Some of My Highlights from the ISSCR

Well, I’m home.  Time to sit back and think about what I can remember about what was certainly an informative conference.  Click the more button to read some summaries of some of the talks. I’ll keep adding to this as my motivation piques. 

The conference itself had some teething problems. The acoustics in the main room rendered the speakers incomprehensible, and there was no food.  By far the worst thing was the time limit imposed on the poster sessions at night.  That didn’t deter from the quality of science however, and I shouldn’t be a whino about how money was spend, since the ISSCR budget isn’t quite that of some of the larger conferences. 

One of my favorite talks was Peter Lansdorp’s discussion about whether there may be functional differences between sister chromatin that could result in asymmetric cell division.  To visualize individual sister chromatin, he utilized a clever strategy called ‘chromosome orientation FISH’ or CO-FISH.   This technique involved labeling the telomere repeats to visualize the 5′ and 3′ ends of the chromosomes, while simultaneously labeling the A rich and T rich sequences that are present near the centromere.  One strand would therefore look like this:   5’Asequence-3′, and the other one 3’tsequence-5′. He calls of  them the ‘Watson strand’ and the other the ‘Crick strand’ .  By labeling the cells with BrDU, he was then able to use Hoescht dye, UV light and endonuclease, in a way that I didn’t quite catch, to kill the newly replicated strands.  By counting the distribution of leftover Watson and Crick strands he was then able to deduce whether an asymmetric cell division had occurred.  He studied what must have been hundreds of sections from mouse intestinal epithelium of mice that were fed BrdU.  He was able to demonstrate individual examples of non-random template segregation of individual chromosome in vivo using the CO-FISH technique. Interestingly, he observed this phenomena in later replicating cells outside of the defined stem cell niche of the epithelial crypt, leading him to believe that the asymmetry may not be specific to stem cells per se.  At the moment, it seems that technical limitations are holding back the work, although tremendous progress is being made.  It would be great to see some of the stuff done in vivo to get more clear pictures. 

The question period got a bit heated when the moderator called up his scientific ‘SkeletorThomas Rando, to discuss the ‘immortal strand hypothesis’.  For those who didn’t witness, the two had back to back commentaries in Cell regarding the possible reasons for retaining a parent strand of DNA as discussed previously on this site. 

Speaking of Thomas Rando, he gave a pretty captivating talk about muscle stem cell function.  He’s shown in the past that muscle regeneration capacity decreases with age, but this doesn’t correlate with the function of the muscle satellite stem cell.  Instead, it seems to be the satellite cell microenvironment that makes the difference. He has discussed some of these factors in a recent review as well as a recent paper in Cell Stem Cell and Science.  In general, the development of the muscle satellite cells is directed towards myoblasts via transit amplifying cells.  In aged animals, however, the satellite cells tend to proliferate and become more fibroblastic. The take home message was that that extrinsic and systemic signals led to the regenerative failure of satellite cells.  Heterochronic parabiosis (the grossest of gross surgeries) was used to study the contribution of the Wnt signalling pathway to the abberant differentiation of the satellite cells.  Inhibition of the Wnt signalling using DKK-1 and SFRPs reversed the phenotype. 


To move on, Sally Temple, got people excited about the identification of a new population of adult stem cells that share similar properties with embryonic stem cells. The cells reside within the back of the retina in a place called the Retinal Pigment Epithelium. The RPE forms early on, about day 32 in human embryos, and day 9.5 in mice, and apparently sits quite dormant and minimally used during the life of the organism.  The cells were isolated from retinal epithelium from Cadavers, but she has also been able to isolate them from live patients undergoing some horrible eye surgery or something along those lines.  Interestingly, these cells had limited passages that they could undergo, but there was no correlation with age, as she checked from cells isolated from patients from 22-99 years of age.  Of course she was able to show that they expressed the regular panel of stem cell associated markers, but only by PCR, and she was able to direct them along differentiation pathways as with ES cells.   I don’t remember if she did teratoma studies, but she did do Chorioallantoic Membrane (CAM) transplants to see if masses developed that contained cells of different origins.  The masses were smaller than those of ES cells but did display a heterogenous population of cells. 

Questions arose about whether she has been able to isolate cells from patient with such diseases as retinal neuropathy. 

There were some strange things about these cells that I couldn’t wrap my mind around.  They could be isolated as adherent, and then be taken back into canonical ES spheres repeatedly, despite the massive changes that must be occurring to the cells as they are passaged in culture. 

 

Sean Morrison was quite prolific at the conference. He gave a motivational speech at the Junior Investigator meeting, was treasurer for the ISSCR, and hosted one of the breakfasts.  His talk was kind cool. In the first half of his talk he discussed the difference between the traditional model of cancer growth and the cancer stem cell (CSC) model of cancer growth. He was quick to remind everyone (to my liking) that the CSC paradigm does not explain all cancers, so what he did was isolate metastatic melanoma cells, created single cells suspensions, and was able to get those single cells to form tumours between 15-20% of the time. He concluded that the CSC model did not apply to these cells, and thus could not be over-stretched to include all cancer.  My only criticism is that he did the study using already metastatic melanomas that likely have a higher proportion of cells that have undergone the necessary changes toward a population of tumour initiating cells. 

During the second half of his talk he discussed the inverse relationship between self renewal and age. He did microarray analyses of cells to determine genes that were stem cells specific and associated  with age.  He identified only a single gene that followed a the pattern with age, HMGA2.   He showed, in a nutshell, that this gene was required for NSC self renewal, but not for the proliferation of normal cells. He studied it in the background of different knock out mice, that I didn’t write all the names down for, and showed that its involved, but is not likely the only factor. 

 

 

 

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5 Responses to “Some of My Highlights from the ISSCR”


  1. 1 Alethea June 16, 2008 at 11:11 pm

    Hey – this is the solution – if only more people would post notes for the various talks and posters! Good resumes. I’ll see if I can chip in a couple more.

    In particular for the excellent talk by Peter Lansdorp, which I agree came out high on the cool factor scale. I was scribbling intensely, but since it’s published work, I suppose I could go brush up on it. I don’t know how I missed what sounds like a fun (controversy!) Q&A session, perhaps I was ru

    I was paying particular attention to Sally’s talk, and she didn’t do the teratoma test. But I think she was planning to.

    Sean is inspiring, indeed – and a former neural crest cell researcher 🙂

  2. 2 Mr. Gunn June 16, 2008 at 11:19 pm

    That’s fascinating stuff, Rando’s work. Thanks for the heads-up.

    I think Sean’s right to issue a cautionary note, and it’s not likely that he had 15% CSCs in his suspension. However, skin seems like one of those areas where you wouldn’t expect stem cells to play a big role, since it’s constantly in turnover, unlike the liver which is also constantly exposed to damage, but doesn’t turnover as rapidly.

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  1. 1 Humans in Science » Must. Get. Sleep. End of ISSCR conference 2008. Trackback on June 17, 2008 at 6:13 am

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