This scientific debate cannot be ignored – too many lives are at stake



The Human Papillomavirus (HPV) Causes Cervical Cancer Hypothesis states that HPV encodes proteins which cause cancers as the virus replicates.

However this hypothesis raises many questions

a) Why would only 1 in 10,000 HPV-infected women develop cervical cancer?
b) Why would cervical cancers only develop 20 to 50 years after infection? – In other words, why would the virus not cause cancers when it is biochemically active and causing warts, namely before it is neutralized by natural anti-viral immunity?
c) Why are cervical carcinomas individually very distinct from each other in terms of malignancy, drug-resistance, cell histology, as originally described by Papanicolaou et al. in Science in 1952, although they are presumably caused by the same viral proteins?
d) Why are cervical carcinomas that are presumably generated by Human Papillomavirus proteins not immunogenic and thus not eliminated by natural antibodies?

Despite over 25 years of research on the HPV causes cancer hypothesis, there have been no direct answers to these questions. Until now.

In What if HPV does not cause cervical cancer?  Norma Erickson and Peter H. Duesberg, PhD discuss a paper recently published by McCormack et al in Molecular Cytogenetics, titled “Individual karyotypes at the origins of cervical carcinomas.” The authors suggest that if the findings in this paper are true, a vaccine against human papillomavirus (HPV) is extremely unlikely to protect against cervical cancer.

According to this research neither genetic predisposition nor HPV infections are necessary for the development of cervical cancer but rather individual karyotypes. The authors explain that most living things have chromosomes, or units of genetic information, in their cells, and that a karyotype is the number, size, and shape of chromosomes in any given organism. All cervical cancer cells investigated during the course of this study contained new abnormal karyotypes with the genetic makeup of these new abnormal karyotypes indicating that the cervical cancers originated with these karyotypes and not from a virus such as the Human Papilloma Virus or HPV.

All cancers have individual clonal cells which are descended from and genetically identical to the parent cell karyotypes and thus phenotypes (expressed physical traits).  No two cancers are the same. The HPV causes cervical cancer hypothesis, states that HPV encodes proteins which cause cancers as the virus replicates. But if this were so then all cervical carcinomas would be more or less the same for they would have had common transforming proteins.

According to this latest theory, karyotypic evolutions generate new cancer species from normal cells after exposure to carcinogens (e.g. cigarette smoke or X-rays) or after spontaneous mitotic accidents.

Erickson and Duesberg state that the Karyotypic speciation theory answers the questions presented by the HPV causes cancer hypothesis.

Why would only 1 in 10,000 HPV-infected women develop cervical cancer?

The authors suggest that this is because HPV infection and carcinogenesis are two different events:

No specific correlation exists between HPV and cervical carcinoma. HPV is very common, about 70 to 80% endemic in the American population.  The rest of the population is HPV-free.  The virus is typically sexually transmitted at young age.  Since cervical carcinomas occur in both HPV-positive and HPV-negative  females, there is no specific correlative evidence that HPV plays any role in causing cervical cancer. There is also no specific functional correlation between HPV-infection and carcinogenesis. As shown from the clonal karyotypes of cervical cancers, cancers originate from a major rearrangement of the karyotypes of normal cells.  Since this is true for cervical carcinomas of HPV-positive and of HPV-negative females – and is indeed true for all cancers – there is no functional evidence that HPV plays a role in the development of carcinomas.  

Why would cervical cancers only develop 20 to 50 years after HPV infection?

These events such as HPV infections and cervical cancer are two entirely difference events.

Infection with a sexually transmitted, benign Human Papillomavirus at young age, and a cervical cancer diagnosis – 90% of which occur over the age of 50. The authors conclude that the chronological discrepancies between HPV infection and carcinogenesis exclude a direct mechanism of action connecting viral infection and the development of cancer. Instead the time-dependent evolution of a new cancer-specific karyotype supports the karyotypic theory of the origin of cervical carcinomas.

Why do cervical carcinomas have individual karyotypes and phenotypes – rather than common phenotypes as predicted by the virus hypothesis?

The probability of forming the karyotype of a new autonomous cancer-species by random karyotype variations is very low and thus unlikely to ever generate the same new species twice – much again as in conventional speciation.  Thus all cancers caused by karyotypic speciation will have individual, if sometimes similar phenotypes.

Why are presumably viral cervical carcinomas not immunogenic and thus not eliminated by natural antibodies?

The karyotypic speciation theory explains why presumably viral cervical carcinomas are not immunogenic and are thus able to grow in HPV-DNA-positive people, which contain anti-HPV antibodies produced as a result of prior infection(s) by the virus.

According to the karyotypic cancer theory, carcinomas are generated de novo from cellular chromosomes, genes and proteins, which are not immunogenic in the host of origin (just like all other cancers).  By contrast, hypothetical cancer cells generated by viral proteins would be immediately eliminated by antiviral immunity.

Since cervical carcinomas have clonal carcinoma-specific karyotypes, we know they were generated via chromosomal rearrangements of thousands of normal cellular genes, which are not immunogenic.

According to the authors, fragments of inert HPV DNA found in 70 to 80% of cervical cancers (and in 70 to 80% of all women in the US) are left-overs of by-gone infections or warts that occurred 20-50 years prior to carcinogenesis.  Infections and resultant symptoms were eliminated by natural anti-HPV antibodies.

So where to now?

The authors insist that until such time as scientists can verify or disprove the Karyotypic Speciation Theory of cervical cancer development, medical consumers must proceed with caution. The precautionary principal must be followed with the suspension of the use of HPV vaccines and the continued use of the already proven, safe and effective method of controlling cervical cancer – Pap screening. The Pap smear introduced by George Papanicolaou et al. in Science in 1952, reduced the incidence of cervical cancer in the US from the most common of the 10 most common cancers of women to one that no longer belongs to this list.

This is indeed a scientific debate which cannot be ignored.






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