The correlation between infections by human papillomavirus types 6/11 and 16/18 and mammary gland hyperplasia with glandular thickening

Deng, Xiao-qun; Long, Xiaoli; Li, Jun

doi:10.14715/cmb/2019.65.5.8

Cited by 1 publication

(1 citation statement)

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“…This is concordant with findings on how a pathogenic stimulus in epidermal cells induces inflammation and, when unresolved, can lead to carcinogenesis [158] or to precancerous hyperplasia and endometrial cancer [159]. Even breast cancer shows such a sequence as when pathogenic stimuli, such as (HPV) type 6/11 and 16/18 infections, are followed by fibrosis with its remodeling increases the risk of such cancers [160].…”

Section: Chronic Inflammation Evoked By Pathogenic Stimulussupporting

confidence: 84%

Synopsis: Special Issue on “Disruption of signaling homeostasis induced crosstalk in the carcinogenesis paradigmEpistemology of the origin of cancer”

Brücher

Jamall

2019

4open

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It is increasingly evident that carcinogenesis, in the vast majority of cancers, cannot be explained simply through an accumulation of somatic mutations, or epigenetics, the stem cell theory, or the Warburg effect. Here, decades of thinking based on incorrect assumptions has resulted in an incorrect hypothesis on the origin of cancer. Many papers studying DNA, genetics, RNA, miRNA, proteomics, and epigenetics have increased our understanding of biology. Our paradigm, though more complex, is more reliable and plausible. It states that cancer originates from a disruption of homeostasis. This essential biological phenomenon, homeostasis, maintains the interrelationships of various signaling pathways and induced crosstalk which modify cellular functions together with the interactions of surrounding cells and structures such that the equilibrium lies towards the optimal health of the organism. This Special Issue “Disruption of signaling homeostasis induced crosstalk in the carcinogenesis paradigm Epistemology of the origin of cancer” provides compelling evidence that carcinogenesis is explained by a six-step sequence of events for the vast majority of cancers. These six steps include, (1) a pathogenic stimulus followed by (2) chronic inflammation, from which develops (3) fibrosis with associated remodeling in the cellular microenvironment. From these changes a (4) pre-cancerous niche develops which triggers the deployment of (5) a chronic stress escape strategy, and when this fails to resolve, and (6) the transition of a normal cell to a cancer cell occurs. This paradigm provides opportunities to move away from a symptom-oriented understanding of cancer and is much closer to a cause-based understanding, which opens the door for early preventative strategies to mitigate cancer as a disease, and to interdict metastases. This is underpinned by the fact that an independent recently published proof of this paradigm showed how a stimulus trigger the proposed multi-sequence cascade of events as abrupt involution-induced chronic inflammation, followed by fibrosis with remodeling, which describes the pre-cancerous niche followed by hyperplasia, metaplasia, and cancer.

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Section: Chronic Inflammation Evoked By Pathogenic Stimulussupporting

confidence: 84%