Nothing is ever as simple as it fears appears. 
For instance, here's a letter I just received:

"Here are a couple of things that Merck told me: 
girls under 18 were only tracked for 18 months, 
so no they don't know the long term effects or 
the long term efficacy by my way of thinking. 
9,700 women had cervical cancer last year, 3,700 
died. Of those diagnosed, about 30% of them 
[1,100] had no known origin (cause) of the 
cervical cancer. That means they have no idea why 
these women got it and HPV was not present. Of 
the rest [2,600] some did indeed have an HPV 
causal relationship (no numbers for how many) but 
many had a causal relationship with other 
viruses. So in terms of numbers, HPV is a pretty weak case."

Now, I wouldn't go so far as the writer above who 
says that HPV is a pretty weak case. There 
clearly is SOME sort of correlation. But, and this has not yet been discussed,

1) how many people get genital warts (HPV) each 
year, and how many of those people get cervical cancer? and,

2) how many cases of cervical cancer are there 
each year among people who do not have genital warts?

Mitchel Cohen

At 07:59 AM 2/27/2007, you wrote:
>This paper suggests that Vitamin C might have a 
>therapeutic effect in treating cervical cancer, 
>although we would want to see clinical results 
>that it actually works in practice. If an 
>effective vaccine is indeed available, we would 
>have few cervical cancer cases to treat in the first place.
>On 2/27/07, Jonathan Campbell <<mailto:[log in to unmask]>[log in to unmask]> wrote:
>Biophys Res Commun 2001 (Mar 30);   282 (2):   40915
>Reddy VG, Khanna N, Singh N
>Department of Biochemistry, All India Institute 
>of Medical Sciences, New Delhi, India
>Human Papilloma Virus (HPV) is associated in 
>most instances with cervical cancer. The HPV 
>oncoproteins target P53 protein for degradation, 
>leading to deregulation of cell cycle. We 
>investigated whether stabilization of P53 in 
>cervical cancer cells, by downregulating HPV 
>transcription would restore the apoptotic 
>ability of these cells. Our findings show that 
>vitamin C downregulates the redox sensitive 
>transcription factor AP-1 and decreases one of 
>its transcription targets HPV E6, and stabilizes 
>P53. This was associated with an increase in Bax 
>and decrease in Bcl-2 and telomerase activity. 
>Accumulation of P53 and its target gene bax then 
>sensitized HeLa cells to cell-cycle arrest, cell 
>death/apoptosis induced by cisplatin, and 
>etoposide. Increasing drug sensitivity of 
>cervical carcinoma cells by stabilizing P53 
>using vitamin C is a novel approach and has potential clinical relevance.
>Michael Balter
>Contributing Correspondent, Science
><mailto:[log in to unmask]>[log in to unmask]