The causal organisms of the numerous sexually transmitted infections (STIs) may be bacteria, viruses, fungi or protozoa. Apart from the known STIs these organisms cause, along with their accompanying physical, psychological and social effects, these organisms have also been implicated in oncogenesis. Each pathogen has its unique mechanisms of action, however, one representative organism was examined for each of the groups of microbes that cause STIs, namely: viruses, bacteria, fungi and protozoa, to show their oncogenic association. The human papillomavirus, which causes genital warts, is associated with oropharyngeal, cervical, anogenital, testicular and prostate cancer by the actions of the E5, E6 and E7 oncogenes, which have different functions. Chlamydia trachomatis, the etiological agent of Chlamydia infection, is linked to lymphogranuloma venereum, trachoma, cervical, and ovarian cancers by squamous cell metaplasia, and by the inhibition of apoptosis factors: caspase 3 and mitcochondrial cytochrome c; which consequently inhibits apoptosis. Candida albicans, the causal organism of thrush in the mouth and the vagina, could cause cancer by producing carcinogenic by-products, triggering inflammation, molecular mimicry, and induction of the TH17 response. Trichomonas vaginalis, the protozoon which causes trichomoniasis, is known to cause the influx of pro-inflammatory molecules: chemoattractant protein-1, interleukin-8, and leukotriene B4, d neutrophils, and IL-6, and this may play a role in carcinogenesis. Expression of the oncogenes PIM1, HMGA1, and COX-2 by T. vaginalis has also been associated with the onset of cancer. Vaccination, healthy lifestyles, a mutually-monogamous sexual relationship, completing treatment regimen, use of sterile medical equipment, and not sharing sharp or invasive materials, are recommended in prevention and control of the STI pathogens and consequently, the cancers they cause.
| Published in |
Cell Biology (Volume 8, Issue 1)
This article belongs to the Special Issue Cell Death and Mechanisms in Cancer |
| DOI | 10.11648/j.cb.20200801.13 |
| Page(s) | 12-21 |
| Creative Commons |
This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited. |
| Copyright |
Copyright © The Author(s), 2020. Published by Science Publishing Group |
Sexually Transmitted Infections, Cancer, Oncogene, Inflammation
| [1] | United States National Institutes of Health (2017) What are Some Types of and Treatments for Sexually Transmitted Diseases (STDs) or Sexually Transmitted Infections (STIs)? Available online: https://www.nichd.nih.gov/health/topics/stds/conditioninfo/types. Accessed 26-02-2020, 9: 50 hours. |
| [2] | World Health Organisation (2019) Sexually Transmitted Infections (STIs). Available onlline: https://www.who.int/news-room/fact-sheets/detail/sexually-transmitted-infections-(stis). Accessed 26-02-2020, 10: 08 hours. |
| [3] | World Health Organisation. Cancer. Available online: https://www.who.int/cancer/en/. Accessed 20-01-2019, 19: 42 hours. |
| [4] | United States National Cancer Institute (2015) What is Cancer? Available: www.cancer.gov/about-cancer/understanding/what-is-cancer. Accessed 27-12-2017, 19: 00 hours. |
| [5] | Paul, C., Mistriotis, P. and Konstantatopoulos, K. (2017) Cancer Cell Motility: Lessons from Migration in Confined Spaces. Nature Reviews—Cancer. 17 (2): Pp 131-140. DOI: http://dx.doi.org/10.1038/nrc.2016.123. |
| [6] | World Health Organisation Media Centre (2017b) Fact sheet: The Top 10 Causes of Death. Available: www.int/mediacentre/factsheets/fs310/en/. Accessed 27-12-2017. |
