Tumor Escape and Progression under Immune Pressure
1Department of Microbiology & Immunology, Virginia Commonwealth University Massey Cancer Center, Richmond, VA 23298, USA
2Department of Immunology, Mayo Clinic College of Medicine, 200 First Street SW, Guggenheim 3-42D, Rochester, MN 55906, USA
3Departments of CITI and Hem/HCT, Beckman Research Institute, City of Hope National Medical Center, Beckman Center 3rd Floor, 1500 East Duarte Road, Duarte, CA 91010-3000, USA
Tumor Escape and Progression under Immune Pressure
Description
The fact that cancers develop and progress in immunocompetent hosts makes immunotherapy of cancer a daunting task. In the past decade, we have learned that interactions between tumor cells and cells of the immune system result in the induction of epigenetic changes in the tumor cells and selection of less immunogenic clones as well as alterations in the immune responses including an increased myeloid-derived suppressor cells (MDSCs) and/or Tregs. Knowledge and understanding of cross-talk between nascent transformed cells and cells of the immune system have led to the development of combinatorial immunotherapeutic strategies to overcome cancer.
We invite authors to submit original research as well as review articles that seek to define the interaction between nascent transformed cells and the host immune system. We are particularly interested in articles that explore cooperation of the innate and adaptive immune systems to overcome or to facilitate cancer progression. Potential topics include, but are not limited to:
- Role of host immune system in the induction of epigenetic changes in the tumors
- Interaction of cancer stem cells with cells of the immune system
- Role of the innate immune system in determining the outcome of adaptive immune responses to cancer
- New animal models in tumor immunology research
- Role of infectious diseases in changing the cross-talk between tumor cells and the immune system
- Homeostatic counterregulation in cancer immune therapy. This topic would include both T-cell intrinsic negative checkpoint molecules (CTLA-4, PD-1, etc.) and posttherapy T-regulatory cell expansion
- Role of proteinases and inhibitors, made by immune cells and the tumor environment, as well as their catalytic and noncatalytic effects on tumor cell proliferation, antiapoptosis, invasion, and metastasis
Before submission authors should carefully read over the journal's Author Guidelines, which are located at http://www.hindawi.com/journals/jir/guidelines/. Prospective authors should submit an electronic copy of their complete manuscript through the journal Manuscript Tracking System at http://mts.hindawi.com/ according to the following timetable:
Manuscript Due Friday, 27 January 2012 First Round of Reviews Friday, 27 April 2012 Publication Date Friday, 27 July 2012
Lead Guest Editor
- Masoud H. Manjili, Department of Microbiology & Immunology, Virginia Commonwealth University Massey Cancer Center, Richmond, VA 23298, USA
Guest Editors
- Nejat Egilmez, Department of Microbiology and Immunology, University at Buffalo, 138 Farber Hall, 3435 Main Street, Buffalo, NY 14214, USA
- Keith L. Knutson, Department of Immunology, Mayo Clinic College of Medicine, 200 First Street SW, Guggenheim 3-42D, Rochester, MN 55906, USA
- Senthamil R. Selvan, Department of Medical Oncology, Thomas Jefferson University, Curtis Building, 10th Floor, 1021 Walnut Street, Philadelphia, PA 19107, USA
- Julie R. Ostberg, Departments of CITI and Hem/HCT, Beckman Research Institute, City of Hope National Medical Center, Beckman Center 3rd Floor, 1500 East Duarte Road, Duarte, CA 91010-3000, USA