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The gene encoding the main signaling molecules of the Wnt signaling pathways (the Wnt proteins) was discovered almost four decades ago by Nüsslein-Volhard and Wieschaus. They identified and originally named the gene "wingless" (wg) after a phenotype discovered during their landmark genetic screen in Drosophila for body pattern defects. At around the same time, another researcher named Harold Varmus found that a murine tumor virus activates the mammalian wg homolog, Int-1, which...
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Sequencing of the human genome has opened up several best-kept secrets of the genome. Scientists have identified thousands of genome variations that exist within a population. These variations can be a single nucleotide or a larger chromosomal variation.
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Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
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A single nucleotide polymorphism or SNP is a single nucleotide variation at a specific genomic position in a large population. It is the most prevalent type of sequence variation found in the human genome. Point mutations that occur in more than 1% of the population qualify as SNPs. These are present once every 1000 nucleotides on an average in the human genome. Replacement of a purine with another purine (A/G) or a pyrimidine with another pyrimidine (C/T) is known as a transition. In contrast,...
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Coding Variants of the Genitourinary Development Gene WNT9B Carry High Risk for Prostate Cancer.

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  • 1Medical Research Service, Department of Veterans Affairs, Tennessee Valley Healthcare System, Nashville, TN.

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This summary is machine-generated.

New research identifies WNT9B gene variants as a significant risk factor for hereditary prostate cancer (HPC). These findings link embryonic genitourinary development genes to prostate cancer susceptibility.

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Area of Science:

  • Genetics
  • Oncology
  • Developmental Biology

Background:

  • Hereditary prostate cancer (HPC) exhibits significant genetic heterogeneity.
  • Most HPC families lack identified pathogenic variants, indicating undiscovered genetic factors.

Purpose of the Study:

  • To identify novel pathogenic variants predisposing individuals to prostate cancer.
  • To explore the genetic underpinnings of familial prostate cancer.

Main Methods:

  • Conducted a familial case-control association study using genome-wide single-allele and identity-by-descent analyses.
  • Sequenced high-risk haplotype carriers for variant detection.
  • Validated candidate variants across independent biobanks.

Main Results:

  • Identified pathogenic variants in WNT9B associated with familial prostate cancer, replicated across four biobanks.
  • WNT9B E152K conferred a 2.5-fold risk, reaching genome-wide significance in meta-analyses of half a million patients.
  • WNT9B Q47R showed genome-wide significance in Finns, with founder effect confirmed by identity-by-descent analysis.
  • WNT9B, HOXB13, and HNF1B are crucial for embryonic prostate development.
  • KMT2D and DHCR7, involved in genitourinary development, were nominally associated with prostate cancer.

Conclusions:

  • WNT9B variants are implicated in hereditary prostate cancer.
  • Genes essential for early genitourinary development play a role in prostate cancer development.