| [7] | World Health Organisation (2017) 10 Facts About Cancer. Available online: https://www.who.int/features/factfiles/cancer/en/. Accessed 25-02-2020, 13: 13 hours. |
| [8] | World Health Organisation (2018) Cancer. Available online: www.who.int/news-room/fact-sheets/detail/cancer. Accessed 08-10-2018. |
| [9] | De Martel, C., Ferlay, J., Franchesci, S., Vignat, J., Bray, F., Forman, D. et al. (2012) Global Burden of Cancers Attributable to Infections in 2008: A Review and Synthetic Analysis. The Lancet—Oncology. DOI: https://doi.org/10.1016/S1470-2045(12)70137-7. |
| [10] | Stolte, M., Bayerdörffer, E., Morgner, A., Alpen, B., Wündisch, T. Thiede, C. and Neubauer. Helicobacter and Gastric MALT Lymphoma. Gut. 50 (Suppl III): Ppiii19-iii24. DOI: http://doi.org/10.1136/gut.50.suppl_3.iii19. |
| [11] | Crowe, S. E. (2005) Helicobacter Infection, Chronic Inflammation, and the Development of Malignancy. Current Opinions in Gastroenterology. 1: 32-8. |
| [12] | Correa, P. and Piazuelo, B. (2011) Helicobacter pylori Infection and Gastric Adenocarcinoma. US Gastroenterology and Hepatology Review. 7 (1): Pp 59-64. PMID: 21857882. |
| [13] | Callaway, E. (2012) E. coli Strain Linked to Cancer in Mice. Nature—News. DOI: http://doi.org/10.1038/nature.2012.11211. |
| [14] | American Cancer Society (2016a) Bacteria That Can Lead to Cancer. Available online: www.cancer.org/cancer/cancer-causes/infectious-agents/infections-that-can-lead-to-cancer/bacteria.html. Accessed 08-10-2018. |
| [15] | El-Mosalamy, H., Salman, T. M., Ashmawey, A. M. and Osama, N. (2012) Role of Chronic E. coli Infection in the Process of Bladder Cancer- An Experimental Study. Infectious Agents and Cancer. 7: 19. DOI: http://doi.org/10.1186/1750-9378-7-19. |
| [16] | Meehan, B. (2016) What You Can Do to Reduce the Risk of Bowel Cancer Caused by E. coli Bacteria. The Conversation. Available online: https://theconversation.com/amp/what-you-can-do-to-reduce-the-risk-of-bowel-cancer-caused-by-e-coli-bacteria-60264. Accessed 08-12-2018, 21: 55 hours. |
| [17] | Mischaud, D. S., Platz, E. A. and Giovannucci, E. (2007) Gonorrhoea and Male Bladder Cancer in a Prospective Study. British Journal of Cancer. 96: Pp 169-171. DOI: http://10.1038/sj.bjc.6603510. |
| [18] | Lian, W-Q., Luo, F., Song, X-L. and Zhao, S-C. (2015) Gonorrhoea and Prostate Cancer Incidence: An Updated Meta-Analysis of 21 Epidemiologic Studies. Medical Science Monitor. 21: Pp 1895-1903. DOI: http://doi.org/10.12659/MSM.893579.e-ISSN 1643-3750. |
| [19] | Zhu, H., Shen, Z., Luo, H., Zhang, W. and Zhu, X. (2016) Chlamydia trachomatis Infection-Associated Risk of Cervical Cancer: AA Meta-Analysis. Medicine. 95 (13): e3077. |
| [20] | Das, M. (2018) Chlamydia Infection and Ovarian Cancer Risk. The Lancet—Oncology. 17 (7): Pe 338. DOI: https://doi.org/10.1016/S1470-2045(18)30421-2. |
| [21] | Trabert, B. Waterboer, T., Idahl, A., Brennerm N., Brinton, L. A., Butt, J. et al. (2018) Antibodies Against Chlamydia trachomatis and Ovarian Cancer Risk in Two Independent Populations. Journal of the National Cancer Institute. 111 (2): djy084. DOI: https://10.1093/jcni/djy084. |
| [22] | Spaargaren, J., Fennema, H. S. A., Morré, S. A., de Vries, H. J. C. and Coutinho, R. A. (2005) New Lymphogranuloma Venereum Chlamydia trachomatis Variant, Amsterdam. Emerging Infectious Diseases. 11 (7): Pp 1090-2. DOI: http://doi.org/10.3201/eid1107.040883. |
| [23] | Huang, S., Li, J. Y., Wu, J., Meng, L. and Shou, C. C. (2001) Mycoplasma Infections and Different Human Carcinomas. World Journal of Gastroenterology. 7: Pp 266-9. |
