Home | Community | Get Involved | Donate | | Site Index | Search Go Button
The mark, American Cancer Society, is a registered trademark of the American Cancer Society, Inc., and may not be copied, reproduced, transmitted, displayed, performed, distributed, sublicensed, altered, stored for subsequent use or otherwise used in whole or in part in any manner without ACS's prior written consent.
 
My Planner Register | Sign In Sign In


Prevention and Early Detection
 
    Prevention
    Early Detection
    Stories of Hope
    Tobacco and Cancer
    Great American Smokeout
    Food and Fitness
    Great American Health Check
    Great American Eat Right Challenge
    Environmental Carcinogens
Glossary
    I Want to Help
  You can help in the fight against cancer. Donate and volunteer. It's easy and fun!
  Learn more
   
Infectious Agents and Cancer

Since the beginning of the 20th century, we have known that some infections play a role in cancer in animals. But only recently has infection with certain viruses, bacteria, and parasites been recognized as a risk factor for several types of cancer in humans.

Worldwide, infections are linked to about 15% to 20% of cancers. In the United States and other developed countries, it is thought that fewer than 10% of all cancers are linked to infectious agents. In developing countries, infections can account for as much as 20% of all cancers.

Some infections may cause long-term inflammation, suppress a person's immune system, or directly affect a cell's DNA. Any of these pathways may lead to a higher risk of cancer.

Even though the infections described below can raise a person's risk of certain types of cancer, most people with these infections never develop cancer.

The risk of developing a cancer is also influenced by other factors. For example, infection with Helicobacter pylori (H. pylori) bacteria may increase your risk of developing stomach cancer, but what you eat, whether or not you smoke, and other factors also influence your risk.

Although the infections that influence cancer risk are usually contagious (especially viral infections), cancer itself is not a contagious disease. A healthy person cannot get cancer from someone who has the disease.

Viruses

Viruses are very small organisms -- most cannot even be seen with an ordinary microscope. They are made up of a small group of genes (in the form of DNA or RNA) surrounded by a protein coating. Viruses cannot reproduce on their own. They need to enter a living cell and "hijack" the cell's machinery to make more viruses. Some viruses do this by inserting their own DNA (or RNA) into that of the host cell. When this insertion affects the host cell's genes, it may push the cell toward becoming cancerous.

Several viruses are now known or suspected of being linked with cancer in humans. Our growing knowledge of the role of viruses as a cause of cancer may lead to vaccines that prevent or treat certain human cancers in the future.

Human papilloma viruses (HPVs)

HPVs are a group of over 100 related viruses that can cause warts on the skin, mouth, genital organs, and larynx. They are spread by contact (touch), including through sex. HPV infections are very common in people who are sexually active. There are no effective treatments for HPV other than removing or destroying cells that are known to be infected. Most genital HPV infections go away over time with the help of the body's immune system.

Certain types of HPV are the main cause of cervical cancer, which is the second most common cancer among women worldwide. It is much rarer in the United States because of the use of the Pap test. This test can detect pre-cancerous changes in cells in the cervix that might be due to HPV infection, which can then be treated, if needed. This treatment can prevent the development of cancer.

While nearly all women who develop cervical cancer shows signs of HPV infection, most women infected with HPV will not develop cervical cancer. Even though doctors can test women for HPV, there is no treatment for the HPV infection itself. If the HPV causes abnormal cells to start growing, these cells can be treated. Women with HPV infection may be checked for abnormal cells more often than those who don't have it. For more information, see the American Cancer Society document, Thinking About Testing for HPV?.

HPVs also have a role in causing some cancers of the penis, anus, vagina, and vulva. They have also been linked to cancers of the mouth, throat, head, and neck. Again, while HPVs have been linked to these cancers, most people infected with HPV never develop cancer. Smoking and drinking, which are also linked with these cancers, may work together with HPV to increase cancer risk.

