Of note, HSCs derived from animals with disseminated prostate carcinoma were found to express lower levels of niche adhesion molecules and receptors (e.g. NOTCH, angiopoietin-1 receptor (TIE2)) and transcription factors regulating HSC self-renewal and proliferation (B-cell specific Moloney murine virus integration site 1 (BMI1) and inhibitors of CDK4 A (INK4A)) [190], suggesting that these aggressive prostate carcinoma cells actively alter HSCs to vacate the niche. This evidence concerns the gene CDKN2A and prostate carcinoma.