Biochemical Pathways in Cancer

The revolutionary advances in cellular and molecular biochemistry in the last quarter century have provided an unprecedented opportunity for systematic approaches to understand the cancer process. With these new advances and the knowledge acquired as a direct result, an enormous impact has positively affected the clinical areas of cancer prevention, disease management, and treatment of malig-nancy. Despite these scientific achievements, we are still faced with the challenge of fully understanding the complex nature of cancer, including issues of disease recurrence and drug resistance. Therefore, dissecting biochemical pathways that underlie the development of cancer should be given high priority to improve knowledge of human health. In this special issue, we will explore the various aspects of cancer-related biochemical pathways. The papers in this issue discuss multiple signaling pathways involved in the regulation of proliferation, senescence, and death of cancer cells. M. K. Altman et al. demonstrated that the regulator of G-protein signaling 5 (RGS5) is able to reduce the proliferation of ovarian cancer cells and extend the survival of mice. The tumor suppressor p53 plays an essential role in cell proliferation , cell cycle progression, cell death, and senescence [1, 2]. Reisman et al. reviewed the evidence that DNA-binding factors RBP-Jκ and C/EBPβ-2 transcriptionally activate p53 to ensure a rapid cellular response to DNA damage. p53 is also involved in complex networks of mitotic kinase signaling in response to mitotic spindle damage to ensure the proper cell cycle progression. a mutual regulation network between mitotic kinase and p53 signaling. The tumor suppressor p16 INK4A has shown to be implicated in replicative senescence. Here, the role of p16 INK4A in replicative senescence and DNA damage-induced premature senescence in the absence of p53 was reviewed by R. Mirzayans et al. The authors also discussed a possible existence of a negative regulatory relationship between p53 and p16 INK4A. R. Jäger and H. O. Fearnhead reviewed cancer cell proliferation and death in a different point of view. These authors suggested that cancer cell proliferation might be a consequence of inappropriate or corrupted tissue-repair programs, initiated by a signal from dying cells. Mounting evidence suggested that dissecting the biochemical process of genetic alterations will help us understand mechanisms underlying the genesis and spread of cancer and develop novel strategies for targeted therapy and tailored cancer management [3, 4]. J. L. Johnson et al. discussed the genetic and biochemical alternations in heterogeneous cell signaling pathways in non-small-cell …