Vaccines against the types of HPV that cause cancer are now under development. One of these vaccines (Gardasil®) has been shown to help protect against infection from 2 of these HPV types, and is now approved for use in females aged 9 to 26. Because it is still fairly new, it is not yet known how well it will protect against cervical cancer. Further studies of this vaccine and others like it are still under way.

Epstein-Barr virus (EBV)

EBV is another type of herpes virus. It is probably best known for causing infectious mononucleosis, also known as "mono" or the "kissing disease." In addition to kissing, it can be passed from person to person by coughing, sneezing, or sharing drinking or eating utensils. Most people in the United States are infected with EBV before the age of 20, although not everyone develops the symptoms of mono. As with other herpes viruses, the virus remains in the body throughout life, but after the first few weeks of infection most people never have any other symptoms.

EBV infects and stays in certain white blood cells in the body called B lymphocytes (also called B cells). Infection with EBV increases a person's risk of getting nasopharyngeal cancer (cancer of the area in the back of the nose) and certain types of fast-growing lymphomas such as Burkitt lymphoma. It may also be linked to Hodgkin disease and some cases of stomach cancer. These cancers are more common in Africa and parts of Southeast Asia. Overall, very few people who have been infected with EBV will ever develop these cancers.

Hepatitis B virus (HBV) and hepatitis C virus (HCV)

HBV and HCV cause viral hepatitis, a type of liver infection. While other viruses can also cause hepatitis (hepatitis A virus, for example), only HBV and HCV can cause chronic (long-term) infections that increase a person’s chance of developing liver cancer. In the United States, about 30% of liver cancers are related to HBV or HCV infection. This number is much higher in certain other countries, where both the infections and liver cancer are much more common.

HBV and HCV are spread from person to person in much the same way as HIV (see section on HIV below) -- through sharing needles, unprotected sex, or childbirth. They can also be passed on through blood transfusions, although this has rarely happened in the United States since blood products began to be tested for these viruses.

Of the 2 viruses, infection with HBV is more likely to cause symptoms, such as a flu-like illness and a yellowing of the eyes and skin (jaundice). But most people recover completely from HBV infection within a few months. Only a very small percentage go on to become chronic carriers. These people have a higher risk for liver cancer.

HCV, on the other hand, is less likely to cause symptoms. But most people with HCV develop chronic infections, which are more likely to lead to liver damage or even cancer. This means that many of the estimated 3.2 million people in the United States who have chronic HCV infection do not know they have it.

While there are few drugs effective in treating hepatitis B or C, a vaccine is available to prevent HBV infection. In the United States, the vaccine is recommended for all children and for adults who are at risk, such as healthcare workers and injection drug users. Unfortunately, there is no vaccine to prevent HCV at this time.

For more information, see the American Cancer Society Document, Liver Cancer.

Human immunodeficiency virus (HIV)

HIV, the virus that causes acquired immune deficiency syndrome (AIDS), does not appear to cause cancers directly. But HIV infection increases a person's risk of getting several types of cancer, especially some linked to other viruses such as HHV-8 (see section below) and HPV.

HIV is acquired through intimate contact with blood, vaginal secretions, breast milk, or semen from an HIV-infected person. Known routes of spread include:

  • unprotected sex (oral, vaginal, or anal) with an HIV-infected person
  • injections with needles or injection equipment previously used on an HIV-infected person
  • prenatal and perinatal (during birth) exposure of infants from mothers with HIV
  • breast-feeding by mothers with HIV
  • transfusion of blood products containing HIV (blood has been tested since 1985)
  • organ transplants from an HIV-infected person (donors are now tested for HIV)

HIV is not spread by insects, through water, or by casual contact such as talking, shaking hands, hugging, sneezing, sharing dishes, sharing a bathroom or kitchen, sharing telephones, or sharing computers.

HIV infects and destroys white blood cells known as helper T cells, which weakens the body's immune system. When the body is less able to fight off infections, other viruses such as HPV may be able to cause more damage to the cells. This damage may trigger cancer.

