Dna Testing in Early Cervical Cancer Detection

December 21, 2009 by admin · Comments Off 

Pap smears has been traditionally used in cervical cancer detection that look for the the presence of human papillomavirus (HPV) in cervical cells which is the cause of most cervical cancer.

In addition to the traditional Pap smears, DNA testing for HPV from cervical cells has higher significance in detecting high-grade precancerous lesions.

An early detection able to avoid cancer from spreading to other parts of body.

It is matter of life and death if high accuracy and high sensitivity precancerous lesions detection able to be performed within a short period of time. Removal of benign tumor should be done as soon as possible.

Time is gold – The faster it detects, the faster it can save one’s life.

However, DNA testing cannot be a replacement for Pap smears as it had created more false alarms that could force more woman to have further unnecessary medical workup. Few things you need to know about HPV DNA Test:1. It is only meant for woman over 30 years of age.

Women under 30 years of age will have asymptomatic infection with HPV. Woman after 30 and older have higher risk of high-grade precancerous lesions.2. Highly-sensitive and specific molecular techniques for identifying HPV DNA in cervical specimens.

HPV DNA test was found to have slightly worse specificity than Pap smears due to the improving sensitivity of the test. This has created higher false positives rate than Pap testing. 3. Women over 30 to be tested every three years if they add the HPV DNA test to their regular testing regime.

If both tests (Pap and DNA Testing) are negative, screening is not repeated for three years.

Eventually, with the advancement of DNA testing of HPV, Pap smears testing can be replaced and women will have less frequent cervical cancer screenings.

Genital Wart Treatment: What Works & What Does Not

December 21, 2009 by admin · Comments Off 


A genital wart can look like a common wart or be pink or red in color.  They can appear like a rough cauliflower like a hand wart.  These warts grow in the genital area where it is moist. Sometimes they cause burning or itching. 


In women they may appear on the vulva, anus or cervix.  In men they are often found on the penis or scrotum.  They can spread to the groin and inner thigh area in men and women.


There is no cure for HPV but it is possible to find genital wart treatment.  Sometimes Genital Warts disappear on their own, without any treatment.  Genital wart treatment involves medications and sometimes surgery.  There are prescription topical genital wart treatments which include Trichloroacetic acid, Imiquimod and Podofilox.


Surgical treatment for Genital Warts includes laser treatment, electrocautery and cryosurgery.  Laser and electrocautery works by burning off the warts and cryosurgery uses liquid nitrogen to freeze the wart.  The wart will fall off after cryosurgery.


There is an antiviral drug called Interferon which is injected into the wart. However this is not usually used as a primary treatment method. This is an expensive treatment and is usually used when warts reappear after other treatments have been used.


Once you have HPV you will always carry it even if you have no symptoms.  There is no cure.  When you are asymptomatic the virus lies dormant in your system.  The virus is transmitted sexually or by skin to skin contact.


There is an HPV vaccine called Gardisil available for young women to protect against cervical cancer and it may prevent Genital Warts.  Condoms do not protect against HPV 100 percent.  Since HPV can be caused by skin to skin contact and lesions can be on other areas besides the penis condoms cannot provide complete protection.  However, condoms should be used during sexual intercourse to prevent transmission of other sexually transmitted diseases.  Condoms can still decrease the risk of the spread of HPV.


Having an STD can be an embarrassing and sensitive issue.  Do not let this stop you from getting genital wart treatment.  It is a medical problem that can be treated.


Sometimes genital warts are so small they may go undetected by the individual.  A woman may find out she has HPV following a gynecological exam and Pap smear.


Genital wart treatments are not a cure.  Sometimes genital warts disappear on their own.  Other times they reappear after treatment.


If you are sexually active and you have genital warts, the best thing you can do is to tell your sexual partner that you carry HPV and make it a practices to use a condom when having sex. Try to abstain if you have an active wart.  If you detect a genital wart seek genital wart treatment right away.

