??????
I guess you're talking prostrate cancer.
No need to guess: I explicitly stated ME/CFS
and prostate cancer in the quote you cited.
I think only the Hanson and Lo/Alter studies found more MLV's in CFS patients;
In ME/CFS patients, I think the following found more MLVs in patients than controls:
- Lombardi et al
- Lo/Alter
- Hanson's latest study
- A previous small-scale study (also by Hanson, I think?)
- Singh's original results (later found to be contamination, but originally higher levels in patients than controls I think)
In other studies:
- A German study into immune-compromised patients
- Silverman's original prostate cancer study
- some other prostate cancer studies (not sure how many, I think there were at least 3 PC studies in total)
I'm glad you've provoked me to list them, because that's more like 9 or 10...and there may be more I've forgotten.
Lo/Alter revoked their findings...
I haven't seen that, but it doesn't affect the argument. They still found more in patients than in controls. The statistical argument is not affected by anybody's withdrawal of the results.
I havent read the latest Hanson study but at her presentation at the Ottawa she warned about contamination in her study...
That was months ago, the study was only just published. I suggest you read the study, or even just the abstract: the conclusion does not say that the results were contamination and makes it clear that they consider the question still open.
Huber found more XMRV in the controls than CFS patients; she didn't find any XMRV in the CFS patients - it was controls - that was what sparked her search for a contaminant.
Esther has cited that, and I believe that's correct though I haven't confirmed it. I don't recall the details, my vague recollection is that she found evidence of contamination right from the start, and found higher levels of contamination than anybody else has observed, and the nature of the contamination was a known problem that Lombardi et al had controlled for...but still, I think you're right that she did initially find more in controls.
So we have one example where it was the other way round. That brings down the odds of this happening by chance to the same as flipping a coin 10 times and once it's tails. Still unlikely...I won't calculate it right now...
In the Blood Safety group Mikovits consistently found more XMRV in the controls and so did her mentor Ruscetti....In fact they found XMRV in different samples from each other and in different samples using different runs.
That particular test is rather a different matter, and yes it was a big fail. But I think it's a misrepresentation to say they found more in controls than in patients. I don't know what the percentages and sample sizes were in that case, but they were very small, and the difference was small, pretty much the same I thought, and not enough to even reach statistical significance I think. So that doesn't count towards the point I'm making, which is that
out of those studies that found a statistically significant difference between patients and controls, something like 9 out of 10 found more in patients than in controls.
I think a more pertinent way to look at this subject is look at the multitude of studies from highly respected labs that found neither XMRV in CFS patients or controls using techniques that were more far more rigorous than employed in the original study. I haven't looked at the XMRV studies in quite a while but the number of negative studies was over 40 as I remember in all sorts of disorders. Not only was XMRV never found in the ill patients it was never found even in background levels. That speaks volumes to me....
I know you find that compelling, but it's certainly not relevant to the point I'm making that lots and lots of studies found nothing at all. Singh did an excellent job in her paper of listing all the problems with the methodology of those negative studies:
http://forums.phoenixrising.me/index.php?threads/cleaning-up-after-xmrv.17517/page-2#post-267193
Specifically, she re-iterated comments made by members here: in particular, they generally only searched using PCR assays that rely on conservation of viral sequence, the limits of detection, reproducibility and precision of their assays were unknown, they didn't include enough negative controls, and none of them included positive samples from Lombardi et al. Most of them were looking specifically for the VP62 contaminant XMRV, so most of those results don't speak to the wider question of MLVs at all.
But regardless of that, no number of negative studies affects my point that of those studies that found a statistically significant difference, nearly all of them found more in patients than controls.
Hanson and Bell's paper lays this out quite clearly: they found more in patients than in controls on their first run, but then couldn't find any on subsequent runs using different techniques. They couldn't explain their first results as contamination.
O'Keefe's findings seem particularly relevant: she found that after a successful PCR run, subsequent runs were becoming contaminated in such a way that detection of MLVs was actually being inhibited by artefacts left over from the first positive run. This is a new discovery of previously unknown problems with PCR which can give false negatives.
If you remember the Singh study,. XMRV also appeared and disappeared; It took her six months to track the contamination but she finally did.
Sure, and that was one of the examples I was noting. I noted that of these anomalous results, many of which have now been withdrawn or have been concluded to be caused by contamination, nearly all of them (Huber being the sole known exception so far) found more MLVs in patients than in controls. The point is that if the explanation of this is batch contamination, and nothing systematically different about the patient samples, then one would expect that there would also be lots of cases where more was found in controls than in patients. That may perhaps have happened, but it hasn't been reported as far as I'm aware.