Many scientists believe that the immune system is also important in attacking and destroying newly formed cancers. So a weak immune system may allow new cancers to survive long enough to become a serious, life-threatening tumor.

HIV infection has been linked to a higher risk of developing of Kaposi sarcoma, invasive cervical cancer, and certain kinds of lymphoma, especially non-Hodgkin lymphoma and central nervous system lymphoma. Anti-HIV drugs may be used to reduce the risk of Kaposi sarcoma and cervical cancer.

Other forms of cancer that may be more likely to develop in people with HIV infection include:

  • invasive anal cancer
  • Hodgkin disease
  • lung cancer
  • cancer of the mouth and throat
  • cancer of the testicles
  • skin cancers, including basal cell, squamous cell, and even malignant melanomas

For more information, see the American Cancer Society document, HIV Infection and AIDS.

Human herpes virus 8 (HHV-8)

HHV-8, also known as Kaposi sarcoma-associated herpes virus (KSHV), has been found in nearly all tumors in patients with Kaposi sarcoma (KS). KS is a rare, slow-growing cancer that often appears as reddish-purple or blue-brown tumors just underneath the skin. KS has been known to exist in central Africa and the Middle East for some time, but was rare in the United States until it started appearing in patients with AIDS in the early 1980s. The number of people with KS has dropped in the United States since peaking in the early 1990s, most likely due to better treatment of HIV infection.

HHV-8 is transmitted sexually and appears to be spread by other means as well. Blood tests show less than 10% of the US population is infected with this virus. HHV-8 does not appear to cause disease in most healthy people. In the United States, almost all people who develop KS have other conditions that have affected their immune system, such as infection with the HIV or immune suppression after an organ transplant.

HHV-8 is related to other herpes viruses, such as the viruses that cause cold sores and genital herpes, Epstein-Barr virus (EBV), and cytomegalovirus (CMV). But these other viruses are not the same as HHV-8 and do not cause KS. Like other herpes virus infections, HHV-8 infections never go away, even when there are no signs of disease.

Researchers are not yet sure how HHV-8 contributes to the development of KS. Because many more people are infected with HHV-8 than ever develop the disease, it is likely that other factors are also needed for KS to develop. As mentioned above, having a weakened immune system appears to be one such factor. For more information, see the American Cancer Society document, Kaposi Sarcoma.

HHV-8 infection has been linked to some rare blood cancers, such as primary effusion lymphoma. The virus has also been found in many people with multicentric Castleman disease, an overgrowth of lymph nodes that acts very much like lymphoma. (For more information, see the American Cancer Society document, Castleman Disease.) Further study is needed to better understand the role of HHV-8 in these diseases.

Human T-lymphotrophic virus-1 (HTLV-1)

HTLV-1 has been linked with a type of lymphocytic leukemia and non-Hodgkin lymphoma called adult T-cell leukemia/lymphoma (ATL). This cancer is found mostly in southern Japan, the Caribbean, Central Africa, parts of South America, and in some immigrant groups in the southeastern United States. In addition to ATL, the virus also causes a form of degenerative nerve disease called tropical spastic paraparesis (TSP), which is most common in Japan and in the Caribbean basin.

HTLV-1 belongs to a class of viruses called retroviruses. These viruses use RNA (instead of DNA) for their genetic code. To reproduce, they must go through an extra step using an enzyme called reverse transcriptase. This allows them to change their RNA genes into DNA. Some of the new DNA genes can then become part of the chromosomes of the human cell infected by the virus. This can change the genes (cause genetic mutations) in human cells that normally control how often the cell divides. This change can sometimes cause cancer. Retroviruses have long been known to cause leukemia in some animals.

HTLV-1 is something like HIV, since it is another human retrovirus. But HTLV-1 cannot cause AIDS. In humans, HTLV-1 can be spread in the same ways as HIV:

  • unprotected sex with an HTLV-1-infected partner
  • injection with a needle or injection equipment after an infected person has used it
  • blood transfusion from an infected donor (blood donations are now tested for this virus in developed countries)
  • from infected mother to child during pregnancy, childbirth, or breastfeeding

Not everyone exposed to the virus becomes infected. For example, mothers infected with HTLV-1 have about a 10% to 30% chance of passing on the virus to their children.

