FinnGen 3 (2023-2027)

The third phase of FinnGen began in August 2023. During this four year period, the data resource created during FinnGen 1 and 2 will be deepened with more data to understand the onset, progression and treatment response of the diseases discovered in the first stages of the project.

In its third phase, the FinnGen project takes a deeper dive into the diseases and variants uncovered in FinnGen 1 and 2. FinnGen 3 will continue producing data and results of core analyses, but there are no current plans to expand the cohort of 520 000 biobank participants.

Instead, FinnGen 3 will:

  1. perform expanded, longitudinal analyses of pre- and post-diagnostic states including disease progression and therapeutic response and 
  2. look at the biological mechanism of the genetic signals.

This will be done by focusing on selected disease areas of interest, namely pulmonology, fibrotic diseases, neurodegenerative diseases, heart failure, inflammatory bowel disease, rheumatic diseases, atopic diseases, eye diseases, kidney diseases and oncology. 

The plan is to introduce new data to the analyses, including laboratory values from the national KANTA register, hospital administered drugs and other relevant clinical data, such as procedures. These data can be used, together with the data already in FinnGen, to draw a more comprehensive picture of how genetic variants influence disease onset, progression and treatment response. 

As a new effort, FinnGen 3 plans to conduct omics analyses on samples collected from the individuals geno- and phenotyped in FinnGen 1 and 2.  Proteomics, single cell sequencing and immune profiling  on samples collected before and after diagnoses can help to identify predictive and indicative biomarkers. Omics data can be further complemented by introducing metabolomics data and whole exome and whole genome sequences from legacy collections, which are available through the FinnGen partner biobanks. Protein, metabolite and RNA signatures are expected  to offer clues into the biological mechanisms that are in place when carriers of a given genetic variant develop a disease.