You work in a lab and you have discovered a brilliant way to specifically control chromatin remodeling on a gene by gene basis. You work in a lab and you have discovered a brilliant method for targeted control of chromatin remodeling on a gene-by-gene basis. You are specifically interested in modifying the transcription of oncogenes, which are genes whose overexpression can lead to cancer. Select modifications you would make in cancer cells that are over expressing oncogenes.
Increase acetylation of histones
Decrease acetylation of histones
Decrease phosphorylation of histones
Increase phosphorylation of histones Increase methylation of histones Decrease methylation of histones

In response to dysregulated oncogenic signals, a vast number of genomic loci that are repressed in the physiologic state are activated by abnormal expression and/or activity of remodelers in malignant cells.

Therefore, altered gene activation and/or inappropriate gene silencing result from chromatin deregulation. Recent findings demonstrate that gene‐translocations leading to fusions of transcription factors increase oncogenesis by changing chromatin architecture.

A number of tumour suppressors, including retinoblastoma (pRb), p53, and Ini1/hSNF5, are also misregulated in some malignancies and use chromatin remodelling as part of their regular roles. Additionally, in cancer, the epigenetic landscape is constantly and dynamically regulated.

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