A survey of people coming to donate blood in several locations around the United States showed that, overall, about 1 out of every 4,000 people had HTLV-1 (about 0.025%). Around 2% to 10% of people who use intravenous drugs or who have gotten multiple transfusions become infected with HTLV-1. Screening of all donated blood in the United States has greatly reduced the chance of infection through transfusion and has helped control the potential spread of HTLV-1 infection.

Once infected, a person's chance of developing adult T-cell lymphoma can be up to about 5%, usually after a long period with no symptoms (20 or more years).

Viruses with uncertain or unproven links to cancer in humans

Feline leukemia virus (FeLV)

FeLV causes feline leukemia, a fatal disease in American domestic cats. A vaccine to protect cats against FeLV is available, and all healthy cats can be immunized against feline leukemia. FeLV has not been known to be transmitted to humans.

Simian virus 40 (SV40)

SV40 is a virus that usually infects monkeys. Some polio vaccines prepared between 1955 and 1963, which were produced from monkey cells, were found to be contaminated with SV40.

Some recent studies have raised the possibility that infection with SV40 might increase a person's risk of developing mesothelioma (a rare cancer of the lining of the lungs or abdomen), as well as some brain cancers, bone cancers, and lymphomas.

Scientists have found that intentional infection of some lab animals, such as hamsters, with SV40 causes mesotheliomas to develop. Researchers have also noticed that SV40 can cause mouse cells grown in the lab to become cancerous, and asbestos increases the cancer-causing effect of SV40 on these cells. Other researchers have studied biopsy specimens of certain human cancers and found fragments that appear to be SV40 DNA. But not all researchers have found this, and fragments much like these can also be found in non-cancerous human tissues.

So far, the largest studies looking at this issue in humans have not found any increased risk for mesothelioma or other cancers among people who got the contaminated vaccines as children. For example, the recent increase in lung mesothelioma cases has been seen mainly in men aged 75 and older, most of whom would not have received the vaccine. Another observation is that, among the age groups who were known to have gotten the vaccine, mesothelioma rates have actually gone down. And even though women were just as likely to have had the vaccine, many more men continue to be diagnosed with mesothelioma. But the peak age range for diagnosis of mesothelioma is 50 to 70 years. Some researchers have pointed out that this issue may remain unresolved until more of the people exposed to SV40 between 1955 and 1963 get into that age range.

Recent findings have suggested that the number of people exposed to SV40 may have been underestimated in earlier studies. Some of the oral polio vaccine that was made in Eastern Europe and used throughout the world may have contained SV40 up until the late 1970s. Research into this important topic is still under way.

Bacteria

Helicobacter pylori (H. pylori)

While stomach cancer is fairly rare in the United States, it is the fourth most common cancer worldwide. Long-term infection of the stomach with H. pylori may lead to chronic inflammation and damage to the inner layer of the stomach, including ulcers. Some of these changes could lead to cancer over time, especially cancer in the lower part of the stomach. H. pylori infection is also linked with some types of lymphoma of the stomach.

More than half of all cases of stomach cancer are thought to be linked to H. pylori infection. But most people who have these bacteria in their stomachs never develop cancer.

About 1 in 3 adults has evidence of infection with H. pylori, and the rate of infection is higher in older age groups. Researchers aren't exactly sure how H. pylori may be spread from one person to another, but a likely route of spread is through a fecal-oral route, such as through contaminated water sources. In fact, contaminated well water has been linked to H. pylori infection in the United States. Because the bacteria's DNA is found in saliva, it may also be transmitted from mouth to mouth.

Other factors also play a role in whether or not someone develops stomach cancer. For example, nitrites are substances commonly found in cured meats, some drinking water, and certain vegetables. They can be converted by certain bacteria, such as H. pylori, into compounds that have been found to cause stomach cancer in animals.