| [24] | Namiki, K., Goodison, S., Porvasnik, S., Allan, R. W., Iczkowski, K. A., Urbanek, C. et al. (2009) Persistent Exposure to Mycoplasma Induces Malignant Transformation of Human Prostate Cells. Plos One. 4 (9): e6872. DOI: http://doi.org/10.1371/journal.pone.0006872. |
| [25] | Barykova, Y. A., Logunov, D. Y., Shmarov, M. M., Vinarov, A. Z., Fiev, D. N., Vinarova, N. A. et al. (2011) Association of Mycoplasma hominis Infection with Prostate Cancer. Oncotarget. 2 (4): Pp 280-97. DOI: http://doi.org/10.18632/oncotarget.256. |
| [26] | Yang, H., Qu, L., Ma, H., Chen, L., Liu, W., Liu, C. et al. (2010) Mycoplasma hyorhinis Infection in Gastric Carcinomas and Its Effect on the Malignant Phenotypes of Gastric Cancer Cells. BMC Gastroenterology. 10: P132. DOI: http://doi.org/10.1186/1471-230X-10-132. |
| [27] | Mitin, V., Tumanova, L. and Botnariuc, N. (2016) Mycoplasma faucium and Breast Cancer. bioRxiv. DOI: http://doi.org/10.1101/089128. |
| [28] | Pehlivan, M., Pehlivan, S., Onay, H., Koyuncuoglu, M. and Kirkali, Z. (2005) Can Mycoplasma-mediated Oncogenesis be responsible for Formation of Conventional Renal Cell Carcinoma? Urology. 65 (2): Pp 411-4. |
| [29] | Kumar, R., Herold, J. L., Schady, D., Davis, J., Kopetz, S. Martinez-Moczygemba et al. (2017) Streptococcus gallolyticus subsp. Gallolyticus Promotes Colorectal Cancer Tumour Development. Plos Pathogens. 13 (7): e1006440. DOI: https://doi.org/10.1371/journal.ppat.1006440. |
| [30] | Koshiol, J., Wozniak, A., Cook, P., Adaniel, C., Acevedo, J, Azócar, et al. (2016) Salmonella enterica serovar typhi and gallbladder cancer: a Case-Control Study and Meta-Analysis. Cancer Medicine. 5 (11): Pp 3310-25. DOI: http://doi.org/10.1002/cam4.915. |
| [31] | Di Domenico, E. G., Cavallo, I., Pontone, M., Toma, L. and Ensoli, F. (2017) Biofilm Producing Salmonella typhi: Chronic Colonisation and Development of Gallbladder Cancer. International Journal of Molecular Sciences. 18 (9): P1887. DOI: https://doi.org/10.3390/ijms18091887. |
| [32] | Mughini-Gras, L., Schaapveld, M., Kramers, J., Mooij, S., Neefjes-Borst, E. A., Pelt, W. V. et al. (2018) Increased Colon Cancer Risk After Severe Salmonella Infection. Plos One. 13 (1) e0189721. DOI: http://doi.org/10.1371/journal.pobe.0189721. |
| [33] | American Cancer Society (2016b) Viruses That Can Lead to Cancer. Available online: www.cancer.org/cancer/cancer-causes/infectious-agents/infections-that-can-lead-to-cancer/viruses.html. Accessed 08-10-2018. |
| [34] | DeNoon, D. J. (2011) Higher Cancer Risk in People With HIV. WedMD. Available online: https://webmd.com/hiv-aids/news/20111122/higher_cancer_risk_in_people_with_hiv. Accessed 10-10-2018. |
| [35] | Mesri, E. A., Cesarman, E. and Boshoff, C. (2010) Kaposi’s Sarcoma Herpesvirus/Human Herpesvirus-8 (KSHV/HHV8) and the Oncogenesis of Kaposi’s Sarcoma. Nature Reviews—Cancer. 10 (10): Pp 707-19. |
| [36] | Rafferty, K. A. Jnr. (1973) Herpes Viruses and Cancer. Scientific American. 229 (4): Pp 26-33. |
| [37] | Herbein, G. and Kumar, A. (2014) The Oncogenic Potential of Human Cytomegalovirus and Breast Cancer. Frontiers in Oncology. 4: P230. DOI: http://doi.org/10.3389/fonc.2014.00230. |
| [38] | Geder, K. M., Lausch, R., O’Neill, F. and Rapp, F. (1976) Oncogenic Transformation of Human Embryo Lung Cells by Human Cytomegalovirus. Science. 192: Pp 1134-7. |
| [39] | Michaelis, M., Doerr, H. W. and Cinatl, J. (Jr.) (2009) The Story of Human Cytomegalovirus and Cancer: Increasing Evidence and Open Questions. Neoplasia. 11 (1): Pp 1-9. |
