Inflammation initiates cancer by depleting stem cells.

Abstract:

:According to the theory presented herewith, neoplasia results solely from stem cell depletion. Besides serving as tissue progenitors, stem cells are postulated to secrete a vital substance 'A' necessary for proper tissue function. Carcinogens interfere with 'A' production mainly by destroying stem cells and since the latter are not replenished, less 'A' is produced. In order to repair the deficiency, the organism grows a special organ, the neoplasm, dedicated to produce a substitute, denominated here as substance 'B'. Since carcinogens continue depleting stem cells, the neoplasm has to grow more and more in order to keep up with the demand, until reaching a stage of decompensation when the harm inflicted by it is greater than its benefit. Any stem cell depleting substance or process e.g. ablation, chemotherapy and inflammation, is regarded here as a carcinogen. Even animal tumor viruses are postulated here to exert their harm mainly by depleting stem cells. Protracted inflammation e.g. ulcerative colitis or cystic mastopathy, hits stem cells and is followed therefore by neoplasia. Age specific incidence rates of such pathologies resemble precursor-successor curves of tracer kinetics. The precursor inflammation hits young adults, while its successive neoplasia is more prevalent in older individuals. Although most age specific curves of adult cancers are unimodal, at least five are bimodal, resembling precursor-successor curves. These are: Hodgkin's disease, seminoma, nasopharyngeal and retroperitoneal tumors and cancer of bone and joints. It is suggested here that these age specific curves are mixtures of two pathologies, an inflammatory, which is prevalent in young persons, followed by neoplasia.

journal_name

Med Hypotheses

journal_title

Medical hypotheses

authors

Zajicek G

doi

10.1016/0306-9877(85)90026-x

subject

Has Abstract

pub_date

1985-11-01 00:00:00

pages

207-19

issue

3

eissn

0306-9877

issn

1532-2777

pii

0306-9877(85)90026-X

journal_volume

18

pub_type

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