Main Causes For Genital Warts

December 21, 2009 by admin · Comments Off 

Genital Warts is a disease which is sexually transmitted. The below mentioned article will explain Genital Warts and then highlight the main root causes of Genital Warts.
Genital warts are basically small flesh colored bumps and they appeal like small cauliflowers. In the beginning, they may appear like small lesions and they measure about 2 mms in diameter. Later they grow and expand into bigger masses. Most commonly in women they may appear both outside and inside the vagina, uterus, cervix and the area around the anus. For men, they may develop both on anus area, penis shaft and on the scrotum. If you have had oral sex with your partner, sometimes men and women also get genital warts in the throat and mouth areas if your partner has attracted this infection.
The virus causing genital warts is human papillomavirus. There are 100 HPV strains, out of which 30 can cause damage and you could catch the infection. The strains are referred to as genital HPV and at least 50% of both men and women who engage in regular sex can attract this disease.
The virus that causes genital warts is called human papillomavirus (HPV). There are around 100 strains of HPV but only 30 of these can infect the genital area. These strains are called genital HPV, which can infect about 50 percent of men and women who are sexually active.
The two varieties of HPV virus are low risk virus and high risk virus. The High risk type results in cancer of penis, throat, vagina, anus or cervix. These are different from the ones which cause genital warts. The HPV (Type 16) has a maximum potency of causing cervical cancer. As per statistics, 50% may get converted into cervical cancer cases. The other types 31, 16, 18 and 45 may result in the former one.
The lesser risk types may result in genital warts. Close to 90% of these cases occur due to types 6 and 11. There are no symptoms whatsoever and hence it becomes difficult to diagnose the disease. There are many people who are unaware that they are affected by low risk HPV. Hence, the chances of transmitting them are definitely greater. It is advised that you get regular checkups so as to eliminate any doubts.
Genital warts are transmitted through sexual intercourse. It is estimated that close to 66% of people who attract genital warts would have had sexual intercourse with an infected partner. This could be either anal sex, vaginal or even oral.
Childbirth could also bring about these problems. When the baby comes out from the uterus and gets in contact with the infected birth canal, there are chances that the infant would attract genital warts of the throat or mouth, if the mother is infected with genital warts during her delivery.
Though not scientifically proven, fomites are objects which transmit viruses from individual to individual. Make sure you avoid using toiletries and towels of people infected with genital warts. Sometimes, genital warts are also transmitted through contaminated medical equipments too.

Human Papilloma Virus â?? a Review

December 21, 2009 by admin · Comments Off 


Sameera Mohotti (BSc, MSc, MD(MA))


HPV is one of the most common sexually transmitted viral diseases. It is

estimated that 80% of sexually active adults have been infected with one or more genital HPV types at one point of their life time. The prevalence of HPV is increasing worldwide. Although it is

difficult to estimate the overall prevalence of HPV infection, it is estimated that the prevalence could be as high as 20 million (Revzina 2005). The total health care cost associated with the screening and treatment of cervical cancer in the U.S. is estimated to be $6 billion per year (Koutsky 1997). A US sero prevalence study performed by Revizina et al revealed that the highest prevalence of

HPV is among college students and women attending STD clinics Data from clinics in Australia indicate a prevalence of 4- 13% among STD clinic attendants Following initial infection, HPV establishes latent infection, from which symptomatic recurrences may develop periodically (Revzina 2005),(Armstrong 1986).

The main aim of this review was to evaluate the current literature regarding the types of HPV, symptoms and its pathogenesis.


Over 200 types of HPV have been classified on the basis of their DNA sequence homology. 85 HPV genotypes are well characterized.