Antibiotics and other medicines can be used to treat H. pylori infections. It is not yet known if people with chronic H. pylori infection of their stomach lining but no symptoms should be treated for this infection. Some doctors believe that patients with H. pylori who are at high risk of stomach cancer should be treated whether or not they have symptoms. These issues are still being studied.

Doctors have given antibiotics to patients who have had superficial stomach cancers removed in order to get rid of H. pylori infection. This seems to have prevented new stomach cancers in those patients.

Chlamydia trachomatis

Chlamydia trachomatis is a relatively common kind of bacteria that can infect the female reproductive system. It is spread by sexual contact. Although infection may cause symptoms, more than 2 out of 3 women have no symptoms. This means that most women with chlamydia do not know they are infected unless samples taken when they have a Pap test are also studied for this type of bacteria. It is very common in younger women who are sexually active, and may persist for years unless it is detected and treated.

Some studies suggest that women whose blood test results show past or current chlamydia infection are at greater risk for cervical cancer than are women with a negative blood test. Studies have not shown that chlamydia by itself can cause cancer. But it may work with HPV in some way that promotes cancer growth. One possible explanation suggested by 2 recent studies is that chlamydia may affect how long cancer-promoting HPV stays in the cervix. Researchers found that women who had chlamydia along with HPV were more likely to still have HPV when they were re-tested later than the women who had not had chlamydia. Although further studies are needed to confirm these findings, there is already good reason to avoid this infection and to have it treated with antibiotics when it is found. Long-term chlamydia infection is known to be a cause of pelvic inflammation that can lead to infertility. Like other sexually transmitted diseases that irritate or ulcerate the genital area, chlamydia can also increase the risk of becoming infected with HIV during exposure to an HIV-infected sexual partner.

Other bacteria

Chlamydia psittaci is being studied as a possible cause of cancer. It is best known for causing a mild infection sometimes known as "parrot fever" when the germ is inhaled from dried bird droppings or feather dust. (This germ is not like the type of chlamydia discussed above and is not sexually transmitted.) Two recent studies have suggested that Chlamydia psittaci bacteria may also be involved in a rare cancer of the eyes known as ocular adnexal mucosa-associated lymphoid tissue (MALT) lymphoma. In some cases, this lymphoma started to improve when the patient was given an antibiotic to treat the bacteria, but this did not happen in others. Further research is needed to learn more about the link between the bacteria and the cancer.

Other studies have suggested that infection with Borrelia burgdorferi (the bacterium that causes Lyme disease) may be linked with MALT lymphoma of the skin. And Campylobacter jejuni may be linked with MALT lymphomas of the digestive tract. Further research is needed to clarify these links.

Chlamydia pneumoniae is a type of bacteria that can cause lung infections (pneumonia). In several studies, more people with lung cancer had evidence of previous infection with this germ than those who did not have lung cancer. Even though it looks like there may be a link, these types of studies do not show that the bacteria caused the cancer. Studies are under way to explore the chance that this germ can increase the risk of lung cancer.

Parasites

Certain parasitic worms that can live inside the human body can also raise the risk of developing some kinds of cancer. While these organisms are not found in the United States, they can be a concern for people who live in or travel to other parts of the world.

Opisthorchis viverrini and Clonorchis sinensisare liver flukes (a type of flatworm) that have been linked to increased risk of developing cancer of the bile ducts (the tubes that connect the liver to the intestines). These infections come from eating raw or undercooked fish. They are found mostly in East Asia and are rare in other parts of the world.

Schistosoma haematobium is a parasite found in the water of developing countries of Africa and Asia. Infection with this parasite (an illness called schistosomiasis) has been linked to bladder cancer. Possible links to other types of cancer are now being studied as well.

Additional resources

More information from your American Cancer Society

We have selected some related information that may also be helpful to you. These materials may be ordered from our toll-free number, 1-800-ACS-2345.

