Also, it’s worth noting that, whereas ips and SCNT are not yet ready for the widespread clinical use, this might not always stay so, and hence one day it might well provide an option to perform autologous HSC transplants in patients in which it would have been very difficult or impossible otherwise.

I’ve read more than 1-2 article (I cited here only 3) and I am familiar with Dr. Zavazava’s (PlosONE) paper and induction of immune tolerance by ES-derivates. I don’t think used any false logic. When I wrote about possible mutations I wrote “increased risk of mutation with increased expansion”.

Also I didn’t make any claims that expansion of CD34+ cells is robust and it’s a clinical standard. I pointed out instead that it’s on the way to clinic because there are many clinical trials going on last 5 years and right now and next 2-3 years more likely we will get an approved clinical-grade expansion protocol for BMT patients.

Double unit cord blood transplantation works very well in clinic right now, but nobody has gotten close to the mechanism of how samples compete for engraftment yet - that’s true. Also, except expansion, we have mobilization technique and intra-bone BMT. More of that, pharmacological methods of increasing engraftment on the way.

About “Nobel comittee” - everything that I said in the post is based on published or reported findings and I can link to them. In particular about this technology you can see the lecture of Irv Weissman (min. 11-13). So notify the Nobel comittee about him, I think Weissman is worth it.

So, overall I still think that improving technologies for somatic HSC transplantation have a better chance of success than hES-derivates in clinical settings.

Also I have to notice, that after I posted this article, I didn’t get any feedback and replies that I wanted, there was NO discussion here. I guess that physicians and scientists mostly don’t care (or are too busy to care) about whatever blog posts and maybe nobody is taking it very seriously. That’s why for me being a little bit provocative is one of the ways to facilitate discussion. I even linked my post to some prominent scientists in the field via email and i got some replies, but they didn’t go to the blog.

I hope you can tell us about your findings or give us some links which confute my thoughts and we can get close to the point of discussion.

Finally, I want to note that you can be as critical as you would like to, but be respectful to the author in your comment.

First, the differences seen between somatic and ESC-derived HSC are interesting on many levels, and provide mechanistic development models for the blood cell lineage specification. With the recent developments in iPS cell generation, ES-HSC issues become even more important as scientists apply lineage specification to iPS cells from patients with diseases in order to study the disease etiology. Discoveries made while examining the inefficient ESC-HSC transition will be applicable to iPS cell differentiation as well as onset of malignancy. I’d say those are worthwhile reason for “why do we need to make HSCs from ES cells?”

As to your second point, you should have read more than one paper from Bhatia, or Zavazava in PlosOne, or countless other papers detailing induction of immune tolerance by cells derived from ESC, a result confirmed in mouse, rat, sheep, and human Bhatia specifically details the immune-privilege of ESC-derived HSC. Further, application of the technology to iPS cells would result in perfectly donor-matched transplant cells, thus obviating concern for immune tolerance.

To false logic, you maintain that cell division=mutation=cancer, yet your own body is replenishing your gut, skin, and yes, even your very own blood cells from a pool of stem cells in each system that expand thousands of fold during your lifetime. Wow, that mitosis sure does work well.

Finally, to plain old misinformation, CD34 expansion in vitro is NOT robust, and is NOT the clinical standard for transplantation; in EVERY case, donors will be mobilized multiple times versus ex vivo expansion. Additionally, cord blood does not yield adequate CD34 cells for transplantation of anyone past a few months old. The only successful clinically-relevant results to date have been with work using mixed-cord transplants, which face the same immunological difficulties that you don’t understand very well. And finally, I’m sure researchers will be thrilled to hear that you ‘know or can develop some technologies of separating malignant cells in bone marrow from healthy HSC, so adult transplant could be autologous.’

I’ll notify the Nobel committee and start enrolling patients in your trial.

Edinburgh experts used blood stem cells from mice to mimic how humans produce the stem cells and found they were able to multiply them by 150 times.

Would you inject yourself cells that you expanded in petridish for 150 times?? I won’t!

We need expand cord blood HSC only 2-3 times from one sample to make patients happy and it’s already work in clinic!

I’d agree with Dr. Medvinsky - it’s very long way to go. I’d add: so long, better concentrate to another - real things…

Here, we demonstrate that despite expressing functional Notch-1, CD34+ cells from hESCs did not derive T cells when co-cultured with OP9 cells expressing Delta-like 1, or in fetal thymus organ culture. hESC-derived CD34+ cells also did not produce B cells in vitro. In contrast, CD34+ cells isolated from UCB routinely generated T and B cells when cultured in the same conditions.
Together, these results demonstrate fundamental differences between hESC-derived hematopoietic progenitors and analogous primary human cells.