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Throat cancer from HPV proves treatable
Study also suggests that low incidence of HPV-positive throat cancers in blacks may explain poor survival rates
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Cancer of the throat that stems from a human papillomavirus infection responds to treatment better than throat cancer that’s triggered by other causes, researchers report online July 29 in Cancer Prevention Research.

The scientists also find that blacks are less likely than whites to have throat cancer that’s attributable to HPV, which may explain why the cancer also proved more deadly in blacks in this study.

Throat cancer, formally known as oropharyngeal cancer, includes malignancies at the base of the tongue, on the tonsils, in the back of the mouth or on the walls of the throat. The cancer has been linked to smoking and alcohol use, but it can also arise from HPV infections acquired via oral sex (SN: 5/12/07, p. 291).

In the new study, researchers analyzed two sets of people with throat cancer.

One group included 196 whites and 28 blacks participating in an ongoing international medical trial. While 66 of the white patients had HPV-positive cancer, only one of the blacks did. All received chemotherapy and radiation.

Looking at survival among these patients over more than five years, the researchers found that HPV-negative throat cancer patients had a median survival of only 20 months. Race didn’t change this data significantly.

In contrast, patients with HPV-positive throat cancer lived substantially longer. Their median survival time could not be accurately discerned because many patients were still alive when the study data were analyzed, says study coauthor Kevin Cullen, a medical oncologist at the University of Maryland Medical Center in Baltimore. This bolsters previous studies showing HPV-positive throat cancer responds well to chemotherapy and radiation.

Cullen and his colleagues decided to examine survival rates among an additional group of patients treated for throat cancer in Baltimore. They identified 124 patients who had been monitored for more than five years, including 54 blacks and 70 whites. The two racial groups had comparable disease progression and received similar treatments. But median survival time for the whites was 69 months, compared with only 25 months for the blacks.

“The better outcome of white versus black oropharyngeal cancer patients in an equal-care setting can be explained by the larger proportion of white patients with better-prognosis HPV-positive tumors,” says oncologist Otis Brawley of the American Cancer Society in Atlanta, in a perspective article accompanying the report.

Differences in sexual practices are a very plausible explanation, he says. Brawley cites a survey showing that white males and females age 15 to 19 are more likely to engage in oral sex than are their black counterparts. Blacks that age are more likely than whites to have experienced genital-to-genital sex.

As the impact of HPV status on throat cancer becomes clearer, treatment for the malignancy will change, says Maura Gillison, a medical oncologist at Ohio State University in Columbus. Patients who test positive for HPV might get by with lighter doses of chemotherapy or radiation, she says.

But those with HPV-negative throat cancers — the kind brought on by smoking and alcohol — face a stiffer challenge because they benefit less from chemo and radiation.

“We’ve got to look at HPV-negative patients to see whether they have a good surgical option,” Cullen says.

Meanwhile, vaccines that prevent cervical cancer from HPV infection may have newfound value, Gillison says. “There is considerable optimism in the medical community that these vaccines will be effective in other sites,” including the throat, she says.


Found in: Body & Brain
Comments 7
  • A casual role for Human Papilloma virus-16 for the Head and Neck Cancers word wide-and role of HPV vaccine altering the carriage rate of oropharyngeal HPV16?

    By
    Authors_:*Professor Pranab kumar Bhattacharya MD(cal), FIC path(Ind.) , Professor of Pathology, In charge of Histopathology Unit, in charge Blood Bank &VCCTC, Cytogenetics. Institute of Post Graduate Medical Education & Research, 244a AJC Bose Road, Kolkta-20, West Bengal, India; **Mr. Ritwik Bhattacharya, B.Com(cal); ***Mr. Rupak Bhattacharya BSc(Cal)MSc(JU) of 7/51 purbapalli, Sodepur Dist 24 parganas(North) Kol-110, West Bengal, India; ****Mrs Dahlia Mukherjee BA(hons), Swamiji Road, Habra N-24 parganas, W.B, India, *****Miss upasana Bhattacharya of Mahamyatala, Garia kol-86,Daughter of Prof. Bhattacharya**** Mrs. Chandrani Dutta Bsc(Zoology)****** Dr Debasis Bhattacharya Ms(cal) FRCS(Eng). Associate Professor, dept. of Surgery IPGME&R, Dr. Tarun Biswas MBBS(cal)DEmonstrator , Dr. Ananya Pal MD(PGT) Pathology Dept. Of Pathology Institute of Post Graduate Medical Education & Research, 244a AJC Bose Road, Kolkta-20, West Bengal, India


