Scientific MOOCs follower. Author of Airpocalypse, a techno-medical thriller (Out Summer 2017)

Welcome to the digital era of biology (and to this modest blog I started in early 2005).

To cure many diseases, like cancer or cystic fibrosis, we will need to target genes (mutations, for ex.), not organs! I am convinced that the future of replacement medicine (organ transplant) is genomics (the science of the human genome). In 10 years we will be replacing (modifying) genes; not organs!

Anticipating the $100 genome era and the P4™ medicine revolution. P4 Medicine (Predictive, Personalized, Preventive, & Participatory): Catalyzing a Revolution from Reactive to Proactive Medicine.

I am an early adopter of scientific MOOCs. I've earned myself four MIT digital diplomas: 7.00x, 7.28x1, 7.28.x2 and 7QBWx. Instructor of 7.00x: Eric Lander PhD.

Upcoming books: Airpocalypse, a medical thriller (action taking place in Beijing) 2017; Jesus CRISPR Superstar, a sci-fi -- French title: La Passion du CRISPR (2018).

I love Genomics. Would you rather donate your data, or... your vital organs? Imagine all the people sharing their data...

Audio files on this blog are Windows files ; if you have a Mac, you might want to use VLC ( to read them.

Concernant les fichiers son ou audio (audio files) sur ce blog : ce sont des fichiers Windows ; pour les lire sur Mac, il faut les ouvrir avec VLC (

"Rational Medicine in Cancer" - "The Secret of Life" MITx 7.00

What if we can no longer hide from... data? What if people were in charge of their own health? Should we become the risk manager of our own genome? Wouldn't that give us the Wilis, sorry, I meant to say, the willies?

National Ballet’s Giselle: Why the Wilis give you the willies

"In the United States, we see about 1.2 million new cases per year of which half of these people will go on to die from their cancer. Actually, all are going to die, but half of them are going to die from their cancer. And this accounts for, we all die, but half are dying of their cancer, and this accounts for about a quarter of deaths in the United States. This is a serious big deal. Now, when cancers begin to grow, it's a single cell. And a single cell, there-- so, I mean, first off, usually, cancers derive from a single cell. That's the first thing to be said is cancers usually-- and many things I'll say tonight are usually-- usually derive from a single cell that goes bad. And it divides and divides and divides and divides and divides, and it's lost its control of its growth. But you won't know it, because when there's two cells there or 100 cells there, it's way too tiny for you to know. You only can see a cancer in an X-ray when it's about 10 to the 8th cells. So only when you get to about 10 to the 8th cells is it detectable by radiography, for example. By imaging. When It gets to 10 to the 9th cells, you can actually feel it. It's what they say, palpable. So this is on the order of maybe one centimeter or so in diameter. By the time you've got 10 to the 12th cells, the patient is usually dead. So you have all these logs of growth that are essentially invisible, and then these logs of growth can become fatal at that point.

By the way, this indicates why it would be really good if you could detect cancers at 10 to the 4th cells and 10 to the 6th cells. And people are working on ways that they might be able to do that.

Now, these cancer, when I say they derive from a single cell, I also want to say that they arise because of mutations in the genome of a single cell. So the cancers usually arise from mutations in the genome. When you think about it, in your body from the time that you were a fertilized egg to now, you've had a total of about, well, during your lifetime, about 10 to the 16th cell divisions, give or take. That's what you've got; in your life, there's probably 10 to the 16th cell divisions, and the chance of a mutation arising in any particular gene per cell division is about 10 to the minus 6th: this is the chance of a mutation in a given gene. That varies between genes and all that, but that's a good guess. So if you had 10 to the 16th divisions and 1 in 10 to the 6th chance of mutation in a given gene per division, every gene has had mutations in it. Every gene has had mutations in it, despite the impressive fidelity of DNA replication that we talked about earlier in the course, that only one error per 10 to the 9th bases. A gene is 10 to the 3rd bases long. So that's about 1 in 10 to the 6th, and you've got 10 to the 16th divisions. That's a lot. Now, these mutations, most of them are happening during development. Some of them could happen before birth. You could have inherited some critical mutations as well. But the mutations can happen by chance, or you can accelerate your rate of mutations. (...)

Cancers usually start by random mutations in a single cell. Some mutations create a protein that fails to function properly increasing the likelihood for additional mutations. For example, if a protein in the mismatch repair pathway did not function properly, then more mutations would occur during replication. Cancers develop as a result of a variety of mutations. Although mutant forms of some proteins are found more commonly in cancers. Some mutations that occur in one cell can increase the likelihood of additional mutations occurring in the same cell." Eric Lander PhD. "Intro to Biology. The Secret of Life" MITx 7.00 MOOC.

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