Patho-Epigenetics of Disease

  • Janos Minarovits
  • Hans Helmut Niller

Table of contents

  1. Front Matter
    Pages i-xiii
  2. Sole Gatto, Maurizio D’Esposito, Maria R. Matarazzo
    Pages 15-41
  3. Gaston Calfa, Alan K. Percy, Lucas Pozzo-Miller
    Pages 43-69
  4. Amanda Ewart Toland
    Pages 91-122
  5. Christian Arsov, Wolfgang Goering, Wolfgang A. Schulz
    Pages 123-157
  6. András Kádár, Tibor A. Rauch
    Pages 159-177
  7. Hans Helmut Niller, Ferenc Banati, Eva Ay, Janos Minarovits
    Pages 179-225
  8. Barbara Klausz, József Haller, Áron Tulogdi, Dóra Zelena
    Pages 227-280
  9. Lorenzo de la Rica, Esteban Ballestar
    Pages 349-378
  10. Thomas Eggermann
    Pages 379-395
  11. Einari Aavik, Mikko P. Turunen, Seppo Ylä-Herttuala
    Pages 397-418
  12. Hans Helmut Niller, Ferenc Banati, Eva Ay, Janos Minarovits
    Pages 419-455
  13. Back Matter
    Pages 457-465

About this book

Introduction

In multicellular organisms the establishment, maintenance, and programmed alterations of cell-type specific gene expression patterns are regulated by epigenetic mechanisms. Thus, epigenetic alterations (DNA methylation, DNA associated Polycomb-Trithorax protein complexes, histone modifications) ensure the unique transcriptional activity and phenotypic diversity of diploid cells that carry identical or nearly identical DNA sequences.

Because DNA methyltransferase I (DNMT1) associates with replication foci during S phase and prefers hemimethylated DNA as a substrate, DNMT1 ensures the clonal propagation of cytosine methylation patterns (maintenance methylation). Thus, DNA methylation may provide a memory function by helping progeny cells to “remember” their proper cellular identity.

An alternative system of epigenetic memory, the Polycomb and Trithorax groups of protein complexes, that may operate both independently from and in concert with DNA methylation, ensures the heritable regulation of gene expression via modification of histone tails.

The complex interplay of epigenetic regulatory mechanisms permits both the dynamic modulation of gene expression and the faithful transmission of gene expression patterns to each progeny cell upon division. These carefully orchestrated processes can go wrong, however, resulting in epigenetic reprogramming of the cells that may manifest in pathological changes, as it was first realized during the studies of epigenetic alterations in malignant tumors. By now it became a well established fact that not only genetic changes, but also the disruption of epigenetic regulation can result in carcinogenesis and tumor progression. Scientists working in other fields soon followed the pioneering work of cancer researchers, and revealed that epigenetic dysregulation forms the basis of a wide spectrum of human diseases.

Editors and affiliations

  • Janos Minarovits
    • 1
  • Hans Helmut Niller
    • 2
  1. 1.Microbiological Research GroupNational Center for EpidemiologyBudapestHungary
  2. 2.University of RegensburgRegensburgGermany

Bibliographic information

  • DOI https://doi.org/10.1007/978-1-4614-3345-3
  • Copyright Information Springer Science+Business Media New York 2012
  • Publisher Name Springer, New York, NY
  • eBook Packages Biomedical and Life Sciences
  • Print ISBN 978-1-4614-3344-6
  • Online ISBN 978-1-4614-3345-3
  • About this book