There are more than 100 types of HPV. About 30 or so types can cause genital infections. Some can cause genital warts; other types can cause cervical or other genital cancers.
The other 70 or so HPV types can cause infections and warts elsewhere on the body, such as on the hands. Many sexually active women and men will contract HPV at some point in their lifetime. Most will never even know it. Usually, this virus does not cause any symptoms and doesn't cause disease. Often, the body can clear HPV infection on its own within two years or less.
The title of a paper recently published by McCormack et al in Molecular Cytogenetics says it all, “Individual karyotypes at the origins of cervical carcinomas.” 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 paper neither genetic predisposition nor HPV infections are necessary for the development of cervical cancer.
All cervical cancer cells investigated during the course of this study contained new abnormal karyotypes. The clonality (genetic makeup) of these new abnormal karyotypes indicates the cervical cancers originated with these karyotypes – NOT from a virus.
Cancer-specific karyotypes explained
All cancers have individual clonal (cells descended from and genetically identical to the parent cell) karyotypes (number, size and shape of chromosomes) and thus phenotypes (expressed physical traits). No two cancers are the same. See the karyotype arrays in the paper named above and referenced at the end of this article. The karyotype determines the phenotype via thousands of messenger RNAs (about a thousand per chromosome), which in turn make thousands of proteins – at concentrations (copy numbers) that are cancer karyotype-specific – all cancer cells are individually very different from normal cells.
In this respect, cancer cells resemble a new cellular species existing within the human body, much like a parasite. The genes and proteins within cancer cells are expressed at very abnormal concentrations when compared to the normal cells surrounding them. However, since all genes and proteins expressed within cancer cells originated from human cells, cancers are not immunogenic (able to produce an immune response) – despite their huge biological differences from surrounding normal cells. This is the reason the immune system cannot “see” cancers.
The Human Papillomavirus (HPV) Causes Cervical Cancer Hypothesis
This hypothesis states that HPV encodes proteins which cause cancers as the virus replicates. Having common transforming proteins, all cervical carcinomas would be more or less the same if this were accurate. Since viral proteins are foreign to humans, viruses, virus-infected cells and possibly virus-transformed tumor cells would inevitably be immunogenic and as such eliminated by the host’s immune system within weeks to months after infection. This is the reason why HPV-induced warts are eliminated by the immune system within weeks to months after infection. This hypothesis raises four questions:
- Why would only 1 in 10,000 HPV-infected women develop cervical cancer?
- 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?
- 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?
- Why are cervical carcinomas that are presumably generated by Human Papillomavirus proteins not immunogenic and thus not eliminated by natural antibodies?
The Karyotypic Speciation Theory of Cervical Cancer Development
The McCormack et al. study, ”Individual karyotypes at the origins of cervical carcinomas” advances the theory that carcinogenesis is a form of speciation (See Duesberg et al., “Is carcinogenesis a form of speciation?” Cell Cycle 2011). According to this 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. The common function of carcinogens is the induction of aneuploidy (chromosomal disruption, either gains or losses).
By unbalancing thousands of genes aneuploidy automatically destabilizes the normal human cell karyotype and thus catalyzes random karyotypic variations. Selections of variants with proliferative phenotypes form nonclonal pre-neoplastic hyperplasias (enhanced growth of non-neoplastic cells in a tissue or an organ) with persistently varying karyotypes.
Very rare karyotypic variations form autonomous (capable of replicating without influence from surrounding host cells) new cancer species with individual clonal karyotypes. Cancer karyotypes are stabilized within narrow margins of variation by clonal selections for cancer-specific autonomy. Since this mechanism is very inefficient, it predicts long latent periods from carcinogen exposures to cancers with individual clonal cancer karyotypes. Furthermore, they discovered the individual karyotypes of each carcinoma correspond 1 to 1 to their individual phenotypes (e.g. invasiveness and resistance to chemotherapeutic drugs). This is proof-of-principle that these karyotypes determine the phenotypes of cancers – rather than the defective and latent Papilloma-virus DNAs. According to the karyotypic speciation theory, the defective viral DNAs of “HPV DNA-positive” carcinomas are functionally irrelevant, because they are not expressing any viral proteins. Instead they are non-immunogenic fossils of long past Papilloma-virus infections.
As such they are no matches for the thousands of cellular genes that are abnormally expressed in cervical carcinomas.
Karyotypic speciation theory explains paradoxes presented by the HPV causes cancer hypothesis
Why would only 1 in 10,000 HPV-infected women develop cervical cancer?
According to the karyotypic carcinoma theory this discrepancy is the result of the facts that HPV infection and carcinogenesis are two entirely independent 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. This conclusion is consistent with the fact that carcinomas with new clonal karyotypes arise only 20 to 50 years (!) after infection by HPV, which we discuss next.
Why would cervical cancers only develop 20 to 50 years after HPV infection? The karyotypic cancer theory sheds light on the presumed long latent periods from HPV infection to cancer. This huge latent period suggests evidence of two entirely unrelated 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 presumed long latent period could be a result of the low probability of forming a new autonomous cancer species from a normal somatic cell by random karyotypic rearrangements. The evolution of a new individual species of cells (cervical cancer cells) with the ability to reproduce independent of influence from surrounding human cells by random karyotypic variations of precursor cells takes time.
The very low probability of evolving a new autonomous cancer species by random karyotypic evolution explains not only the long and unpredictable time intervals between HPV infection (if it occurs) and cervical carcinomas, but aso the classical age bias of all cancers.
The age bias of cancer says that over 90% of all cancers only occur at ages over 50 years. The authors concluded 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 hyothesis?
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.
What do we do now?
Until such time as scientists can verify or disprove the Karyotypic Speciation Theory of cervical cancer development, medical comsumers must proceed with caution. This is a scientific debate which cannot be ignored. Public health authorities and medical professionals must apply the precautionary principal by suspending the use of HPV vaccines and supporting the already proven, safe and effective method of controlling cervical cancer – Pap screening. It is this method which, after its introduction 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.
There are HPV tests that can be used to screen for cervical cancer. These tests are recommended for screening only in women aged 30 years and older. They are not recommended to screen men, adolescents, or women under the age of 30 years. Most people with HPV do not know they are infected and never develop symptoms or health problems from it. Some people find out they have HPV when they get genital warts. Women may find out they have HPV when they get an abnormal Pap test result (during cervical cancer screening). Others may only find out once they've developed more serious problems from HPV, such as cancers.
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