How Parasites Can Drive Cancer: The Mechanisms

Table of Contents

1. What the Presentation Said
2. Which Parasites the Mechanisms Apply To
3. Chronic Inflammation: The Common Thread
4. Oxidative and Nitrative DNA Damage
5. Parasite Secretions That Make Cells Divide
6. Epigenetic Change
7. Immune Suppression and Tumour Escape
8. Immune Surveillance and the “50 to 100 Cancer Cells a Day” Figure
9. When Worms Work Against Tumours
10. How the Claim Compares With the Research
11. What Is Not Known
12. Connections
13. Key Research Papers
14. Featured Videos

What the Presentation Said

The speaker, the medical director of an integrative cancer clinic, presented a slide titled around parasite-driven oncogenesis (oncogenesis means the formation of cancer). The argument ran in steps:

• Infection with parasites and other microbes promotes inflammation, and the speaker described cancer as an inflammatory disease.
• Next comes immune dysregulation: in the speaker’s words, the immune system cannot detect these parasites and other microbes, which makes a person more susceptible to tumours.
• Four mechanisms were listed: chronic inflammation, oxidative stress, immune suppression and epigenetic modulation (changes in how genes are switched on and off without changes to the DNA sequence itself).
• The speaker described parasites as “changing the terrain”, shifting epigenetic factors so that cancer genes are activated, while a suppressed immune system lets the tumour escape. Oxidative stress was said to create more mutations, and chronic inflammation to cause DNA damage.
• Later, the speaker said parasites release secretions, distort cell signals, block oxygen and “poison the terrain” where cancer forms, calling this biological sabotage. Parasites were said to settle first in the gut and liver and then migrate to other organs, including the brain.
• Near the end of the talk, the speaker said that studies have shown people produce 50 to 100 cancer cells a day, which the immune system takes care of, and suggested that heavy-metal and parasite detoxification would lower cancer risk.

The speaker did not name a study for the mechanism slide or for the 50-to-100 figure. A related slide, which the speaker said came from an online group, claimed that parasites feed on decay, metals and toxins until cells mutate; that point is covered on the page about parasites and heavy metals, and the claim that parasites carry viruses and bacteria is covered on Do Parasites Harbour Bacteria and Viruses?

Which Parasites the Mechanisms Apply To

The research on how parasites cause cancer is almost entirely about a short list of organisms. The International Agency for Research on Cancer (International Agency for Research on Cancer (IARC), the World Health Organization’s cancer agency) classes three parasites as Group 1 human carcinogens: the bladder blood fluke Schistosoma haematobium and the two Asian liver flukes Opisthorchis viverrini and Clonorchis sinensis. Malaria (Plasmodium falciparum) is classed as probably carcinogenic, acting together with Epstein-Barr virus in Burkitt lymphoma. The full list is on the page about parasites classified as cancer-causing agents.

Each of these causes a specific cancer in a specific organ:

• Schistosoma haematobium — bladder cancer, often of the squamous-cell type.
• Opisthorchis viverrini and Clonorchis sinensis — cholangiocarcinoma (bile duct cancer).
• Plasmodium falciparum, with Epstein-Barr virus — endemic Burkitt lymphoma in children.

Researchers at Mie University in Japan, who have studied DNA damage in infection-related cancers for many years, group these parasites with Helicobacter pylori (stomach cancer), hepatitis B and C viruses (liver cancer), human papillomavirus (cervical cancer) and Epstein-Barr virus (nasopharyngeal cancer) as infections that share a common route to cancer through chronic inflammation (Kawanishi and colleagues, 2016). The mechanisms below are therefore not unique to parasites. They are the mechanisms of long-lasting infection and inflammation in general, and they have been shown in detail for only a handful of parasites. Most of the common worm and protozoan infections in the world are not on the International Agency for Research on Cancer list of carcinogens.

Chronic Inflammation: The Common Thread

Inflammation is the body’s response to injury or infection: white blood cells move in, release signalling proteins (cytokines) and reactive chemicals, and the tissue repairs itself. Short bursts are protective. The problem arises when the trigger never goes away — a fluke that lives in a bile duct for years, or schistosome eggs lodged in the bladder wall.

Cancers that arise at sites of inflammation

A widely cited review in Nature summarised the evidence that many cancers arise from sites of infection, chronic irritation and inflammation. It described the tumour microenvironment — the non-cancer cells, blood vessels and signalling molecules surrounding a tumour — as largely shaped by inflammatory cells, which help tumour cells multiply, survive and spread (Coussens and Werb, 2002).

