Thursday, July 06, 2006

Preventing Cervical Cancer Deaths

10,000 women develop and nearly 4000 women die from cervical cancer each year in the U.S.. Most of the deaths are of poor and/or minority women. Pap testing (done on a regular basis) can most often catch cervical cellular changes at a pre-malignant or early malignant stage, allowing for treatment that is most often very successful. But many lack access to and/or do not avail themselves of these health maintenance services.

It is, however, always better to prevent the occurrence of a disease, than to try and catch it and then treat it before it gets “bad”.

The major cause of cervical cancer is certain “types” of HPV (Human Papillomavirus). If you can prevent infection with HPV you can prevent a large percentage of cervical cancers. Three things prevent cervical infection with HPV: 1) no genital-to-genital contact, 2) HPV vaccine (recently approved for use by the FDA), and 3) condoms. All 3 of these preventatives must be taught about, the public informed about them, and they must be used to be effective (i.e. used alone and/or in combination).

The FDA vaccine advisory panel, last week, recommended that all 11 and 12 year old girls should routinely receive the new anti-HPV vaccine. The vaccine is active against 2 types of the HPV responsible for 70% of cervical cancer cases. What a step forward in preventative medicine.

While practitioners who deal with STD care and treatment have been of the opinion that consistent and “proper” condom use prevents most STD transmission, including HPV, only recently has there been a “good” study with proven benefit (good = well done clinical control comparison trial). [Keep in mind that “proper” condom use isn’t as easy as it may seem] Published last month, the study demonstrated a 70% reduction in risk of becoming infected with HPV. There has also been recent research demonstrating condom protection from herpes, chlamydia and syphilis (again it was always “known”, but now there is better clinical proof).

Lives can be saved with widespread vaccination and consistent, “proper” condom use as disease prevention measures.

2 comments:

KM said...

Um, Dr. Keller -

The cervical cancer vaccine "Gardasil" has only confirmed immunity for 3.5 years. The cost for the 3 shot series is $360.00. So when the 12 year-old's immunity is up by the time they are 16, will they need a booster? Is a booster safe and effective? Who knows. Can you say, "Cha-Ching"?

The problem with most medical professionals is that they believe that vaccines will prevent all diseases all the time with no side effects. Since the late 80's when the HiB (Haemophilius Influenza) and Hepatitis B (also a sexually transmitted virus) were added to the childhood vaccine schedule, there has been an epidemic increase in neurodevelopmental disorders (autism, ADD), chidhood diabetes, asthma, and obesity. Of course, the health agencies, most notably the CDC and the AAP refute the claim that vaccines have anything to do with this increase. However, the CDC oversees the national vaccine program and the AAP gets millions of dollars from the vaccine industry.

There is currently an abundance of lab and clinical science linking a vaccine preservative, thimerosal, to the epidemic of autism in this country.(http://www.generationrescue.org/evidence_reports.html) Thimerosal is nearly 50% ethylmercury and infants born in the late 80's up until very recently were greatly over-exposed to this known neurotoxin (based on EPA guidelines). My own son, who was diagnosed at age three with autism spectrum disorder, is now recovering because he is being treated for mercury toxicity.

Doctor, it might be best if you'd read the science before blogging about the benefits of a vaccine, whose safety testing is sparse at best. Think of all the children and their families who wouldn't be suffering with the devestating disorder of autism had their pediatricians done the same.

Anonymous said...

http://www.virusmyth.net/aids/data/pdlatvir3.htm

The following epidemiological and biochemical arguments cast doubt on these HPV-cancer hypotheses:
1. Random allelic mutation of suppressor genes, as postulated by zur Hausen, predicts a few cancers soon, and more long after infection. Since cancers only appear 20-50 years after infection, cooperation between HPV and mutations cannot be sufficient for carcinogenesis.
2. Further, the proposal of zur Hausen that inactivation of host suppressor genes is necessary for viral transformation is not compatible with HPV survival. Since HPV, like all small DNA viruses, needs all of its 8-kb DNA for virus replication (13), suppression of one or more HPV proteins by normal cellular genes would effectively inhibit virus replication in all normal cells. Conversely, if viral transforming proteins were not suppressed by normal cells, virus-replicating wart cells should be tumorigenic because all viral genes are highly expressed in virus replication (1, 13, 191).
3. The clonality of cervical cancers rules out the Howley hypothesis.
4. The lack of a consistent HPV DNA sequence and of consistent HPV gene _expression in HPV DNA-positive tumors is inconsistent with the zur Hausen and Howley hypotheses and indicates that HPV is not necessary to maintain cervical cancer.
5. The presence of HPV in no more than 67% of age-matched women with cervical cancer (198) also indicates that HPV is not necessary for cervical cancer.
6. The hypothesis also fails to explain the presence of clonal chromosome abnormalities consistently seen in cervical cancer (16, 192-194)-except if one makes the additional odd assumption that only cells with preexisting chromosome abnormalities are transformed by HPV.
It follows that neither HPV nor HSV plays a direct role in cervical carcinomagenesis. Moreover, the HPV-cancer hypothesis offers no explanation for the absence of a reciprocal venereal male carcinoma.
Thus, detecting inactive and defective viral DNA from past infections in non-tumorigenic cells with a commercial hybridization test (Vira/Pap, Digene Diagnostics, Silver Spring, Maryland) or with the PCR (199) seems worthless as a predictor of rare carcinomas appearing decades later, in view of the "ubiquity" (191) of these viruses in women and the total lack of evidence that cervical cancer occurs in women with HPV more often than in those without. This test, at $30-150, is currently recommended for the 7 million Pap smears that appear "atypical" in the U.S. per year (Digene Diagnostics, personal communication, 1991). By contrast only 13,000 cervical cancers are observed annually in both HPV-positive and -negative women in the U.S. (197). Indeed, the test may be harmful, considering the anxiety a positive result induces in believers of the virus-cancer hypothesis.
An alternative cervical carcinoma hypothesis suggests that rare spontaneous or chemically induced chromosome abnormalities, which are consistently observed in both HPV and HSV DNA-negative and -positive cervical cancers (192-194), induce cervical cancer. For example, smoking has been identified as a cervical cancer risk (204). The controlled study of age-matched women described above suggests that 52% of the women with cervical cancer were smokers compared to only 27% of those without (198). Indeed, carcinogens may be primary inducers of abnormal cell proliferation rather than HPV or HSV. Since proliferating cells would be more susceptible to infection than resting cells, the viruses would be just indicators, rather than causes of abnormal proliferation. Activation of latent retroviruses like HTLV-I (Section III,A) (2), herpes viruses (12), and lambda phages (205) by chemical or radiation-induced cell damage and subsequent proliferation are classical examples of such indicators. Indeed, Rous first demonstrated that the virus indicates hydrocarbon-induced papillomas; it "... localized in these and urged them on ..." and suggested that enhanced proliferation is a risk factor for carcinogenesis (203).
According to this hypothesis, HPV or HSV DNAs in tumor cells reflect defective and latent viral genomes accidentally integrated into normal or hyperplastic cells, from which the tumor is derived. This hypothesis readily reconciles the clonal chromosome abnormalities with the clonal viral DNA insertions of the "viral" carcinomas. The inactive and defective viral DNA in the carcinomas would be a fossil record of a prior infection that was irrelevant to carcinogenesis.