National organizations and Web sites*

In addition to the American Cancer Society, other sources of patient information include:

Centers for Disease Control and Prevention (CDC)
Toll-free number: 1-800-CDC-INFO (1-800-232-4636)
Web site: www.cdc.gov

National Cancer Institute
Toll-free number: 1-800-4-CANCER (1-800-422-6237)
Web site: www.cancer.gov

*Inclusion on this list does not imply endorsement by the American Cancer Society.

No matter who you are, we can help. Contact us anytime, day or night, for information and support. Call us at 1-800-ACS-2345 or visit www.cancer.org.

References

American Cancer Society. Cancers linked to infectious disease. In: Cancer Facts & Figures 2005. Atlanta, GA: American Cancer Society; 2005.

Anttila T, Saikku P, Koskela P, et al. Serotypes of Chlamydia trachomatis and risk for development of cervical squamous cell carcinoma. JAMA. 2001;285:47-51.

Armstrong GL, Wasley A, Simard EP, et al. The Prevalence of Hepatitis C Virus Infection in the United States, 1999 through 2002. Ann Int Med 2006, 144;705-714.

Ault KA. Epidemiology and natural history of human papillomavirus infections in the female genital tract. Infect Dis Obstet Gynecol. 2006;Suppl:40470.

Bonnet F, Lewden C, May T, et al. Malignancy-related causes of death in human immunodeficiency virus-infected patients in the era of highly active antiretroviral therapy. Cancer. 2004;101:317-24.

Brown LM. Helicobacter pylori: epidemiology and routes of transmission. Epidemiol Rev. 2000;22:283-97.

Chen T, Hudnall SD. Anatomical mapping of human herpesvirus reservoirs of infection. Modern Pathology. 2006;19:726–737.

Buchschacher GL, Wong-Staal F. RNA viruses. In DeVita VT, Hellman S, Rosenberg SA, eds. Cancer: Principles and Practice of Oncology. 7th ed. Philadelphia, Pa: Lippincott Williams & Wilkins; 2005:165-173.

Cote TR, Biggar RJ, Rosenberg PS, et al. Non-Hodgkin's lymphoma among people with AIDS: incidence, presentation and public health burden. Int J Cancer. 1997;73:645-650.

Cutrone R, Lednicky J, Dunn G, et al. Some oral poliovirus vaccines were contaminated with infectious SV40 after 1961. Cancer Res. 2005;65:10273-10279.

Du MQ. MALT lymphoma : recent advances in aetiology and molecular genetics. J Clin Exp Hematop. 2007;47:31-42.

Ferreri AJ, Guidoboni M, Ponzoni M, et al. Evidence for an association between Chlamydia psittaci and ocular adnexal lymphomas. J Natl Cancer Inst. 2004;96:586-594.

Ferreri AJ, Ponzoni M, Viale E, et al. Association between Helicobacter pylori infection and MALT-type lymphoma of the ocular adnexa: clinical and therapeutic implications. Hematol Oncol. 2006;24:33-37.

Ferreri AJM, Ponzoni M, Guidoboni M, et al. Bacteria-eradicating therapy with doxycycline in ocular adnexal MALT lymphoma: a multicenter prospective trial. J Natl Cancer Inst. 2006;98:1375-1382.

Heymann DL (Ed.) Control of Communicable Diseases in Man, 18th ed. Washington DC: American Public Health Association; 2004:432-434.

Holzinger F, Z'graggen K, Buchler MW. Mechanisms of biliary carcinogenesis: a pathogenetic multi-stage cascade towards cholangiocarcinoma. Ann Oncol. 1999;10:122-126.

Howley PM, Ganem D, Kieff E. DNA Viruses. In: DeVita VT, Hellman S, Rosenberg SA, eds. Cancer: Principles and Practice of Oncology. 7th ed. Philadelphia, Pa: Lippincott Williams & Wilkins; 2005:173-184.