A later review of macrophages (large immune cells that engulf debris and microbes) inside tumours went further: an inflammatory component is present in most tumours, including those with no obvious inflammatory cause, and the authors described the evidence that this cancer-associated inflammation promotes tumour growth as strong (Porta and colleagues, 2007).

Inflammation as a hallmark of cancer

In their 2011 update of the “hallmarks of cancer”, the biologists Douglas Hanahan and Robert Weinberg named inflammation as one of two enabling characteristics that help tumours acquire their other abilities (the other is genome instability), and added “evading immune destruction” as an emerging hallmark (Hanahan and Weinberg, 2011).

What this means for the presentation’s point

The research supports inflammation as a major contributor to cancer. It does not show that cancer is simply an inflammatory disease, nor that the inflammation found in most tumours comes from an infection. In the reviews above, much tumour inflammation is produced by the tumour itself, whatever started it.

Oxidative and Nitrative DNA Damage

Inflamed tissue produces reactive oxygen species and reactive nitrogen species — highly reactive molecules, including nitric oxide made by an enzyme called inducible nitric oxide synthase (iNOS). These molecules can chemically damage DNA. Two markers of that damage are 8-oxodG (an oxidised form of one DNA building block) and 8-nitroguanine (a nitrated form of another). If damaged DNA is copied before it is repaired, the result can be a permanent mutation.

In hamsters infected with the liver fluke

The Syrian hamster is the standard laboratory animal for Opisthorchis viverrini. In infected hamsters, both DNA-damage markers appeared in inflammatory cells and in the lining of the bile ducts from day 7, peaked around days 21 to 30, and were still present in the bile duct lining on day 180 — even though a blood test of liver injury (alanine aminotransferase) had returned to normal. The timing of 8-nitroguanine followed the activity of iNOS (Pinlaor and colleagues, Nitric Oxide, 2004).

A companion study compared hamsters infected once, twice or three times. The more often an animal was infected, the more iNOS appeared in the bile duct lining itself and the more DNA damage accumulated there, along with a marker of cell division (proliferating cell nuclear antigen) by day 90. The authors concluded that repeated infection may take part in the start or the promotion of bile duct cancer (Pinlaor and colleagues, Carcinogenesis, 2004). Repeated infection matters because reinfection through raw fish dishes is common in endemic areas, as the liver fluke page describes.

In human tumour tissue

The same research group reports that 8-nitroguanine is strongly formed, together with iNOS, at the cancer sites of patients with Schistosoma-associated bladder cancer and Opisthorchis-associated cholangiocarcinoma, as well as in cancers linked to Helicobacter pylori, hepatitis viruses, human papillomavirus and Epstein-Barr virus. In the two parasite cancers, the damage was found in cells carrying stem-cell markers (Oct3/4 and, in bile duct tumours, CD133), which the authors propose may be where these cancers begin (Kawanishi and colleagues, 2016). An earlier review by the group reports that antibacterial, antiviral and antiparasitic drugs markedly reduced these DNA-damage markers and iNOS expression in the conditions they studied, and proposes 8-nitroguanine as a possible marker of inflammation-related cancer risk (Kawanishi and colleagues, 2006).

Much of this evidence comes from one research network. It is consistent with the wider literature on inflammation and cancer, but finding damaged DNA in a tumour shows association, not on its own that the damage started the tumour.

Parasite Secretions That Make Cells Divide

The presentation said parasites release secretions that distort cell signals. For the Asian liver fluke this has been studied directly. Adult flukes release a mixture called excretory/secretory products — proteins, small RNA molecules and tiny membrane packets (extracellular vesicles) — into the bile.

The first evidence: cells grew faster near live flukes

In a culture dish, mouse fibroblasts (connective-tissue cells) grown in a chamber below live Opisthorchis viverrini, without touching the worms, multiplied markedly faster than cells grown without parasites. The secretions switched on two proteins that push cells through the cell cycle, phosphorylated retinoblastoma protein and cyclin D1 (Thuwajit and colleagues, 2004). This was in mouse cells in culture.