HPV can be grouped as high risk HPV and low risk HPV based on their association with cancer and precursor lesions. High risk HPVâ??s have a high oncogenic potentials. This group includes serotypes 16,18,31,33, 34, 35,39,45,51,52,56,58,59,66,68. Low risk HPVâ??s have less oncogenic potentials and usually results in the formation of low grade precancerous lesions. This group includes

serotypes 6, 11, 42, 43, 44. This difference in the capacity to induce malignant transformation is due to the functional difference seen in E6 and E7 proteins of the two groups (Burd 2003; Longworth and Laimins 2004).

Although many HPV infections are sub clinical, symptomatic HPV infection typically results in lesions. Each HPV serotype infects certain parts of the body and responsible for different types of lesions. According to the current classification system (Bethesda system) of HPV lesions, there are three main groups. They are anoGenital Warts, low grade squamous intraepithelial lesions (cervical / anal intraepithelial neoplasia and mild dysplasia) and high grade squamous intraepithelial lesions (moderate and severe dysplasia).Cervical/anal/vulvar/penile carcinomas usually develop from high grade squamous intraepithelial lesions (University 2001).

Genital Warts (proliferative foci of epithelial keratinocytes infected with HPV) appear as bumps or abnormal growths in the genital area. This is one of the commonest clinically recognized disease manifestations of genital HPV. These are usually found in vulva, urethra, anus, and vagina and on the cervix. Warts are extremely contagious and they occasionally lead to cancer of the cervix in

women or cancer of the penis in men (Lacey 2005).

The presence of abnormal cells on the surface of the skin is called dysplasia.

Dysplasia is not a cancer and mild dysplasia is likely to self resolve. However, mild, moderate and severe dysplasia could be progressed in to a cancer, if not detected and treated at its early stage. Studies indicate that even adolescents with low grade squamous intraepithelial lesions and high grade squamous intraepithelial lesions are also at high risk for progression to high-grade cervical abnormalities (Wright, Pinto et al. 2004).


HPV is a nonenveloped, double stranded circular DNA virus with a diameter of 5.5 nm. The genome is approximately 8 Kb in size and encased in an icosahedral capsid which is composed of 72 capsomeres. Capsid comprises of an outer protein coat which consists of two capsid proteins, L1 (major) and L2 (minor) (Sapp, Volpers et al. 1995).

HPV genome is functionally divided in to 3 regions .They are the upstream regulatory region, early region and the late region. The upstream regulatory region involves in viral replication and also controls the transcription of some sequences in the early region. The early region of the genome encompasses 6 open reading frames (ORFâ??s) named E1, E2, E4, E5, E6 and E7. These encode proteins involved in viral replication, transcription and cellular transformation. E6 and E7 regions are responsible for the oncogenic properties of HPV. The late region encompasses two ORFâ??s and these encode L1 and L2 structural proteins which is necessary for capsid production (Sapp, Volpers et

al. 1995).


HPV gain entry into the host cells through the basal layer of the epithelium. In initial infection HPV is present as an episome. It has been proposed that HPV-6 attaches to the host cells via ?6-intergrin in the epithelium cells; where as, HPV16 and HPV 33 attach to host cells via cell surface heparin sulphate. The papilloma viral gene expressions are linked with the differentiation stages of the epithelium and virus multiplies as it progresses through the natural epithelial cell maturation (Giroglou, Florin et al. 2001).

During viral replication, the E1 gene product (E1 protein) binds to the viral origin of replication and this result in the extra chromosomal replication of the viral genome. The E2 gene product (E2 protein) down-regulates the E6 and E7 regions to allow the normal differentiation process of the cell. The capsid genes L1 and L2 synthesize the capsid protein and envelopes each episomal DNA in a protein capsid. The E4 gene product (E4 protein) is associated with the maturation and release of papilloma virus particles(Burd 2003),(Longworth and Laimins 2004).