    Infection with Human Papilloma Virus (HPV) 16 and 18 mostly is well established for development of cervical cancers in pre and post menopausal women through out the world. Professor H. Zur Housen was awarded the Nobel Prize for medicine and physiology for establishing role of HPV in development of cancer in 2008 instead of HSV2. But a pathogenic role for this HPV in non ano- genital cancer has yet been unclear till days. Tobacco and alcohol is considered till day as important etiological factor for Head and Neck Squamous cell cancers(HNSCC). Epidemiological and laboratory evidences howevver now suggest this conclusion that in addition to tobacco and alcohol, HPV may be also the causative agent for the head and neck SCC. In our Institute at IPGME&R, Kolkata-20, West Bengal, India, from Pathology department the major bulk of cancer are diagnosed in the male population in any year is HNSCC and more then 95% of these sufferers gives however history of either smoking cigarette or local made Bidi or chewing Pan Parag products for long periods. These people are usually older and middle aged male. What about those young people dignosed with HNSCC? As with cervical cancer HNSCC is today a world wide public health problem with more then 9-10 lacks population per year are diagnosed by the histo Pathologists having HNSCC. High risk HPV like HPV16 orHPV18 is probably not necessary for development of HNSCC. In our laboratory, we carried a work for 2 years on Role of HPV 16 and HNSCC mostly in younger people particularly and found HPV type 16 DNA is present in primary[poorly differentiated] and in metastatic cell nucleus in high copy numbers frequently integrated and transcriptionaly active by ISH technique. We are not sure whether these findings is casual association of HPV16 with HNSCC or etiology. Researches over past several years had also shown a string and consistent association between high risk HPV and distinct subset of HNSCC . However in our study these HPV associated HNSCC are characterized clinically by their location within the laryngeal and palatal tonsil of oropharynx. Their poorly differentiated histopatholgy and their frequent occurrence in nonsmoking and young patients then in HNSCC not associated with HPV
    The proportion of HNSCC that is associated with HPV may be greater in nonsmoker. HPV positive cancer may also occur who smokes. However it is unclear before us whether elevated risk of HNSCC for contamination of HPV infection and tobacco addiction is synergistic or additive with HPV?
    Thus screening for HPV in oral cavity and development of oral PAP smear might lead to early diagnosis and treatment for HNSCC. The prevalence of oral HPV infection presently a pre-requisite for HPV associated HNSCC was around 7% in centers without cancer in the IARC study [1]
    Another possibility for prevention of HPV associated HNSCC lies in HPV vaccine as we consider. Systemic Immunization with a protective HPV16 vaccine will be highly effective no doubt in preventing persistence HPV 16 in female genital tract. It is however not known to us whether such a vaccine will also alter the carriage rate of oropharyngial HPV16 and HNSCC.

    Reference
    1] Herrero R, Castellasaguex, Pawlita M etal “ Human Paplloma Virus and Oral Cancer, The international gency for Research on Cancer-a multicenter study J. Natl .cancer Institute 2003:95:1272-83
    copy right- The copy right of the article strictly reserved to Professor Pranab Kumar Bhattacharya as per IPR copy Right Rules. Do not Infringe it
    Bapi Bapi
    Sep. 28, 2009 at 10:36am
  • I didn't see another possible source for the oxidation of iron in ancient seas - UV dissociation of water in the atmosphere. This is a process that supposedly robs Mars of it's atmospheric water. Is it a possibility here too? Before there was significant oxygen in the atmosphere, there would be no ozone layer to prevent UV light from reaching the surface.
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  • Genetic disorders are often caused by sperm DNA that has double strand breaks, copy number variations, point mutations and imprinting mutations that have to do with advancing paternal age. Men need to know about their biological clock and father babies in their 20s and very early



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    Dec. 26, 2009 at 10:26pm
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    Dec. 28, 2009 at 5:11am
  • CHOP used to be an acronym for Cyclophosphamide, drugs starting in H and O and prednisone but they changed the two middle drugs and kept the acronym (and added -R for rituxan). I had this for diffuse large B-cell lymphoma (NHL) in summer-fall 2003, after losing 20 lb of mostly muscle (down to 93 lb). I gained back 30 during and after chemo. Before starting chemo I was too weak to sit up but got progressively stronger during chemo as I regained muscle, except for periods of weakness for a copule of days after the 5 days of prednisone, which prevents muscle growth. My partner dragged me out for walks starting about a week after my first therapy, at first a slow progression to the curb and back (the porch step was a problem), then we made it to the near corner, the far corner, the nearby orchard a few houses away where I sat as he picked windfalls, eventually around the block, to the pharmacy 1/4 mile away (a 'milestone') and after four months I made it to town 1 mile away, rested at the only placeopen Christmas day
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  • Thank you administrator...
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    Jan. 14, 2010 at 7:59pm
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Suggested Reading:
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  • D'Souza G et al. 2009. Oral sexual behaviors associated with prevalent oral human papillomavirus infection. Journal of Infectious Diseases, 199: 1263–1269.
  • Zelkowitz, R. 2009. HPV casts a wider shadow. Science, 323 (Jan. 30): 580-581.
  • Seppa, N. 2007. Risk Factor: Throat cancer linked to virus spread by sex. Science News, 171 (May 12): 291.
  • Gillison, M.L. et al. 2000. Evidence for a causal association between human papillomavirus and a subset of head and neck cancers. Journal of the National Cancer Institute, 92: 709-720.
  • Gypsyamber, D. et al. 2007. Case-control study of human papillomavirus and orophyaryngeal cancer. New England Journal of Medicine, 356: 1944-1956.
  • Mork, J. et al. 2001. Human papillomavirus infection as a risk factor for squamous-cell carcinoma of the head and neck. New England Journal of Medicine, 344: 1125–1131.
  • Brawley, OW. 2009. Oropharyngeal Cancer, Race, and the Human Papillomavirus. Cancer Prevention Research, published online July 29.
    doi:10.1158/1940-6207.CAPR-09-0150
  • Gates, GJ, Sonenstein FL. 2000. Heterosexual genital sexual activity among adolescent males: 1988 and 1995. Family Planning Perspectives, 32: 295–297.
Citations & References:
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  • Settle, K. et al. 2009. Racial Survival Disparity in Head and Neck Cancer: Results from Low Prevalence of Human Papillomavirus Infection in Black Oropharyngeal Cancer Patients. Cancer Prevention Research, published online July 29.
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