Vascular Fractality and Alimentation of Cancer

Szász, András

doi:10.4236/ijcm.2021.127025

Cited by 3 publications

(2 citation statements)

References 66 publications

(51 reference statements)

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“…The size of the colonies is also a matter [160,165]. The basal, resting metabolic rate in a unit of the cancer mass prefers the growing mass in suboptimal alimentation [161,166].…”

Section: Fourth Stage Of Cancer Developmentmentioning

confidence: 99%

“…The current is powered by endogenous field strength, forming an "injury current" [164,169], which is an internal rebalancing of the charge distribution, driving wound healing [165,170]. The injury current ignites cellular migration [166,171] and supports the proliferation to heal the wound [167,168,172,173]. The electric field ignites the cell division, and the field strength correlates with its frequency of it [169,174].…”

Section: Fifth Stage Of Cancer Developmentmentioning

confidence: 99%

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Peto’s “Paradox” and Six Degrees of Cancer Prevalence

Szasz

2024

Cells

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Peto’s paradox and the epidemiologic observation of the average six degrees of tumor prevalence are studied and hypothetically solved. A simple consideration, Petho’s paradox challenges our intuitive understanding of cancer risk and prevalence. Our simple consideration is that the more a cell divides, the higher the chance of acquiring cancerous mutations, and so the larger or longer-lived organisms have more cells and undergo more cell divisions over their lifetime, expecting to have a higher risk of developing cancer. Paradoxically, it is not supported by the observations. The allometric scaling of species could answer the Peto paradox. Another paradoxical human epidemiology observation in six average mutations is necessary for cancer prevalence, despite the random expectations of the tumor causes. To solve this challenge, game theory could be applied. The inherited and random DNA mutations in the replication process nonlinearly drive cancer development. The statistical variance concept does not reasonably describe tumor development. Instead, the Darwinian natural selection principle is applied. The mutations in the healthy organism’s cellular population can serve the species’ evolutionary adaptation by the selective pressure of the circumstances. Still, some cells collect multiple uncorrected mutations, adapt to the extreme stress in the stromal environment, and develop subclinical phases of cancer in the individual. This process needs extensive subsequent DNA replications to heritage and collect additional mutations, which are only marginal alone. Still, together, they are preparing for the first stage of the precancerous condition. In the second stage, when one of the caretaker genes is accidentally mutated, the caused genetic instability prepares the cell to fight for its survival and avoid apoptosis. This can be described as a competitive game. In the third stage, the precancerous cell develops uncontrolled proliferation with the damaged gatekeeper gene and forces the new game strategy with binary cooperation with stromal cells for alimentation. In the fourth stage, the starving conditions cause a game change again, starting a cooperative game, where the malignant cells cooperate and force the cooperation of the stromal host, too. In the fifth stage, the resetting of homeostasis finishes the subclinical stage, and in the fifth stage, the clinical phase starts. The prevention of the development of mutated cells is more complex than averting exposure to mutagens from the environment throughout the organism’s lifetime. Mutagenic exposure can increase the otherwise random imperfect DNA reproduction, increasing the likelihood of cancer development, but mutations exist. Toxic exposure is more challenging; it may select the tolerant cells on this particular toxic stress, so these mutations have more facility to avoid apoptosis in otherwise collected random mutational states.

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“…The size of the colonies is also a matter [160,165]. The basal, resting metabolic rate in a unit of the cancer mass prefers the growing mass in suboptimal alimentation [161,166].…”

Section: Fourth Stage Of Cancer Developmentmentioning

confidence: 99%

Section: Fifth Stage Of Cancer Developmentmentioning

confidence: 99%

Peto’s “Paradox” and Six Degrees of Cancer Prevalence

Szasz

2024

Cells

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Allometric Scaling by the Length of the Circulatory Network

Szász¹

2021

OJBIPHY

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Background: Allometric scaling is a well-known research tool used for the metabolic rates of organisms. It measures the living systems with fractal physiology. The metabolic rate versus the mass of the living species has a definite scaling and behaves like a four-dimensional phenomenon. The extended investigations focus on the mass-dependence of the various physiological parameters. Objective: Proving the length of vascularization is the scaling parameter instead of mass in allometric relation. Method: The description of the energy balance of the ontogenic growth of the tumor is an extended celldeath parameter for studying the mass balance at the cellular level. Results: It is shown that when a malignant cellular cluster tries to maximize its metabolic rate, it changes its allometric scaling exponent. A growth description could follow the heterogenic development of the tumor. The mass in the allometric scaling could be replaced by the average length of the circulatory system in each case. Conclusion: According to this concept, the dependence of the mass in allometric scaling is replaced with a more fundamental parameter, the length character of the circulatory system. The introduced scaling parameter has primary importance in cancer development, where the elongation of the circulatory length by angiogenesis is in significant demand.

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Exploring Biocomplexity in Cancer: A Comprehensive Review

Szasz,

Szigeti

2024

OJBIPHY

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Vascular Fractality and Alimentation of Cancer

Cited by 3 publications

References 66 publications

Peto’s “Paradox” and Six Degrees of Cancer Prevalence

Peto’s “Paradox” and Six Degrees of Cancer Prevalence

Allometric Scaling by the Length of the Circulatory Network

Exploring Biocomplexity in Cancer: A Comprehensive Review

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