The productive viral stage results in flat or papillary lesions. Since the papilloma virus replication goes hand in hand with the epithelial cell differentiations, as the lesions are formed the superficial and intermediate epithelial layers would contain a large amount of viral DNA. The accumulations of viral particles in the superficial epithelial layers provoke the cells to the koilocytosis cytopathic effect. This gives rise to koilocytes, in which the cellular nucleus is displaced to the side with a ‘hollow’ appearance of the cytoplasm. The virus particles are released as dying koilocytes are shed (zur Hausen 1991; Longworth and Laimins 2004).


When a person gets infected with high-risk HPV, it may take up to 20 years for the

cancer changes to appear. This persistency of HPV infection is necessary for the malignant transformation of the cells. In HPV associated benign lesions, the HPV DNA is usually located extra chromosomal where as in HPV associated cancers , the HPV DNA is usually found integrated in to host genome. Integration of high risk HPV DNA in to the host cell disrupts the E2 region. This results in the loss of normal E2 down-regulation of E6 and E7 which leads to the up-regulation of the two HPV viral oncogenes; E6 and E7.These E6 and E7 gene products has the ability to destabilize the cell growth regulatory and modify the cellular environment in which it replicates (Jan M. M. Walboomers 1999; Yoshinouchi, Hongo et al. 1999; Burd 2003).

pRB and pRb related proteins are critical components of the cell cycle as they seize the

transcription factor E2F which is necessary for the functions of the cell cycle. When E7 proteins bind to the pRB, pRB-E2F complex gets disrupted and this results in the E2F liberation. This disruption affects the normal functions of the cell. E6 viral gene product, the E6 protein, targets the immunosuppressor protein p53 (low risk HPV typeâ??s bind p53 in decreased affinity). The p53 protein prevents cells from completing the cell cycle and up-regulates genes involved in DNA repair, if it comes across any DNA damage. Another important function of the p53 protein is to instruct a cell with DNA damage to commit suicide. If the p53 function is inactivated then these damaged cells would continue to divide and accumulate mutations which would eventually lead to the formation of a tumor.

When E6 protein binds to p53, E6 associated ubiquitin ligase catalyzes ubiquitin ligase mediated p53 degradation. This destroys the tumor suppressive properties of p53 (Syrjanen 1999; Ha and Califano 2004).

The ability of E6 and E7 gene products to disrupt the cellular p53 and pRB protein functions result in, increase cell proliferation and genomic instability. Eventually the cell accumulates damaged DNA/mutations which may lead to the formation of fully transformed cancerous cells. The low risk HPVâ??s appear to be unable to integrate in to the host genome. But low risk serotypes like HPV 6, 11 may result in chromosomal instability which would lead to the accumulation of mutational events, which in turn may form fully transformed cancerous cells .In addition to the E6 and E7 protein function, methylation of viral DNA, telomere activations, humoral and immunogenic factors also contribute to the cellular transformations (Holowaty, Miller et al. 1999; Burd 2003).


Armstrong, B. K., O. V. Allen, B. A. Brennan, I. A. Fruzynski, N. H. de Klerk, E. D. Waters, J.

Machin, and M. M. Gollow (1986). “Time trends in prevalence of cervical cytological abnormality in

women attending a sexually transmitted diseases clinic and their relationship to trends in sexual

activity and specific infections.” Br J Cancer 54: 669-75.

Burd, E. M. (2003). “Human Papillomavirus and Cervical Cancer.” Clin. Microbiol. Rev. 16: 1-17.

Burd, E. M. (2003). “Human Papillomavirus and Cervical Cancer.” Clin. Microbiol. Rev. 16(1): 1-17.

Giroglou, T., L. Florin, et al. (2001). “Human Papillomavirus Infection Requires Cell Surface Heparan Sulfate.” J. Virol. 75(3): 1565-1570.

Ha, P. K. and J. A. Califano (2004). “The role of Human Papilloma Virus in oral carcinogenesis.” Crit Rev Oral Biol Med 15(4): 188-196.

Holowaty, P., A. B. Miller, et al. (1999). “Natural History of Dysplasia of the Uterine Cervix.” J. Natl. Cancer Inst. 91(3): 252-258.

