development, speech, behaviour, and occasionally seizures or heart differences. Any subset is possible - including none at all.
written for humans
10 supporting sources
conf 80%
updated today
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