Call for Papers - Focused Issue: Genomic Instability, Clonal Evolution and Oncogenesis

Published: 2018-09-11

Guest Editors:

Masood A. Shammas, PhD, Harvard (Dana Farber) Cancer Institute, Boston, MA, USA;
Pierfrancesco Tassone, MD, Magna Graecia University, Catanzaro, Italy;
Bisweswar Nandi, Harvard Medical School, Boston, MA, USA

Precision Cancer Medicine (PCM, Precis Cancer Med, ISSN: 2617-2216) is an open access, peer-reviewed online journal newly launched in 2018. It aims at better understanding and management of cancers by exploring in pathological mechanism and genetic changes of cancer, tailoring therapeutic decisions and developing targeted therapies or individually customized strategies. For more information, please visit:


DNA in living organisms is constantly exposed to a variety of harmful substances which can either be present or produced within the cell or other organs or present in the environment. These factors which may include radiation, certain viruses, mutagenic and carcinogenic chemicals, oxidative byproducts of food, hydrochloric acid and bile acids in gastroesophageal refluxate, DNA replication errors/stress, errors and/or dysregulation of DNA repair pathways, cytokines, hormones and growth factors, can potentially cause damage to DNA and disrupt genomic integrity of a cell. In normal cells, multiple DNA repair pathways (including homologous recombination, non homologous end joining, base excision repair, nucleotide excision repair and mismatch repair) exist which repair the damage to restore and preserve the information in the genome. Homologous recombination which uses homologous chromosome (in G1) or sister chromatid (in G2 phase of cell cycle) as template to repair the damage, is the most precise known repair mechanism. The accurate repair of DNA damage is achieved by coordinated action of DNA repair and related pathways including cell cycle, immune system and apoptosis etc. These pathways are tightly regulated and operate only ate right time, place and intensity. If a cell acquires extensive and irreparable damage, it undergoes apoptotic death. If damage to DNA is not extensive but escapes repair, it can lead to change/s in the genome. Acquisition of changes in the right set of genes can transform a cell predisposing it to oncogenesis. Immune system has ability to recognize and kill such cells thus providing another shield against oncogenesis. In summary, multiple pathways ensure the integrity and stability of genome to prevent oncogenesis and related disorders. However, these pathways can also contribute to DNA damage, genomic instability and oncogenesis, if dysregulated.  

We invite investigators to contribute research, review or opinion articles describing recent findings in the fields of genomics/genomic evolution, inflammation, and/or the environmental/dietary factors affecting genome stability and/or other parameters related to cancer. The purpose of the research published under this topic will be to:

  • Understand molecular mechanisms and consequences of genomic instability, clonal evolution and inflammation in cancer. Manuscripts may provide novel information in these fields separately or linking them together;
  • Identification of new prognostic tools and novel therapeutic strategies, targeting genomic instability, telomere maintenance, and inflammation;
  • Identification of new potential carcinogens and new ideas to reduce exposure and prevent these cancers.
  • Manuscript Due:
    December 31, 2018

    Review of the manuscripts:
    January 01 -- March 01, 2019

    As an online journal, PCM follows the rapid publication process, which means articles are going to be published promptly once accepted, without delay in fitting the publication frequency.