We investigate the implications of DNA double strand breaks in the human genome, regarding the progression and treatment of various cancer types. During mitosis, the canonical DNA repair mechanisms are suspended while broken chromosomes get temporarily stabilized through so-called adapter proteins. We already knew that TOPBP1 is involved in that process and recently, we identified another Protein which recruits TOPBP1 to sites of damage. After mapping the interaction site on TOPBP1 we attempted to pull down CIP2A using a fragment of the binding domain, followed by chromatography-tandem-mass spectrometry analysis, the results of which we share in this upload.