He was an excellent patient by the description of people who know what the good ones and bad ones act like.
The implications of this statement—that “good” people do what it takes to survive cancer, and “bad” people don’t—is total BS. People survive or don’t survive cancer largely because of factors out of their control. The one thing they can do—if they have enough money, or if they live in a country that doesn’t deny health care to people who aren’t rich—is find good treatment. After that, it’s largely a matter of what type of cancer it is, and how soon after it developed that it was diagnosed and treated. The only relevant factor we know for sure is that LA let the cancer progress far further than he should have before seeking treatment. Probably because he was an athlete accustomed to denying pain or pathology. This is on the record, and indicates that in this respect, he was just damn lucky to survive (though it’s not unusual, see below).
What is upsetting is how he decided to go on an even stronger program after his diagnosis, researching HemAssist as he was lying in a hospital bed.
Do you have a link for this?
What is there to discuss about Armstrong's cancer?
Did doping cause it? Maybe, but we'll never know.
What else is there to discuss on this topic?
As I said before, if he took EPO when he returned in 2009—a question that may very well be answered at some point in the future—that has huge ramifications for his image as a spokesman to cure cancer. Beyond that, a discussion of this topic just might be considered by young riders who are considering the pros and cons of doping.
There are many examples of factors that result in a relatively small but significant increase in cancers (e.g., second-hand smoke; certain kinds of foods). It’s possible that certain PEDs are in that class. Because the effect is relatively small, it might not be at all apparent in looking at a population of riders. Obviously it would be very difficult to do a rigorous epidemiological study of them, particularly when very few of them will admit to doping, and even those that do, we don’t know exactly when, for how long, what, and how much.
There is much to indicate that Cortisone use can activate the HPC virius. It is no surprise that 4 guys on the national team at the same time Lachuga, Strock, Kieter, and Armstrong all developed HVP related issues.
In fact the cancer that Armstrong, and Lachuga, had has an 85% correlation with HPV.
This is a very interesting link, and suggests an actual mechanism that could account for some causative effect of certain PEDs on cancer. This study found, in essence, that while evidence of parvovirus infection is present in the circulation of a majority of subjects (both with and without testicular cancer), it was also found in the testis of a large majority of individuals with testicular cancer, but not in any controls. Antibody examination showed that the virus was not in the blood as a result of acute infection, IOW, it had been around for some time. In individuals who developed testicular cancer, the virus found its way into the testis.
We don’t know why, but one reasonable possibility, as RR notes, is that immunosuppression could result in inadequate neutralization of the virus, allowing it to infect the testis and possibly trigger events leading to cancer. The relationship between viruses and cancer is heavily researched now, and several cancers are known to have viral causes.
85% is persuasive for me.
The same figure appeared in another statistic in this paper:
[testicular] cancer mortality rates are now declining and the 5 year relative survival rate is now over 85 %
This paper was published in 1998, not long after LA’s bout with cancer. I guess 85% of the population has laser-like focus, Polish.
Your "percentage" doesn't factor in the possibility that if HPV started causing cancer it did so independently of the steroid mechanism.
Of course. I think RR was just noting that immunosuppression might increase the chances of a virus--already known to be present in large proportion of the population--infecting a tissue and causing cancer there.
Your "percentage" doesn't factor in the possibility that the "correlation" you identify in that one study does not match up with causation. Given that study, one could conclude that Parvovirus B-19 is caused by cancer or its treatment as easily as you can conclude that B-19 causes cancer. In fact, that increased risk is discussed in at least one article (by Sung-Hsin Kuo in the Journal of Clinical Microbiology). The velonews article you quote says that human parvovirus is "usually benign."
No, the fact that controls have just as great a seroprevalence of the virus is evidence that the virus is not "caused by cancer". You could argue that cancer began from an independent mechanism, and the cancerous tissue in some manner made it possible for the virus to infect it. But given the strong evidence that viruses can have a causative role in cancers, that would probably be considered by most researchers as less likely.
The authors raise both possibilities in their conclusions, though emphasizing the notion that the virus could have caused the cancer:
In conclusion, we believe that parvovirus B19 might play some role, direct or indirect, in the aetiology or development of testicular GCT based on our findings, i.e. the presence of parvovirus B19 DNA sequences in the majority of GCT investigated, the absence of B19 in non-tumour testis and, with the exception of one patient, the absence of acute B19 infection at the time of the surgery. Alternatively, B19 may infect the tumour tissue.
Yes, the virus usually is benign, as are many viruses known to cause cancer. The question is why or how it becomes malignant, and immunosuppression is a very real possibility.
Your "percentage" is based on a study that involved only 39 patients. From that one study, one cannot reasonably conclude that there is an 85% chance of anything regarding Lance Armstrong.
We certainly can't conclude that drug-induced immunosuppression was a cause of LA's cancer, agreed. As I said before, the value and interest of RR's links is that it suggests a possible connection between certain PEDs and cancer, which ought to be of general interest in this forum regardless of whether it's relevant to LA's cancer. And again, if LA was shown to take one of these drugs at a time when evidence for this connection was known, shame on him. The article RR cited was published in 1998. It would be interesting to know if LA's doctors knew about this work, given that his TUE for cortisone was at about the same time.
Bottom line: No one is saying this work proves anything, for anyone let alone LA. But I find it very relevant to this thread.
http://www.ncbi.nlm.nih.gov/pubmed/18539403
http://www.ncbi.nlm.nih.gov/pubmed/12185288
http://www.ncbi.nlm.nih.gov/pubmed/10748869
Some studies since have found an association of the virus with germ cell tumors, though in a lower proportion of subjects. AFAIK, whether the virus precedes the tumor or vice-versa has not yet been settled. The second of the three studies linked above concludes that the tumor comes first, followed by infection of the virus. But as I understand it, they came to this conclusion by showing there was no difference in seropositivity (virus infection in the bloodstream) between controls and individuals with cancer. This does not speak to the possibility that some individuals in the cancer group might have had different environmental circumstances--such as exposure to immunosuppressive agents--that would increase the likelihood of any virus present going to the testis and causing cancer. As far as I can see, these authors and others are assuming that if the virus causes cancer, the initial infection should be more prevalent in those who get the cancer. This is not necessarily the case if other circumstances are necessary for the virus to act.