A fluke version of a human growth factor

In 2009, researchers identified in the fluke’s secretions a protein closely resembling human granulin, a growth factor involved in wound healing. The fluke protein, named Ov-GRN-1, was found on the surface of bile duct cells in infected hamsters. In the laboratory it made mouse fibroblasts multiply at nanomolar (very low) concentrations, and antibodies against it blocked the secretions’ ability to make mouse fibroblasts and a human cholangiocarcinoma cell line multiply. The authors described it as the first secreted growth factor from a parasitic worm shown to drive host-cell proliferation (Smout and colleagues, 2009). Granulin is described in more detail on the liver fluke page.

How the secretions get inside human cells

Normal human bile duct cells in culture took up the fluke’s secretions through endocytosis (the cell wrapping its membrane around material to draw it in). The secretions made liver-derived cells multiply but not a colon cell line, and drove the normal bile duct cells to release the inflammatory cytokine interleukin-6. Blocking endocytosis reduced both effects (Chaiyadet and colleagues, 2015).

Newer findings

• One microRNA (a short RNA molecule that regulates genes) carried in the fluke’s extracellular vesicles was predicted to target cancer-related pathways and made two human bile duct cell lines multiply faster in culture (Tan and colleagues, 2024).
• For Clonorchis sinensis, the Chinese liver fluke, a 2025 study combined patient tumour tissue with cell experiments. Liver cancer (hepatocellular carcinoma) in infected patients showed higher levels of a protein called CD24; in culture, the fluke’s secretions raised CD24 through a gene-control protein called E2F1, increased cell multiplication, reduced cell death, and raised immune-checkpoint molecules (CTLA-4 and LAG-3) in co-cultures with blood immune cells (Lu and colleagues, 2025).

A clinical review from Thailand lists the main proposed pathways from fluke to bile duct cancer as mechanical damage to the duct lining from the worms’ feeding, immune and cellular reactions to the fluke’s antigens and secretions, fluke-induced changes in the bile duct’s bacteria, and the effects of repeated treatment; it adds that the presence of the fluke together with outside carcinogens magnifies the risk for people in endemic areas (Prueksapanich and colleagues, 2018).

The research on secretions is strongest for the liver flukes and almost entirely from cell culture and hamsters. No study was found showing that the secretions of the common intestinal worms do the same.

Epigenetic Change

Epigenetic changes alter which genes are active without changing the DNA sequence. The best-studied is DNA methylation: small chemical tags added to a gene’s control region (promoter) that can silence it. When the silenced gene is one that normally holds cell growth in check (a tumour-suppressor gene), cells can grow unchecked. The presentation described this as cancer genes being switched on; in the research it is more often protective genes being switched off.

Liver fluke bile duct cancer

A 2024 scoping review screened the literature on epigenetics in Opisthorchis-associated cholangiocarcinoma and included 81 articles, 11 of which examined the tumours themselves. It reports a predominant hypermethylation pattern (many genes with excess methylation tags) in these tumours, together with disturbance of the Wnt/β-catenin pathway, a growth-signalling route. The authors state that these findings still need validation before any clinical use (Kafle and colleagues, 2024).

Schistosoma and the bladder

In a pilot study from Ghana, researchers measured methylation of seven genes in urine from 57 adults, infected and uninfected. Methylation of two tumour-suppressor genes, RASSF1A and TIMP3, was associated with severe bladder damage on ultrasound; the two together gave an area under the curve of about 78%, a moderate ability to tell people with severe damage from those without (Zhong and colleagues, 2013). The study measured bladder damage, not cancer.

These studies show that epigenetic changes are present in parasite-associated tumours and damaged tissue. They do not establish whether the parasite causes the methylation directly or whether it follows from years of inflammation and cell turnover.

Immune Suppression and Tumour Escape

The presentation said the immune system cannot detect parasites. The research describes something different: worms do provoke immune responses, and many survive by actively turning those responses down.

How worms damp the immune response

A 2020 review from the University of Glasgow describes how helminths (parasitic worms) induce a state of reduced immune responsiveness. A central route is the expansion of regulatory T cells (Tregs), immune cells whose job is to restrain other immune cells. Worms do this directly, through secreted molecules such as a mimic of the human signalling protein TGF-β made by a mouse gut worm, and indirectly through other immune cells. Tregs help the parasite persist and, in filarial infections, also limit the damage the infection causes. The review notes that these worm-induced Tregs have been linked to suppression of allergy and autoimmune inflammation (White and colleagues, 2020). This line of research is about parasite survival, allergy and autoimmunity; it is not a study of cancer.

