Chromatin, a complex of DNA wrapped around a core of histone proteins, greatly reduces the size of DNA.  Processes like replication and transcription are dependent upon chromatin density because tightly packaged DNA cannot be accessed by proteins involved in these activities.  Histone post-translational modifications (PTMs) can alter chromatin density enabling or inhibiting replication and transcription.  Alterations in levels of transcriptional activating and inactivating PTMs have been associated with progression of numerous cancers.  A recent study has shown that expression of estrogen receptor in breast cancer is regulated by epigenetic aberrations.  Described here is a mass spectrometric approach for correlating PTM status with hormone responsiveness in two breast cancer cell lines.  It is hypothesized that differences in histone modifications exist between cancer cell lines derived from ER+ and ER- breast tumors.  Identification of differences in PTMs between the tumor types may provide insights into new treatments that target histone-modifying enzymes.

Deciphering the breast cancer histone code

245th National Meeting (2013)

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