Publications by authors named "Kegan O Skalitzky"

Among the most significant discoveries from cancer genomics efforts has been the critical role of epigenetic dysregulation in cancer development and progression. Studies across diverse cancer types have revealed frequent mutations in genes encoding epigenetic regulators, alterations in DNA methylation and histone modifications, and a dramatic reorganization of chromatin structure. Epigenetic changes are especially relevant to pediatric cancers, which are often characterized by a low rate of genetic mutations.

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Article Synopsis
  • Prostate cancer risk factors include age, race, and genetic variants, with the CREBRF gene showing notable alterations in Pacific Islanders, a group with high incidence rates.
  • Analysis revealed that 4.05% of prostate tumors had likely damaging CREBRF mutations, which correlated to significantly shorter survival rates—41.23 months for affected patients versus 131 months for those without.
  • In mice lacking CREBRF, there was decreased prostate cell growth and increased cell death, along with altered levels of specific circulating proteins, indicating CREBRF may be important for maintaining prostate health and regulating cancer progression.
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Benign prostatic hyperplasia (BPH) occurs progressively with aging in men and drives deteriorating symptoms collectively known as lower urinary tract symptoms (LUTS). Age-associated changes in circulating steroid hormones, and prostate inflammation have been postulated in the etiology of BPH/LUTS. The link between hormones and inflammation in the development of BPH/LUTS is conflicting because they may occur independently or as sequential steps in disease pathogenesis.

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Fibrogenic and inflammatory processes in the prostate are linked to the development of lower urinary tract symptoms (LUTS) in men. Our previous studies identified that osteopontin (OPN), a pro-fibrotic cytokine, is abundant in the prostate of men with LUTS, and its secretion is stimulated by inflammatory cytokines potentially to drive fibrosis. This study investigates whether the lack of OPN ameliorates inflammation and fibrosis in the mouse prostate.

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