Immune suppression in parasite-associated tumours

Direct evidence linking parasite-driven immune suppression to cancer is limited to the liver flukes. In the 2025 Clonorchis study above, the fluke’s secretions raised immune-checkpoint molecules (brakes that tumours exploit to switch off attacking immune cells) in laboratory co-cultures (Lu and colleagues, 2025). The liver fluke page describes a patient study linking Clonorchis infection to a more immune-suppressed tumour environment and poorer response to immunotherapy.

The wider picture

Escaping immune destruction is recognised as a hallmark of cancer in general (Hanahan and Weinberg, 2011). Whether a common worm infection, by turning down immunity, makes cancers in general more likely has not been shown in people. The page on how parasites evade the immune system covers the evasion strategies themselves.

Immune Surveillance and the “50 to 100 Cancer Cells a Day” Figure

The figure

The presentation stated that studies have shown the body produces 50 to 100 cancer cells a day, which the immune system removes. This page found no primary study that measured that number. A PubMed search made for this page did not find a study that counted them. The figure circulates widely in health writing, but how many cells in a body acquire cancer-like changes each day, and how many of those the immune system clears, has not been measured directly in people.

What immune surveillance research shows

The underlying idea — that the immune system finds and destroys early cancer cells — is real and has a long history. It was proposed by Macfarlane Burnet and Lewis Thomas, then largely abandoned for lack of evidence, and revived when better experiments were done (Dunn and colleagues, 2002).

• In mice, animals lacking lymphocytes (a type of white blood cell) and the immune signal interferon-gamma developed carcinogen-induced sarcomas and spontaneous epithelial cancers more often than normal mice. Tumours that grew in normal mice were less visible to the immune system, as if the immune system had already weeded out the more visible ones (Shankaran and colleagues, 2001).
• This led to the theory of “cancer immunoediting” in three phases: elimination (the immune system destroys early cancer cells), equilibrium (cancer cells survive but are held in check), and escape (cells that can evade the immune system grow into a tumour). The authors base it on strong data from mice and on supporting, correlative data from human cancers (Dunn and colleagues, 2004).
• A 2011 review in Science stresses that the immune system plays a dual role: it can suppress tumours, but it can also promote them by selecting for cancer cells better able to survive and by creating conditions inside the tumour that help it grow (Schreiber and colleagues, 2011).

Evidence in people

A 2007 meta-analysis in The Lancet compared cancer rates in 444,172 people with human immunodeficiency virus (HIV)/acquired immunodeficiency syndrome (AIDS) and 31,977 organ-transplant recipients on immune-suppressing drugs. Both groups had significantly higher rates of 20 of 28 cancer types. Most of these were cancers with a known infectious cause — for example, liver cancer was about 5.2 times more common with human immunodeficiency virus/acquired immunodeficiency syndrome and 2.1 times more common after transplant, and Hodgkin lymphoma about 11 and 3.9 times. Most common epithelial cancers (cancers of lining tissues) did not occur at increased rates (Grulich and colleagues, 2007).

That pattern matters for the presentation’s argument. A weakened immune system in people mainly lets infection-driven cancers through, which fits the idea that immunity keeps cancer-causing infections in check. It does not fit a simple picture in which the immune system is the main thing standing between everyone and every common cancer.

When Worms Work Against Tumours

The research does not run in one direction. A 2014 review titled “The bifacial role of helminths in cancer” describes reports that some worms, and components made from them, can trigger anti-tumour immune responses, protecting against tumour formation or leading to tumour regression in experimental settings. The review covers immune, genetic, epigenetic, hormonal and metabolic changes caused by helminths that could push cancer risk either way, and notes that the functions behind this two-way influence are not well understood (Oikonomopoulou and colleagues, 2014).

The page on other suspected links between parasites and cancer covers studies in which worm infection appeared protective, and the page on Toxoplasma and brain tumours describes research using a weakened parasite as an anti-tumour tool in mice. These findings are a reminder that “parasites drive cancer” is true for a few specific infections, not a rule for parasites as a group.

How the Claim Compares With the Research

Supported

• Chronic infection and inflammation contribute to cancer. This is well established, and inflammation is recognised as an enabling characteristic of cancer (Coussens and Werb, 2002; Hanahan and Weinberg, 2011).
• For the carcinogenic flukes, oxidative and nitrative DNA damage, parasite secretions that make cells divide, epigenetic changes and immune-environment changes have all been documented, in hamsters, cell culture and human tumour tissue.
• Parasites do release secretions that alter host-cell signalling: a fluke growth factor, microRNAs and other secreted products drive cell multiplication in laboratory studies.

