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Infectious causes of cancer and their detection.

Dalton-Griffin L, Kellam P - J. Biol. (2009)

Bottom Line: Molecular techniques for identifying pathogens associated with cancer continue to be developed, including one reported recently in BMC Medical Genomics.Identifying a causal infectious agent helps in understanding the biology of these cancers and can lead ultimately to the development of antimicrobial drugs and vaccines for their treatment and prevention.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Infection, University College London, Cleveland Street, London W1T 4JF, UK.

ABSTRACT
Molecular techniques for identifying pathogens associated with cancer continue to be developed, including one reported recently in BMC Medical Genomics. Identifying a causal infectious agent helps in understanding the biology of these cancers and can lead ultimately to the development of antimicrobial drugs and vaccines for their treatment and prevention.

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Related in: MedlinePlus

Infectious agents can contribute to malignant transformation by several mechanisms. These can be broadly divided into: chronic inflammation, which drives abnormal levels of cell proliferation (yellow); direct virus-induced transformation of infected cells, leading to increased cell survival (red); and immunosuppression, which allows the pathogen to evade the immune system and persist (blue). The colour coding is maintained from Figure 1. Chronic inflammation leads to the production of inflammatory cytokines as well as reactive oxygen and nitrogen oxide species (ROS and RNOS) by phagocytes at the site of infection, which can lead to DNA damage as well as cellular damage and increased cell cycling. Virus-induced transformation is caused by the actions of pathogen-encoded oncogenic proteins as well as by integration into the host genome (HPV). The transforming events outlined in this figure do not necessarily lead directly to cancer formation; for example, despite encoding similar proteins, other infectious agents do not cause cancer. The fact that some pathogens have evolved to persist without causing tumorigenesis also highlights that persistence is maybe a prerequisite for, but is on its own insufficient for, oncogenesis in humans. Immune evasion mechanisms include control of the adaptive and innate immune system, allowing avoidance of tumor surveillance. EBV, Epstein-Barr virus; HBV, human hepatitis virus B; HCV, hepatitis virus C; HIV, human immunodeficiency virus; HPV, human papillomavirus; HTLV-1, human T-lymphotropic virus 1; KSHV, Kaposi sarcoma-associated herpesvirus.
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Figure 2: Infectious agents can contribute to malignant transformation by several mechanisms. These can be broadly divided into: chronic inflammation, which drives abnormal levels of cell proliferation (yellow); direct virus-induced transformation of infected cells, leading to increased cell survival (red); and immunosuppression, which allows the pathogen to evade the immune system and persist (blue). The colour coding is maintained from Figure 1. Chronic inflammation leads to the production of inflammatory cytokines as well as reactive oxygen and nitrogen oxide species (ROS and RNOS) by phagocytes at the site of infection, which can lead to DNA damage as well as cellular damage and increased cell cycling. Virus-induced transformation is caused by the actions of pathogen-encoded oncogenic proteins as well as by integration into the host genome (HPV). The transforming events outlined in this figure do not necessarily lead directly to cancer formation; for example, despite encoding similar proteins, other infectious agents do not cause cancer. The fact that some pathogens have evolved to persist without causing tumorigenesis also highlights that persistence is maybe a prerequisite for, but is on its own insufficient for, oncogenesis in humans. Immune evasion mechanisms include control of the adaptive and innate immune system, allowing avoidance of tumor surveillance. EBV, Epstein-Barr virus; HBV, human hepatitis virus B; HCV, hepatitis virus C; HIV, human immunodeficiency virus; HPV, human papillomavirus; HTLV-1, human T-lymphotropic virus 1; KSHV, Kaposi sarcoma-associated herpesvirus.

Mentions: The major mechanisms by which infectious agents can promote and maintain tumor formation can be divided broadly into three main categories (Figure 2). The first is the induction of chronic inflammation as a result of a continuing immune response to a persistent infection. This occurs, for example, in the case of hepatitis C virus (HCV), associated with liver cancer, which continually replicates in the liver, setting up a chronic state of inflammation there. Similarly, the blood fluke Schistosoma haematobium and the Gram-negative bacterium Helicobacter pylori can both directly contribute to cancer formation through persistence within the host causing chronic inflammation [4]. H. pylori is a good example of this category, and was classified by the World Health Organization as a class 1 carcinogen in 1994. There is a high prevalence of persistent infection with H. pylori: worldwide, 75% of people are infected, with prevalence being higher in sub-Saharan Africa, where H. pylori is associated with 63.4% of all stomach cancers [1]. However, the fact that not all people infected with H. pylori develop gastric cancer clearly shows that the infectious agent is a risk factor, but that other environmental and genetic influences are involved in cancer formation.


Infectious causes of cancer and their detection.

