How do normal cells transition into cancer cell work?

10 February 2015 100 8K Report

The transition from one cell function to another, as well as the transition of one cell type to another seems to be a routine event rather than a rare one. It has been shown that an epithelial mesenchymal transition (EMT) in embryogenesis/morphogenesis acts in a direction opposite to that of a mesenchymal-epithelial transition (MET) [Cell 2009, 139(5):871–890]. Furthermore, EMT can induce non-cancer stem cells to become cancer stem cells [Cell 2008, 133(4):704–715 & PLoS One 2008, 3(8):e2888].

Braun recognized some 60 y ago that a gram negative bacterium Agrobacterium tumefaciens could initiate the in vitro transformation of normal plant cells into tumor cells; he showed that transformation occurs in a short time period, resulting in tumor cells with slower growth and less progression [Am J Biol 1947, 34(4):234–240 & Proc Natl Acad Sci U S A 1958, 44(4):344–349 & Phytopathology 1951, 41:963–966]. Zaenen et al. revealed, and Mary-Ann Chilton’s group subsequently proved, that a small DNA plasmid within A. tumefaciens was responsible for the transformation [J Mol Biol 1974, 86(1):109–127.]: tumor inducing DNA (Ti-DNA), after infection, was integrated into the plant genome in tobacco plants [Cell 1977, 11(2):263–271]. Chilton also showed that Braun’s findings were based on the same principle: although the T-DNA from the A. tumefaciens Ti-plasmids was not at first detected [Proc Natl Acad Sci U S A 1974, 71(9):3672–3676], it was later proven to be in the nuclear DNA fraction of crown-gall tumors [Proc Natl Acad Sci U S A 1980, 77(7):4060–4064]. More evidence comes from research on mesothelial cells. In 1966, Eskeland, based on silver-staining electron microscopy studies, first suggested that injured or destroyed mesothelial cells are replaced in location and function by free-floating “peritoneal macrophages,” which are transformed from their original role to that of mesothelial cells [Acta Pathol Microbiol Scand 1966, 68(3):379–395 & Acta Pathol Microbiol Scand 1966, 68(3):353–378.].

As a consequence of a pathogenic stimulus such as inflammation or wound healing, EMT can change MCs into cells with mesenchymal or epithelial characteristics [Int J Biochem Cell Biol 1997, 29(1):5–17]. Recently it was reported that the transition from one cell function to another, as well as the transition of one cell type to another seems to be a routine event rather than a rare one [BMC Cancer. 2014 May 10;14:331] AND due to the above findings within the human, animal and plant kingdom it was proposed that carcinogenesis occurs by a multistep sequence and that its last step is a transition of a normal cell into a cancer cell.

http://www.biomedcentral.com/content/pdf/1471-2407-14-331.pdf

An actual paper in PLoS ONE 2015 supports the proposal as chronic lung injury results into a transition of a normal cell into a cancer cell.

Kitamura et al.: Chronic Lung Injury by Constitutive Expression of Activation-Induced Cytidine Deaminase Leads to Focal Mucous Cell Metaplasia and Cancer. PLoS One. 2015 Feb 6;10(2):e0117986.

http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0117986

Kulvinder kochar kaur

A VERY DIFFICULT QUESTION TO ANSWER BUT IN NORMAL EMBRYOGENESIS AS YOU DISCUSSED THE ROLES OF HOW A PLACENTA NORMALLY INVADES AND ROLES OF VARIOUS ADAM/TACE FUNCTIONS, and roles of various EGF receptors MMPS etc IT IS NORMALLY SEEN THAT EVEN NO GESTATIONAL TROPHOBLASTIC DISEASE DEVELOPS AND PLACENTAL INVASION REMAINS LIMITED WITH THE USE OF PROKINETICINS and limited VEGF whatever is required but sometimes one comes across cases where ou meet gestationalchorio carcinoma and i happened to see a very interesting case of a youngunmarried girl with no history of contact presenting with a solid intrauterine tumour which kept n increasing and reached 26 weeks pregnant uterus size and MRI pictures revealed a highly invasive tumour in myometrium and with an unmarried girl whokept on bleeding profusely with markedly getting deranged immune system and repeated bouts of super infection nodiagnosiswasbeing made and ultimately ahe was kept for aTAH with BSO and although she had a transrectal biosy which showed HCG staining villi no diagnosis was made when i first saw her and decided totry to treat her as a case of nongeatational choriocarcinoma of uterine body and gave her EMA-CO therapy after treating her infections with iv antibiotics and blood transfusions and gradually her tumor shrunk and loss anchor from myometrium and she expelled a huge tumor vagially -although this was totally against conventional norms of a 26wks choriocarc8inoma with a vrty low secreting hcgand sometimes i got a negative uot and beta hcg fluctated around 1200 in contrast to lakhs in a 26 weeks ize choriocarcinoma although i tried to publish in gyneoncology nobody knew what the diagnosis fitted nto although it isa wonder i will send youall her MRIS as well asc photographs but it is a surprise how a transformationoccurs and this penetration beyond myometrium occurs and kkeeps occuring and what would lne put this into as an initiating factorbbecause this tumor was just rapidly increasing in size ad unmarried girl with intact hymen .

Joseph ( Jozsef in Hungarian) -- Molnar

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