Supported only in part

• “Cancer is an inflammatory disease”: inflammation is present in most tumours, but published reviews describe it as one contributor among several, much of it produced by the tumour itself rather than by an infection.
• Immune suppression: worms do turn down host immunity, mainly through regulatory T cells. Evidence that this raises cancer risk exists only for the liver flukes, largely from laboratory work.
• Epigenetic change: present in fluke-associated tumours and schistosome-damaged bladders. Research more often reports protective genes silenced than cancer genes switched on, and whether the parasite causes the change directly is unknown.
• Immune surveillance: real and supported by animal studies and by the pattern of cancers in immune-suppressed people, but the research describes a two-sided process, not a simple daily clean-up.

Contradicted

• That the immune system cannot detect parasites: the published research describes immune responses to worms, which many worms then actively damp down.
• That these mechanisms apply to parasites in general: they have been shown in detail for a few organisms that cause specific cancers in specific organs. Most common parasite infections are not classed as causes of cancer, and some worm studies point the other way.

No research found

• No primary study was found for the figure of 50 to 100 cancer cells produced a day.
• No study was found showing that parasites block oxygen or “poison the terrain” as a general cancer mechanism; these phrases do not correspond to measured processes in the papers reviewed here.
• No clinical trial was found showing that parasite or heavy-metal detoxification in people without a diagnosed infection lowers cancer risk. Where research does show a benefit from treatment, it concerns diagnosed, specific infections such as liver flukes and Schistosoma in endemic areas — covered on the sibling pages.

Decisions about cancer treatment and antiparasitic medicines belong with a clinician.

What Is Not Known

• How much each mechanism contributes. In fluke-associated cancers, mechanical damage, inflammation, DNA damage, secretions, epigenetic change, bile bacteria and dietary carcinogens all appear to act together, and their relative weight in people is not known.
• Why only a minority of infected people develop cancer. Millions carry liver flukes or Schistosoma haematobium; most never develop the related cancer. Genetic, dietary and infection-intensity factors are suspected but not fully mapped.
• Whether the laboratory findings transfer to people. Much of the mechanism research comes from hamsters and cell lines; the doses of parasite secretions used in culture may not match what bile duct cells meet in the body.
• Whether clearing an infection reverses changes already made. DNA-damage markers persisted in hamster bile ducts for months, and it is not known how long epigenetic changes last after treatment.
• How many early cancer cells the human body forms and clears each day. No direct measurement exists.
• Whether the immune-damping effect of common worms changes the risk of cancers that are not caused by infection, in either direction.

Connections

• Cancer and Parasites
• Parasites Classified as Cancer-Causing Agents
• Liver Flukes and Bile Duct Cancer
• Schistosoma and Bladder Cancer
• How Parasites Evade the Immune System
• Parasites
• Clonorchis Sinensis
• Schistosoma
• Malaria
• Cancer
• Cholangiocarcinoma
• Helicobacter Pylori: Cancer Risk and Complications
• Oxidative Stress
• Inflammatory Markers
• The Immune Response (Animation)