Jan M. M. Walboomers, M. V. J., M. Michele Manos, F. Xavier Bosch, J. Alain Kummer, Keerti V. Shah,

Peter J. F. Snijders, Julian Peto, Chris J. L. M. Meijer, Nubia Muñoz, (1999). “Human papillomavirus is a necessary cause of invasive cervical cancer worldwide.” The Journal of Pathology 189(1): 12-19.

Koutsky, P., Laura. (1997). “Epidemiology of Genital Human Papillomavirus Infection.” The American Journal of Medicine 102: 3-8.

Lacey, C. J. N. (2005). “Therapy for genital human papillomavirus-related disease.” Journal of

Clinical Virology Supplement: Human Papillomaviruses 32(Supplement 1): 82-90.

Longworth, M. S. and L. A. Laimins (2004). “Pathogenesis of Human Papillomaviruses in Differentiating Epithelia.” Microbiol. Mol. Biol. Rev. 68(2): 362-372.

Revzina, N. V., and R. J. Diclemente (2005). “Prevalence and incidence of human papillomavirus infection in women in the USA: a systematic review.” Int J STD AIDS 16: 528-37.

Sapp, M., C. Volpers, et al. (1995). “Organization of the major and minor capsid proteins in human papillomavirus type 33 virus-like particles.” J Gen Virol 76(9): 2407-2412.

Syrjanen, S. M., and K. J. Syrjanen. (1999). “New concepts on the role of human papillomavirus in cell cycle regulation.” Ann Med 31: 175-187.

University, J. s. H. (2001). “HPV-induced Anal Dysplasia: What Do We Know and What Can We Do About It?” (Online)

Wright, J. D., A. B. Pinto, et al. (2004). “Atypical Squamous Cells of Undetermined Significance in Girls and Women .” Obstet Gynecol 103(4): 632-638.

Yoshinouchi, M., A. Hongo, et al. (1999). “Analysis by Multiplex PCR of the Physical Status of Human Papillomavirus Type 16 DNA in Cervical Cancers.” J. Clin. Microbiol. 37(11): 3514-3517.

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184: 9-13.

The Right Talk about Genital Warts

December 21, 2009 by admin · Comments Off 


First the bad news, Genital Warts are caused by the human papilloma virus, which means they are very contagious. Both men and women are at equal risk of contracting and spreading this STD. Genital Warts can be found on and inside of all the skin surfaces associated with sexual activity. They first appear as small bumps, then grow into cauliflower shaped clusters.


Being a virus, papilloma or Genital Warts are very hard to eradicate from your body. A virus is a life from witch rewrites the DNA of the infected cells to reproduce itself. The good news is that these viruses have been around as long as life has been on this planet, so other life form, as well as your own body has the natural compounds and systems to fight off and control these viruses. The trick is to turn on your immune system and feed it with what it needs to fight this virus.


Fortunately your body is a very good machine for controlling viruses, but it needs the vitamins and minerals for fuel. The healthier the choices you make the better your body can rid itself of these foreign life forces that invade it. Make no mistake your body is at war and the healthier your choices, the faster it will respond. There are natural compounds like Arbor Vitae, Potassium, Black Sulphide, Wild yellow indigo, and Nitric Acid that rev up your bodies ability to fight viruses. Especially viruses like papilloma. In addition, a good multi vitamin well help prevent the rest of your body from getting to run down as your immune system learn to fight the virus.

What does the doctor say? Take care not to damage, scratch, or pick at these warts. Inform your partner, use a condom, and practice safe sex. Wash your hands thoroughly with hot water and soap. Avoid touching them because they are so contagious you could spread them with your hand to other areas of your body.

Take action now! Your health and your partners health is at risk, not to mention the health of others you may come into contact with. This is not the end of the world. You and your partners lives will be back to normal in time, but it is a good lesson in healthy life choices.


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