Michael Helmrath · Patient personalized translational tools in cystic fibrosis to transform data from bench to bed-side and back
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Article1 min read·Published May 2021Older

Patient personalized translational tools in cystic fibrosis to transform data from bench to bed-side and back

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Article · May 2021 · 1 min read

In brief

In brief

This study demonstrates a translational pipeline using patient-derived intestinal organoids and human intestinal organoid (HIO) mouse models to predict CFTR modulator response in rare cystic fibrosis mutations. Positive in vitro ivacaftor response in enteroids led to successful N-of-1 clinical trial with improved outcomes, validating personalized therapeutic testing.

Written by the GCMD Library team from the article.

Michael Helmrath

Cystic fibrosis is a deadly multiorgan disorder caused by loss of function mutations in the gene that encodes for the cystic fibrosis transmembrane conductance regulator (CFTR) chloride/bicarbonate ion channel. More than 1,700 CFTR genetic variants exist that can cause CF, and majority of these are extremely rare. Because of genetic and environmental influences, CF patients exhibit large phenotypic variation. These factors make clinical trials difficult and largely impractical due to limited and heterogeneous patient pools. Also, the benefit of approved small-molecule CF modulators in a large number of rare mutation patients remains unknown. The goal of this study is to perform a comprehensive bench-side study using in vitro patient enteroids and in vivo mice implanted human intestinal organoids (HIOs) to test CF modulator-Ivacaftor response for a rare CF mutation patient. Based on the positive Ivacaftor response in the enteroids, the patient was enrolled in a (N = 1) clinical trial and showed improved clinical outcomes upon Ivacaftor treatment. HIO implantation model allowed in vivo modulator dosing and provided an elegant human organ-based demonstration of bench-to-bedside testing of modulator effects. Additionally, using the CF HIO model the role of CFTR function in the maturation of human intestine was reported for the first time. In all, we demonstrate that these models effectively serve to translate data from the lab to the clinic and back so that patient-specific thera

Statements in this article

  1. More than 1,700 CFTR genetic variants exist that can cause cystic fibrosis, and the majority of these are extremely rare.

    Established
  2. Clinical trials in cystic fibrosis are difficult and largely impractical due to limited and heterogeneous patient pools caused by genetic and environmental variation.

    Established
  3. The benefit of approved small-molecule CF modulators in a large number of rare mutation patients remains unknown.

    Open
  4. Patient-derived enteroids can be used in vitro to test CFTR modulator response for rare CF mutations.

    Research
  5. Human intestinal organoids implanted in mice allow in vivo modulator dosing and provide organ-based demonstration of modulator effects.

    Research
  6. A patient with a rare CF mutation showed positive Ivacaftor response in enteroid testing and was subsequently enrolled in an N=1 clinical trial.

    Research
  7. The patient showed improved clinical outcomes upon Ivacaftor treatment following positive enteroid testing.

    Research
  8. The CF human intestinal organoid model demonstrated the role of CFTR function in the maturation of human intestine for the first time.

    Research

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