Husain A, Roberts D, Pro B, McLaughlin P, Esmaeli B. Meta-analyses of the association between Chlamydia psittaci and ocular adnexal lymphoma and the response of ocular adnexal lymphoma to antibiotics. Cancer. 2007;110:809-815.

Lambert PF, Sugden B. Viruses and Human Cancer. In: Abeloff MD, Armitage JO, Niederhuber JE, Kastan MB, McKenna WG, eds. Clinical Oncology. 3rd ed. Philadelphia, Pa: Elsevier Churchill Livingstone; 2004:207-225.

Littman AJ, Jackson LA, Vaughan TL. Chlamydia pneumoniae and lung cancer: epidemiologic evidence. Cancer Epidemiol Biomarkers Prev. 2005;14:773-778.

Manfredi JJ, Dong J, Liu WJ, et al. Aaronson SA. Evidence against a role for SV40 in human mesothelioma. Cancer Research.2005; 65:2602-2609.

Montaño DE, Kasprzyk D, Carlin L, Freeman C. Executive Summary Results from: HPV Provider Survey: Knowledge, Attitudes, and Practices About Genital HPV Infection and Related Conditions, 2005. Available at: www.cdc.gov/std/hpv/HPVProviderSurveyExecSum.pdf. Accessed April 25, 2008.

Mork J, Lie AK, Glattre E, et al. Human papillomavirus infection as a risk factor for squamous-cell carcinoma of the head and neck. N Engl J Med. 2001;344:1125-1131.

Nagachinta T, Duerr A, Suriyanon V, et al. Risk factors for HIV-1 transmission from HIV-seropositive male blood donors to their regular female partners in northern Thailand. AIDS. 1997;11:1765-1772.

National Cancer Institute. Simian Virus 40 and Human Cancer: Fact Sheet. Available at: www.cancer.gov/cancertopics/factsheet/simian-virs-40. Accessed April 23, 2008.

National Cancer Institute, Division of Cancer Epidemiology and Genetics, Infections and Immunoepidemiology Branch Research. Available at: http://dceg.cancer.gov/iib. Accessed April 4, 2008.

Poiesz BJ, Papsidero LD, Ehrlich G, et al. Prevalence of HTLV-I-associated T-cell lymphoma. Am J Hematol. 2001;66:32-38.

Samoff E, Koumans EH, Markowitz LE, et al. Association of Chlamydia trachomatis with persistence of high-risk types of human papillomavirus in a cohort of female adolescents. Am J Epidemiol. 2005;162:668-675.

Silins I, Ryd W, Strand A, et al. Chlamydia trachomatis infection and persistence of human papillomavirus. Int J Cancer. 2005;116:110-115.

Strickler HD, Goedert JJ, Devesa SS, et al. Trends in U.S. pleural mesothelioma incidence rates following simian virus 40 contamination of early poliovirus vaccines. J Natl Cancer Inst. 2003;95:38-45.

Talley NJ, Fock KM, Moayyedi P. Gastric Cancer Consensus Conference Recommends Helicobacter pylori Screening and Treatment in Asymptomatic Persons From High-Risk Populations to Prevent Gastric Cancer. Am J Gastroenterol. 2008;103:510-514.

Vilchez RA, Kozinetz CA, Butel JS. Conventional epidemiology and the link between SV40 and human cancers. Lancet Oncol.2003;4:188-191.

Last medical review: 05/19/2008
Last revised: 10/20/2008

Printer-Friendly Page
Email this Page
Also in this area
General Information About Carcinogens  
Radiation  
Infectious Agents and Cancer  
Air Pollution  
Chemicals  
Consumer Products  
Medical Treatments  
Related Tools & Topics
Statistics  
Not registered yet?
  Register now or see reasons to register.  
Help |  About ACS |  Employment & Volunteer Opportunities |  Legal & Privacy Information |  Press Room
Copyright 2008 © American Cancer Society, Inc.
All content and works posted on this website are owned and
copyrighted by the American Cancer Society, Inc. All rights reserved.