Carcinogenic bacteria

Source: Wikipedia, the free encyclopedia.
Bacteria involved in causing and treating cancers

Cancer bacteria are bacteria infectious organisms that are known or suspected to cause cancer.[1] While cancer-associated bacteria have long been considered to be opportunistic (i.e., infecting healthy tissues after cancer has already established itself), there is some evidence that bacteria may be directly carcinogenic. Evidence has shown that a specific stage in cancer can be associated with bacteria that is pathogenic.[2] The strongest evidence to date involves the bacterium H. pylori and its role in gastric cancer.[1]

Oncoviruses are viral agents that are similarly suspected of causing cancer.

Known to cause cancer

CagA has been implicated in carcinogenesis.[7] Another bacteria that is in this genus is Helicobacter hepaticus, which causes hepatitis and liver cancer in mice.[8]

Chronic inflammation

Chronic inflammation contributes to the pathogenesis of several types of malignant diseases, but it is particularly important for H. pylori.[9] Following a H. pylori infection many circulating immune cells are recruited to the infection site including neutrophils. [10] To destroy the pathogens neutrophils, produce substances with antimicrobial activities such as oxidants like reactive oxygen species (ROS) and reactive nitrogen species (RNS).[11] H. pylori can survive the induced oxidative stress by producing antioxidant enzymes such as e.g., catalase.[12] However, the overproduction of ROS and RNS induces various types of DNA damage in the infected gastric cells.[12]At the same time H. pylori is known to down-regulate major DNA repair pathways.[13] As a result, genomic and mitochondrial mutations accumulate, leading to genomic instability - a well-known Hallmark of Cancer [14] - in the gastric cells.[13]

CagA

The virulence factor

CagA in H. pylori has been linked to the development of gastric cancer.[15] Once CagA is injected into the cytoplasm it can change the gastric cell signaling in both a phosphorylation-dependent and -independent manner. [11] Phosphorylated CagA affects cell adhesion, spread and migration[16] but can also induce the release of the proinflammatory chemokine IL-8.[15] Additionally, interactions of the CRPIA motif in non-phosphorylated CagA were shown to lead to the persistent activation of the PI3K/Akt pathway, a pathway that is often overly active in many human cancers.[17][18] This leads to the activation of the pro-inflammatory NF-κB and β-catenin pathways as well as increased gastric cell proliferation.[17] Furthermore, CagA has also been found to increase tumor suppressor gene hypermethylation and thereby inhibiting the tumor suppressor genes.[19] This is achieved by upregulating the methyltransferase DNMT1 via the AKT–NF-κB pathway.[19][20] Lastly, CagA also induces the expression of the enzyme spermine oxidase (SMOX) that converts spermine to spermidine.[11] As a by-product H2O2 is produced which causes ROS accumulation and contributes to the oxidative stress that the gastric cells experience during chronic inflammation.[11]

Speculative links

A number of bacteria have associations with cancer, although their possible role in carcinogenesis is unclear.

Bacteria Suggested link
Salmonella Typhi, Paratiphi A, Typhimurium is associated with gallbladder cancer.[21][22]
Streptococcus bovis is associated with colorectal cancer.[23][24]
Chlamydia pneumoniae is associated with lung cancer.[23][25]
Mycoplasma may also have a role in the formation of different types of cancer.[26][27]
Helicobacter pylori has been linked with certainty to stomach cancer [28] and may be related to MALT lymphoma, and has also been associated to oral cancer.[2] but may also protect certain individuals from esophageal cancer.[23]
Porphyromonas gingivalis is associated with esophageal cancer, colorectal cancer, pancreatic cancer.[29]
Fusobacterium nucleatum is associated with esophageal cancer, colorectal cancer, pancreatic cancer.[29]
Escherichia coli is associated with colorectal cancer.[29]
Salmonella spp. is associated with colorectal cancer.[29]
Enterotoxigenic Bacteroides fragilis is associated with colorectal cancer.[29]
Chlamydia trachomatis in concert with HPV infection is associated with cervical cancer.[29]
Streptococcus anginosus is associated with esophageal cancer.[30]
Streptococcus mitis is associated with esophageal cancer.[30]
Ruminococcus is associated with colorectal cancer when under aerobic conditions.[31]

chronic inflammation, may also be linked to oral cancers.[33]

The relationship between cancer and bacteria may be complicated by different individuals reacting in different ways to different cancers.[23]

History

In 1890, the Scottish pathologist William Russell reported circumstantial evidence for the bacterial cause of cancer.[34] In 1926, Canadian physician Thomas Glover reported that he could consistently isolate a specific bacterium from the neoplastic tissues of animals and humans.[35] One review summarized Glover's report as follows:

The author reports the isolation of a pleomorphic organism from various types of cancer which can be grown in pure cultures in its several phases. He produced a serum from it which has given remarkable results in a series of 50 reported cases. This is very important, if true. We suppose the Cancer Society will give an opinion later on the reliability of the findings."[36]

Glover was asked to continue his work at the Public Health Service (later incorporated into the National Institutes of Health) completing his studies in 1929 and publishing his findings in 1930.[37] He asserted that a vaccine or anti-serum manufactured from his bacterium could be used to treat cancer patients with varying degrees of success.[37] According to historical accounts, scientists from the Public Health Service challenged Glover's claims and asked him to repeat his research to better establish quality control.[38] Glover refused and opted to continue his research independently; not seeking consensus, Glover's claims and results led to controversy and are today not given serious merit.[39]

In 1950, a Newark-based physician named

neoplasia.[40] Livingston continued to research the alleged bacterium throughout the 1950s and eventually proposed the name Progenitor cryptocides as well as developed a treatment protocol.[41] Ultimately, her claim of a universal cancer bacterium was not supported in follow up studies. In 1990 the National Cancer Institute published a review of Livingston's theories, concluding that her methods of classifying the cancer bacterium contained "remarkable errors" and it was actually a case of misclassification - the bacterium was actually Staphylococcus epidermidis.[39]

Other researchers and clinicians who worked with the theory that bacteria could cause cancer, especially from the 1930s to the 1960s, included Eleanor Alexander-Jackson,

Florence Seibert, Wilhelm von Brehmer, and Ernest Villequez.[42] Alexander-Jackson and Seibert worked with Virginia Livingston. Some of the researchers published reports that also claimed to have found bacteria associated with different types of cancers.[43][44][45][46][47][48]

See also

References

  1. ^
    PMID 30854333
    .
  2. ^
    PMID 25767359
    .
  3. PMID 17578895
    .
  4. S2CID 21288653
    .
  5. S2CID 9289825
    .
  6. PMID 9721161
    .
  7. PMID 16367902
    .
  8. PMID 12810954
    .
  9. PMID 12490959
    .
  10. PMID 26316793
    .
  11. ^
    PMID 36769214
    .
  12. ^
    PMID 28289428
    .
  13. ^
    PMID 20122996
    .
  14. PMID 21376230
    .
  15. ^
    PMID 24629337
    .
  16. PMID 12391297
    .
  17. ^
    PMID 19154985
    .
  18. PMID 34439105
    .
  19. ^
    PMID 28127428
    .
  20. PMID 26848521
    .
  21. PMID 26067598
    .
  22. PMID 26028364
    .
  23. ^
    PMID 16566840
    .
  24. PMID 15249410
    .
  25. PMID 12867569
    .
  26. PMID 15142464
    .
  27. PMID 19721714
    .
  28. S2CID 233900318
    .
  29. ^
    PMID 36834525
    .
  30. ^
    PMID 15245592
    .
  31. PMID 26755640
    .
  32. PMID 15681903
    .
  33. S2CID 27269158
    .
  34. PMID 20753194
    .
  35. ^ Glover TJ (1926). "Progress in Cancer Research". Canada Lancet and Practitioner. 67: 5.
  36. PMC 1581099
    .
  37. ^ a b Glover TJ (1930). "The bacteriology of cancer". Canada Lancet and Practitioner. 74: 92–111.
  38. ^ Glover TJ, Engle JL (1938). Studies in Malignancy. New York: Murdock Foundation.
  39. ^
    PMID 2106368
    .
  40. S2CID 39359507
    .
  41. PMID 4220493
    .
  42. ISBN 978-0-8147-3562-6
    .
  43. PMID 17866459
    .
  44. ^ Mazet G (June–August 1941). Etude bacteriolgigue sur la maladie d'Hodgkin. Montpellier Medicine.
  45. ^ Von Brehmer W. "Siphonosopra polymorpha n. sp.: ein neuer microorganismus des blutes, seine beziehung zur tumorgenese". Med Welt. 8: 1178–1185.
  46. ^ Crofton WM (1936). The True Nature of Viruses. London, England: Staples Press Ltd.
  47. ^ Villesquez EJ (1955). Le Parasitisme Latent des Cellules du Sang chez l' Homme, en Particulier dans le Sang des Cancreeux. Paris, France: Librarie Maloine.
  48. ^ Fonti CJ (1958). Eziopatogenese del Cancro. Milan, Italy: Amadeo Nicola.& c.
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