Origin of Cancer: An Information, Energy, and Matter Disease

被引:30
作者
Hanselmann, Rainer G. [1 ,2 ]
Welter, Cornelius [1 ]
机构
[1] Saarland Univ, Inst Human Genet, Homburg, Germany
[2] Beratungszentrum Hyg, Freiburg, Germany
关键词
entropy; cancer; carcinogenesis; warburg effect; mutations; aneuploidy; microenvironment; matter; SELF-ORGANIZATION; MAMMALIAN-CELLS; SYSTEMS BIOLOGY; BREAST-CANCER; HIGH-RISK; ANEUPLOIDY; TRANSFORMATION; INSTABILITY; METABOLISM; MECHANISMS;
D O I
10.3389/fcell.2016.00121
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Cells are open, highly ordered systems that are far away from equilibrium. For this reason, the first function of any cell is to prevent the permanent threat of disintegration that is described by thermodynamic laws and to preserve highly ordered cell characteristics such as structures, the cell cycle, or metabolism. In this context, three basic categories play a central role: energy, information, and matter. Each of these three categories is equally important to the cell and they are reciprocally dependent. We therefore suggest that energy loss (e.g., through impaired mitochondria) or disturbance of information (e.g., through mutations or aneuploidy) or changes in the composition or distribution of matter (e.g., through micro-environmental changes or toxic agents) can irreversibly disturb molecular mechanisms, leading to increased local entropy of cellular functions and structures. In terms of physics, changes to these normally highly ordered reaction probabilities lead to a state that is irreversibly biologically imbalanced, but that is thermodynamically more stable. This primary change-independent of the initiator-now provokes and drives a complex interplay between the availability of energy, the composition, and distribution of matter and increasing information disturbance that is dependent upon reactions that try to overcome or stabilize this intracellular, irreversible disorder described by entropy. Because a return to the original ordered state is not possible for thermodynamic reasons, the cells either die or else they persist in a metastable state. In the latter case, they enter into a self-driven adaptive and evolutionary process that generates a progression of disordered cells and that results in a broad spectrum of progeny with different characteristics. Possibly, 1 day, one of these cells will show an autonomous and aggressive behavior-it will be a cancer cell.
引用
收藏
页数:12
相关论文
共 99 条
[81]   Aneuploidy: Cells losing their balance [J].
Torres, Eduardo M. ;
Williams, Bret R. ;
Amon, Angelika .
GENETICS, 2008, 179 (02) :737-746
[82]   Neoplastic transformation of cultured mammalian cells by estrogens and estrogenlike chemicals [J].
Tsutsui, T ;
Barrett, JC .
ENVIRONMENTAL HEALTH PERSPECTIVES, 1997, 105 :619-624
[83]  
Tsutsui T, 2000, INT J CANCER, V86, P151, DOI 10.1002/(SICI)1097-0215(20000415)86:2<151::AID-IJC1>3.0.CO
[84]  
2-0
[85]   Chromosomal variability of human mesenchymal stem cells cultured under hypoxic conditions [J].
Ueyama, Hanae ;
Horibe, Tomohisa ;
Hinotsu, Shiro ;
Tanaka, Tomoaki ;
Inoue, Takeomi ;
Urushihara, Hisashi ;
Kitagawa, Akira ;
Kawakami, Koji .
JOURNAL OF CELLULAR AND MOLECULAR MEDICINE, 2012, 16 (01) :72-82
[86]   Physical relationships among matter, energy and information (Reprinted form Cybernetics and Systems '04, 2004) [J].
Umpleby, Stuart A. .
SYSTEMS RESEARCH AND BEHAVIORAL SCIENCE, 2007, 24 (03) :369-372
[87]   Functional roles of transiently and intrinsically disordered regions within proteins [J].
Uversky, Vladimir N. .
FEBS JOURNAL, 2015, 282 (07) :1182-1189
[88]   Correlation Between Dysplasia and Ploidy Status in Oral Leukoplakia [J].
Andre W. van Zyl ;
Marlene B. van Heerden ;
Emil Langenegger ;
Willie F. P. van Heerden .
Head and Neck Pathology, 2012, 6 (3) :322-327
[89]   CANCER Tumours outside the mutation box [J].
Versteeg, Rogier .
NATURE, 2014, 506 (7489) :438-439
[90]  
Virchow Rudolf, 1858, Die Cellularpathologie in ihrer Begrundung auf physiologische und pathologische Gewebelehre: 20 Vorlesungen, gehalten wahrend der Monate Februar, Marz und April 1858 im Pathologischen Institut zu Berlin