Why did Stefan Molyneux develop cancer

A cancer that heals itself: identifying the responsible gene

Extremely rare, but very real: a certain type of skin cancer heals spontaneously without any treatment. Its genetic origins have just been identified, which could help research discover new cancer therapies.

Some skin cancers, very rarely, can heal spontaneously. © XenonR, Wikimedia, CC by-sa 2.0

Unetumeur, which is often synonymous with the beginning of a long battle against cancer, is based on surgery, chemotherapy, deradiotherapy ... That is why the idea of ​​a cancer that cures by itself is at least original. but it does exist! It is a very rare skin cancer known as Ferguson-Smith keratoacanthoma, or spontaneously healing multiple squamous epithelioma (MSSE).

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Characterized by the sudden appearance of a tumor in the skin, this canker sore is made up of keratinizing squamous cells that cause the top layers of the epidermis to form. It usually appears on the head, usually in childhood or adolescence, or even in young adults. When it gradually heals and leaves more or less visible scars, new tumors appear regularly.

Somewhere on chromosome 9 ...

This cancer was already known to be genetic, dominant. Carried by lechromosom9, the leader had not yet been identified before the work of an international team of researchers. Scientists at the Singapore Institute of Medical Biology, the University of Dundee in the UK and the University of California Los Angeles in the US have now linked the disease to mutations in the TGFBR1 protein.

The cellular TGFBR1 receptor interacts with a TGFβ molecule dimer through its association with another receptor, TGFBR2 (a). Mutations prevent this interaction or signal transmission from functioning properly (b). © Natural Genetics

This is a surface cell receptor that is involved in the transmission of the signal given by TGFβ-type hormones ("growth factor"). The interaction of the two proteins causes a number of modifications within the cell, which result in the regulation of cell growth, cell proliferation and differentiation, and apoptosis or programmed cell death. It is therefore a kind of controller to avoid any drift that can lead to the formation of tumors.

Eleven mutations on the same gene.

It is the 24200 base pair sequencing around delocalchromosomal previously identified as associated with the disease, showing the presence of 11 different mutations in the TGFBR1 gene, among 18 families affected by the disease, according to the article published in the Nature Genetics review. Identified, punctual mutations (which lead, for example, to the coding of a leclinin prolin) or deletions (which lead to the disappearance of several amino acids) lie in the regions of the gene which code for the domain of interaction with the hormone or in the kinase domain that it intends around the signal to transmit in the cell.

Under these conditions, cellular regulation is undermined as the TGF & bgr; -Hormone can no longer play its role of control ... which explains the abnormal proliferation of cells. In addition, it is already known that the dysfunction of this cellular receptor is the first genetic cause for the development of colorectal decancers. But if cell proliferation is taking place, why does the phenomenon stop spontaneously?

At this point, scientists are still struggling to find an answer. However, the discovery of the molecular origin of the tumor is already a breakthrough in itself that can help Saguérison understand. Although the disease affects only a handful of people around the world, the discovery of new information on cancer mechanisms may pave the way for the development of treatments that target a larger group of cancer patients.