Dalton-Griffin L, Kellam P - J. Biol. (2009)

Infectious agents can contribute to malignant transformation by several mechanisms. These can be broadly divided into: chronic inflammation, which drives abnormal levels of cell proliferation (yellow); direct virus-induced transformation of infected cells, leading to increased cell survival (red); and immunosuppression, which allows the pathogen to evade the immune system and persist (blue). The colour coding is maintained from Figure 1. Chronic inflammation leads to the production of inflammatory cytokines as well as reactive oxygen and nitrogen oxide species (ROS and RNOS) by phagocytes at the site of infection, which can lead to DNA damage as well as cellular damage and increased cell cycling. Virus-induced transformation is caused by the actions of pathogen-encoded oncogenic proteins as well as by integration into the host genome (HPV). The transforming events outlined in this figure do not necessarily lead directly to cancer formation; for example, despite encoding similar proteins, other infectious agents do not cause cancer. The fact that some pathogens have evolved to persist without causing tumorigenesis also highlights that persistence is maybe a prerequisite for, but is on its own insufficient for, oncogenesis in humans. Immune evasion mechanisms include control of the adaptive and innate immune system, allowing avoidance of tumor surveillance. EBV, Epstein-Barr virus; HBV, human hepatitis virus B; HCV, hepatitis virus C; HIV, human immunodeficiency virus; HPV, human papillomavirus; HTLV-1, human T-lymphotropic virus 1; KSHV, Kaposi sarcoma-associated herpesvirus.
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Related In: Results  -  Collection

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Figure 2: Infectious agents can contribute to malignant transformation by several mechanisms. These can be broadly divided into: chronic inflammation, which drives abnormal levels of cell proliferation (yellow); direct virus-induced transformation of infected cells, leading to increased cell survival (red); and immunosuppression, which allows the pathogen to evade the immune system and persist (blue). The colour coding is maintained from Figure 1. Chronic inflammation leads to the production of inflammatory cytokines as well as reactive oxygen and nitrogen oxide species (ROS and RNOS) by phagocytes at the site of infection, which can lead to DNA damage as well as cellular damage and increased cell cycling. Virus-induced transformation is caused by the actions of pathogen-encoded oncogenic proteins as well as by integration into the host genome (HPV). The transforming events outlined in this figure do not necessarily lead directly to cancer formation; for example, despite encoding similar proteins, other infectious agents do not cause cancer. The fact that some pathogens have evolved to persist without causing tumorigenesis also highlights that persistence is maybe a prerequisite for, but is on its own insufficient for, oncogenesis in humans. Immune evasion mechanisms include control of the adaptive and innate immune system, allowing avoidance of tumor surveillance. EBV, Epstein-Barr virus; HBV, human hepatitis virus B; HCV, hepatitis virus C; HIV, human immunodeficiency virus; HPV, human papillomavirus; HTLV-1, human T-lymphotropic virus 1; KSHV, Kaposi sarcoma-associated herpesvirus.
Mentions: The major mechanisms by which infectious agents can promote and maintain tumor formation can be divided broadly into three main categories (Figure 2). The first is the induction of chronic inflammation as a result of a continuing immune response to a persistent infection. This occurs, for example, in the case of hepatitis C virus (HCV), associated with liver cancer, which continually replicates in the liver, setting up a chronic state of inflammation there. Similarly, the blood fluke Schistosoma haematobium and the Gram-negative bacterium Helicobacter pylori can both directly contribute to cancer formation through persistence within the host causing chronic inflammation [4]. H. pylori is a good example of this category, and was classified by the World Health Organization as a class 1 carcinogen in 1994. There is a high prevalence of persistent infection with H. pylori: worldwide, 75% of people are infected, with prevalence being higher in sub-Saharan Africa, where H. pylori is associated with 63.4% of all stomach cancers [1]. However, the fact that not all people infected with H. pylori develop gastric cancer clearly shows that the infectious agent is a risk factor, but that other environmental and genetic influences are involved in cancer formation.

Bottom Line: Molecular techniques for identifying pathogens associated with cancer continue to be developed, including one reported recently in BMC Medical Genomics.Identifying a causal infectious agent helps in understanding the biology of these cancers and can lead ultimately to the development of antimicrobial drugs and vaccines for their treatment and prevention.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Infection, University College London, Cleveland Street, London W1T 4JF, UK.

ABSTRACT
Molecular techniques for identifying pathogens associated with cancer continue to be developed, including one reported recently in BMC Medical Genomics. Identifying a causal infectious agent helps in understanding the biology of these cancers and can lead ultimately to the development of antimicrobial drugs and vaccines for their treatment and prevention.

Show MeSH
Related in: MedlinePlus