Key Research Papers

1. Coussens LM, Werb Z. Inflammation and cancer. Nature. 2002;420(6917):860-7. PubMed PMID: 12490959
2. Porta C, Subhra Kumar B, Larghi P, et al. Tumor promotion by tumor-associated macrophages. Advances in experimental medicine and biology. 2007;604:67-86. PubMed PMID: 17695721
3. Hanahan D, Weinberg RA. Hallmarks of cancer: the next generation. Cell. 2011;144(5):646-74. PubMed PMID: 21376230
4. Kawanishi S, Ohnishi S, Ma N, et al. Nitrative and oxidative DNA damage in infection-related carcinogenesis in relation to cancer stem cells. Genes and environment. 2016;38:26. PubMed PMID: 28050219
5. Kawanishi S, Hiraku Y, Pinlaor S, et al. Oxidative and nitrative DNA damage in animals and patients with inflammatory diseases in relation to inflammation-related carcinogenesis. Biological chemistry. 2006;387(4):365-72. PubMed PMID: 16606333
6. Pinlaor S, Hiraku Y, Ma N, et al. Mechanism of NO-mediated oxidative and nitrative DNA damage in hamsters infected with Opisthorchis viverrini: a model of inflammation-mediated carcinogenesis. Nitric oxide. 2004;11(2):175-83. PubMed PMID: 15491850
7. Pinlaor S, Ma N, Hiraku Y, et al. Repeated infection with Opisthorchis viverrini induces accumulation of 8-nitroguanine and 8-oxo-7,8-dihydro-2′-deoxyguanine in the bile duct of hamsters via inducible nitric oxide synthase. Carcinogenesis. 2004;25(8):1535-42. PubMed PMID: 15059927
8. Thuwajit C, Thuwajit P, Kaewkes S, et al. Increased cell proliferation of mouse fibroblast NIH-3T3 in vitro induced by excretory/secretory product(s) from Opisthorchis viverrini. Parasitology. 2004;129(Pt 4):455-64. PubMed PMID: 15521634
9. Smout MJ, Laha T, Mulvenna J, et al. A granulin-like growth factor secreted by the carcinogenic liver fluke, Opisthorchis viverrini, promotes proliferation of host cells. PLoS pathogens. 2009;5(10):e1000611. PubMed PMID: 19816559
10. Chaiyadet S, Smout M, Johnson M, et al. Excretory/secretory products of the carcinogenic liver fluke are endocytosed by human cholangiocytes and drive cell proliferation and IL6 production. International journal for parasitology. 2015;45(12):773-81. PubMed PMID: 26187786
11. Tan S, Thanan R, Sripa B, et al. Identification and functional analysis of mitogenic miRNA of the carcinogenic liver fluke Opisthorchis viverrini. Acta tropica. 2024;256:107243. PubMed PMID: 38719083
12. Lu WM, Yan J, Liu ZJ, et al. Clonorchis sinensis-driven hepatocarcinogenesis via E2F1-CD24 transcriptional axis: mechanistic and therapeutic implications. Parasites & vectors. 2025;18(1):353. PubMed PMID: 40830893
13. Prueksapanich P, Piyachaturawat P, Aumpansub P, et al. Liver Fluke-Associated Biliary Tract Cancer. Gut and liver. 2018;12(3):236-245. PubMed PMID: 28783896
14. Kafle A, Suttiprapa S, Muhammad M, et al. Epigenetic Biomarkers and the Wnt/β-Catenin Pathway in Opisthorchis viverrini-associated Cholangiocarcinoma: A Scoping Review on Therapeutic Opportunities. PLoS neglected tropical diseases. 2024;18(9):e0012477. PubMed PMID: 39236081
15. Zhong X, Isharwal S, Naples JM, et al. Hypermethylation of genes detected in urine from Ghanaian adults with bladder pathology associated with Schistosoma haematobium infection. PloS one. 2013;8(3):e59089. PubMed PMID: 23527093
16. White MPJ, McManus CM, Maizels RM. Regulatory T-cells in helminth infection: induction, function and therapeutic potential. Immunology. 2020;160(3):248-260. PubMed PMID: 32153025
17. Oikonomopoulou K, Brinc D, Hadjisavvas A, et al. The bifacial role of helminths in cancer: involvement of immune and non-immune mechanisms. Critical reviews in clinical laboratory sciences. 2014;51(3):138-48. PubMed PMID: 24588712
18. Dunn GP, Bruce AT, Ikeda H, et al. Cancer immunoediting: from immunosurveillance to tumor escape. Nature immunology. 2002;3(11):991-8. PubMed PMID: 12407406
19. Shankaran V, Ikeda H, Bruce AT, et al. IFNgamma and lymphocytes prevent primary tumour development and shape tumour immunogenicity. Nature. 2001;410(6832):1107-11. PubMed PMID: 11323675
20. Dunn GP, Old LJ, Schreiber RD. The immunobiology of cancer immunosurveillance and immunoediting. Immunity. 2004;21(2):137-48. PubMed PMID: 15308095
21. Schreiber RD, Old LJ, Smyth MJ. Cancer immunoediting: integrating immunity’s roles in cancer suppression and promotion. Science. 2011;331(6024):1565-70. PubMed PMID: 21436444
22. Grulich AE, van Leeuwen MT, Falster MO, et al. Incidence of cancers in people with HIV/AIDS compared with immunosuppressed transplant recipients: a meta-analysis. Lancet. 2007;370(9581):59-67. PubMed PMID: 17617273

PubMed Topic Searches

1. Parasite infection and carcinogenesis mechanisms
2. Liver fluke secretions and cell proliferation
3. 8-nitroguanine and inflammation-related carcinogenesis
4. Helminths, regulatory T cells and immune suppression
5. Cancer immunosurveillance and immunoediting

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