BioMed Research International

PGCCs Generating Erythrocytes to Form VM Structure Contributes to Tumor Blood Supply


Publishing date
26 Sep 2014
Status
Published
Submission deadline
09 May 2014

Lead Editor

1Department of Pathology, University of Texas, M.D. Anderson Cancer Center, Houston, TX 77030, USA

2Department of Clinical Cancer Prevention, University of Texas, M.D. Anderson Cancer Center, Houston, TX 77030, USA

3Department of Oncology, Nankai University, Tianjin 300121, China

4Department of medical imaging, Tianjin Union Medicine center, Tianjin 300121, China


PGCCs Generating Erythrocytes to Form VM Structure Contributes to Tumor Blood Supply

Description

Polyploid giant cancer cells (PGCCs) refer to the special subpopulation of cancer cells with giant and multinuclei and contribute to solid tumor heterogeneity. However, to date, their functions are poorly understood. PGCCs differ from normal cells (even the tumor cells) in morphology, size, proliferation pattern, expression of differentiation markers, chromosomal abnormalities, tumor formation, radioresistance, and chemoresistance. These PGCCs had remarkable biologic features of cancer stem cells. Neoangiogenesis is the physiological process involving the growth of new blood vessels from preexisting blood vessels. Cancer development usually undergoes an initial period of avascular growth followed by vasculogenic mimicry (VM) that connects with endothelium-dependent vessels to obtain sufficient blood and oxygen supply to support tumor cell growth, invasion, and metastasis. Accumulating evidence has demonstrated that many different types of cancer utilize VM to form a blood supply network to support tumor cell growth, invasion, and metastasis, and are associated with poor prognosis in different cancers. Recently, we have confirmed that PGCCs can generate erythrocytes expressing hemoglobin. Thus, there is no doubt that tumor cells and their generating erythrocytes can form the VM structure to sustain the blood supply for the tumors.

We invite investigators to contribute original research articles as well as review articles that will stimulate the continuing efforts to understand the molecular mechanism of PGCCs formation and PGCCs generating erythrocytes, which leads to the formation of VM. Furthermore, the relationship between VM structures and other tumor blood supply patterns including mosaic vessels and endothelium-dependent vessels needs to be clarified. Potential topics include, but are not limited to:

  • Potential mechanism of PGCCs formation and the influence of PGCCs in radioresistance and chemoresistance
  • Role of histone 1 families in PGCCs formation
  • Pattern of cell division of PGCCs
  • Role of cell fusion in PGCCs formation
  • Epithelial to mesenchymal transition (EMT) and PGCCs
  • The relationship between PGCCs and cancer stem cells
  • Molecular mechanism of PGCCs generating erythrocytes
  • Identifying correlates of PGCCs generating erythrocytes in VM formation
  • The relationship of VM structures and other tumor blood supply patterns
  • New drug discovery inducing the differentiation of PGCCs

Before submission authors should carefully read over the journal's Author Guidelines, which are located at http://www.hindawi.com/journals/bmri/guidelines/. Prospective authors should submit an electronic copy of their complete manuscript through the journal Manuscript Tracking System at http://mts.hindawi.com/submit/journals/bmri/vascular.medicine/pge/ according to the following timetable:


Articles

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BioMed Research International
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