Theories of cancer origin

Paduch, Roman

doi:10.1097/cej.0000000000000024

Cited by 18 publications

(11 citation statements)

References 61 publications

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“…CSCs are undifferentiated, pluripotent, and have the ability of self-renewal, giving rise to other malignant daughter cells. Tumor cells are usually responsive to conventional chemotherapy, whereas CSCs are resistant to therapy, and will ultimately re-establish the tumor at the local or distant sites [ 35 , 148 , 155 , 156 ] Therefore, a better understanding of the regulatory mechanisms that control the population of CSCs is essential to the development of more efficient therapeutic strategies against HNSCC.…”

Section: Epigenetic Modifications Of Cancer Stem Cellsmentioning

confidence: 99%

Epigenetic Modifications and Head and Neck Cancer: Implications for Tumor Progression and Resistance to Therapy

Castilho

Squarize

Almeida

2017

IJMS

138

121

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Head and neck squamous carcinoma (HNSCC) is the sixth most prevalent cancer and one of the most aggressive malignancies worldwide. Despite continuous efforts to identify molecular markers for early detection, and to develop efficient treatments, the overall survival and prognosis of HNSCC patients remain poor. Accumulated scientific evidences suggest that epigenetic alterations, including DNA methylation, histone covalent modifications, chromatin remodeling and non-coding RNAs, are frequently involved in oral carcinogenesis, tumor progression, and resistance to therapy. Epigenetic alterations occur in an unsystematic manner or as part of the aberrant transcriptional machinery, which promotes selective advantage to the tumor cells. Epigenetic modifications also contribute to cellular plasticity during tumor progression and to the formation of cancer stem cells (CSCs), a small subset of tumor cells with self-renewal ability. CSCs are involved in the development of intrinsic or acquired therapy resistance, and tumor recurrences or relapse. Therefore, the understanding and characterization of epigenetic modifications associated with head and neck carcinogenesis, and the prospective identification of epigenetic markers associated with CSCs, hold the promise for novel therapeutic strategies to fight tumors. In this review, we focus on the current knowledge on epigenetic modifications observed in HNSCC and emerging Epi-drugs capable of sensitizing HNSCC to therapy.

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Section: Epigenetic Modifications Of Cancer Stem Cellsmentioning

confidence: 99%

Epigenetic Modifications and Head and Neck Cancer: Implications for Tumor Progression and Resistance to Therapy

Castilho

Squarize

Almeida

2017

IJMS

138

121

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“…The extreme complexity of cancer has aroused many theories and hypothesis about cancer initiation and progression, typically the theories of somatic gene mutations, chromosomal instability, aneuploidy, speciation, mitochondrial dysfunction, Warburg effect, etc., each of them being partially logical and verifiable on the one hand and meeting with serious challenges on the other [ 4 , 5 ]. A general theory accounting for an exclusive cause of cancer initiation and progression has long been sought [ 124 ].…”

Section: Tumorigenesis Resembles An Uncontrolled Process Of Neural Spmentioning

confidence: 99%

“…Some theories, hypotheses and concepts have been put forward to establish a unified connection between these cancer related genes, gene mutations and the acquirement of cancer properties in cells. However, each of them cannot provide an exclusive explanation for tumorigenesis because of some inconsistencies [ 4 , 5 ]. Epithelial–mesenchymal transition (EMT) is such a concept that seems to link gene expression changes during tumorigenesis and cancer malignant properties, but it has been challenged by some studies.…”

Section: Introductionmentioning

confidence: 99%

Tumorigenesis as a process of gradual loss of original cell identity and gain of properties of neural precursor/progenitor cells

Cao

2017

Cell Biosci

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Cancer is a complex disease without a unified explanation for its cause so far. Our recent work demonstrates that cancer cells share similar regulatory networks and characteristics with embryonic neural cells. Based on the study, I will address the relationship between tumor and neural cells in more details. I collected the evidence from various aspects of cancer development in many other studies, and integrated the information from studies on cancer cell properties, cell fate specification during embryonic development and evolution. Synthesis of the information strongly supports that cancer cells share much more similarities with neural progenitor/stem cells than with mesenchymal-type cells and that tumorigenesis represents a process of gradual loss of cell or lineage identity and gain of characteristics of neural cells. I also discuss cancer EMT, a concept having been under intense debate, and possibly the true meaning of EMT in cancer initiation and development. This synthesis provides fresh insights into a unified explanation for and a previously unrecognized nature of tumorigenesis, which might not be revealed by studies on individual molecular events. The review will also present some brief suggestions for cancer research based on the proposed model of tumorigenesis.

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“…The most cancer development theories have not been able to do so. Various theories of cancer origin can be classified into two broad categories, epigenetic and genetic ones [54]. The genetic theories can be further divided into gene-and genome-based theories.…”

Section: Classical Semiclassical and Quantum Modeling Of Tumor And mentioning

confidence: 99%

Quantum-Mechanical Modeling of Mutations, Aging, Evolution, Tumor, and Cancer Development

Djordjević

2016

Quantum Biological Information Theory

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In this chapter, we will describe the quantum-mechanical models to accurately describe the process of creation of spontaneous, induced, and adaptive mutations. These models will be used to describe the processes of evolution and aging. The various theories of quantum evolution and epievolution will be studied as well. We then describe the Markovian chain-like classical and quantummechanical modeling of mutations and aging. In the same section, the hybrid quantum-classical biological channel model with memory is described as well. After that, various classical, semiclassical, and quantum models of cancer development are studied. The final section concludes the chapter. Quantum-Mechanical and Quantum Mechanics-Like Models for Mutations and EvolutionWe have already discussed the role of mutations in evolution process in Chap. 3; see Sect. 3.4. Based on several recent publications [1][2][3][4][5][6][7][8][9][10][11][12], it has become evident that both Darwinian type of evolution (random mutations followed by selection process) [13] and Lamarckian type of evolution (selected mutations beneficial to the organism) [14] are important. The modernized Lamarckian mechanism, which can also be called neo-Lamarckism, can be described as follows: environmental factors are introducing genomic changes, the mutations are targeted to specific genes, and the mutations provide the adaptation to the original cause. Clearly, this mechanism is well aligned with adaptive mutation mechanism discussed in Sect. 4.3 of the previous chapter (see also [15][16][17][18][19][20][21][22]). The Darwinian mechanism of evaluation is less demanding as no specialized mechanism is required to direct the change of the relevant genomic locus and restrict it to the specific mutations.Based on mutation models we discussed in previous chapter as well as references [1][2][3][4][5][6][7][8][9][10][11][12], it appears that both mechanisms can contribute to the evolution. For low stress levels, the spontaneous mutations seem to be a dominant source to evolution, suggesting Darwinian evolution mode is more relevant. On the other hand, for strong stress levels, the adaptive mutations dominate, indicating that Lamarckian

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Theories of cancer origin

Cited by 18 publications

References 61 publications

Epigenetic Modifications and Head and Neck Cancer: Implications for Tumor Progression and Resistance to Therapy

Epigenetic Modifications and Head and Neck Cancer: Implications for Tumor Progression and Resistance to Therapy

Tumorigenesis as a process of gradual loss of original cell identity and gain of properties of neural precursor/progenitor cells

Quantum-Mechanical Modeling of Mutations, Aging, Evolution, Tumor, and Cancer Development

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