Cancer Pathophysiology

A section of Cancers (ISSN 2072-6694).

Section Information

The major abnormality driving the development of all cancer types is the dysregulated proliferation of cancer cells that grow and divide in an uncontrolled manner, invading normal tissues and organs and eventually spreading throughout the body. Such loss of control in growth is the net result of the accumulation of abnormalities in diverse regulatory systems, resulting in such modifications of cell behavior that distinguish cancerous from normal cells.

Cancer development has historically been seen as a multistep process involving mutation and selection for cells with a progressively increasing capacity for proliferation, survival, invasion, and metastasis. The first step in this process, referred to as tumor initiation, is considered to result from a genetic alteration leading to abnormal proliferation and the generation of a population of clonally derived tumor cells. Further mutations progressively accumulate and are responsible for tumor progression, which confers the so-called property of clonal selection that continues throughout tumor development.

In parallel, more recent findings indicate that epigenetic changes as well as alterations in the noncoding RNA repertoire may occur and significantly contribute to both the initiation and progression of cancer.

This section of Cancers aims to publish contributions on all aspects of cancer pathophysiology. We encourage the submission of all types of manuscripts, including original articles, narrative and systematic reviews, and communications reporting significant advances in the pathophysiology of solid and hematologic cancers. Topics include, but are not limited to:

  • Cancer biology
  • Cancer dependency
  • Cancer epigenetics
  • Cancer phenotype
  • Cancer genetics
  • Cancer-associated miRNAs
  • Cancer stem cells
  • Cancer translational research
  • Cancer-associated noncoding RNAs
  • DNA damage
  • DNA repair systems
  • Hematological cancers
  • Metastasis
  • Oncogenes
  • Pre-malignant conditions
  • Signal transduction pathways
  • Solid cancers
  • Targeted anticancer therapy
  • Tumor angiogenesis
  • Tumor differentiation
  • Tumor suppressor genes

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