| [40] | Wolfe, D. (2016). Is There A Link between Candida albicans and Cancer? The Truth about Cancer. Available online: https://thetruthaboutcancer.com/candida-albicans-cancer/. Accessed 09-12-2018, 23: 42 hours. |
| [41] | Chung, L-M., Liang, J-A., Sun, L-M. and Kao, C-H. (2017) Cancer Risk in Patients with Candidiasis: A Nationwide Population-Based Cohort Study. Oncotarget. 8 (38): Pp 63562-63573. |
| [42] | Gupta, R., Nowakowski, M. and Haseeb, M. A. (2015) Infection and Cancer: Bi-Directorial Interactions. Springer. In: Shurin, M. R., Thanavala, Y. And Ismail, N. (Ed.). eBook ISBN: 978-3-31920669-1. |
| [43] | Tsang, S. H., Peisch, S. F., Rowan, B., Markt, S. C., Gonzalez-Feliciano, A. G., Sutcliffe, S. et al. (2018) Association Between Trcihomonas vaginalis and Prostate Cancer Mortality. International Journal of Cancer. Preprint. DOI: http://doi.org/10.1002/ijc.31885. |
| [44] | Münger, K., Balbwin, A., Edwards, K. M., Hayakawa, H., Nguyen, C. L., Owens, M. et al. (2004) Mechanisms of Human Papillomavirus-Induced Oncogenesis. Journal of Virology. 78 (21): Pp 11451-11460. DOI: https://doi.org/10.1128/JVI.78.21.11451-11460.2004. |
| [45] | United States National Cancer Institute. HPV and Cancer. Available online: https://www.cancer.gov/about-cancer/causes-prevention/risk/infectious-agents/hpv-and-cancer. Accessed 22-04-2018. |
| [46] | World Health Organisation Media Centre (2016) Fact sheet: sexually transmitted infections. Available: www.who.int/mediacentre/factsheets/fs110/en/. Accessed 26-12-2017. |
| [47] | Narisawa-Saito, M. and Kiyono, T. (2007) Basic Mechanisms of High-Risk Human Papillomavirus-Induced Carcinogenesis: Roles of E6 and E7 Proteins. Cancer Science. 98 (10): Pp 1505-11. |
| [48] | Selcuk, O. T. (2016) Human Papillomavirus-Positive Oropharyngeal Cancer: the General Information. Egyptian Journal of Ear, Nose, Throat, and Allied Sciences. 17 (3). Pp. 127-132. DOI: https://doi.org/10.1016/j.ejenta.2016.07.007. |
| [49] | Lehoux, M., D’Abramo, C. M. and Archambault, J. (2009) Molecular Mechanisms of Human Papillomavirus-Induced Carcinogenesis. Canadian Institutes of Health Research. Public Health Genomics. 12 (5-6): Pp 268-280. DOI: http://dx.doi.org/10.1159/000214918. |
| [50] | Oh, J., Kim, J., Cho, E., Song, Y., Kim, W. and Juhnn, Y. (2010) Human Papillomavirus Type 16 E5 Protein Inhibits Hydrogen Peroxide-Induced Apoptosis by Stimulating Ubiquitin-Proteasome-Mediated Degradation of Bax in Human Cervical Cancer Cells. Carcinogenesis. 31 (3): Pp 402-10. DOI: https://doi.org/10.1093/carcin/bgp318. |
| [51] | DiMaio, D. and D. Mattoon (2001) Mechanisms of Cell Transformation by Papillomavirus E5 Proteins. Oncogene 20: 7866-7873. |
| [52] | Benson, E., Li, R., Eisele, D. and Fakhry, C. (2014) The Clinical Impact of HPV Tumor Status Upon Head and Neck Squamous Cell Carcinomas. Oral Oncology. 50: Pp 565-574. |
| [53] | The United States National Library of Medicine (2018) CDKN2A Gene: Cyclin-Dependent Kinase Inhibitor 2A. Available: https://ghr.nlm.nih.gov/gene/CDKN2A. Accessed 14-02-2018. |
| [54] | Matsumura, Y., Nishigori, C., Imamura, S. and Takebe, H. (1998) Mutations of p16 and p15 Tumor-Suppressor Genes and Replication Errors Contribute Independently to the Pathogenesis of Sporadic Malignant Melanoma. Archives of Dermatological Research. 290 (4): Pp 175-80. https://www.ncbi.nlm.nih.gov/pubmed/9617435. |
| [55] | Centres for Disease Control and Prevention (2017a) Gonorrhoea- CDC Fact Sheet (Detailed Version). Available online: www.cdc.gov/std/gonorrhoea/stdfact-gonorrhoea-detailed.htm. Accessed 09-10-2018. |
| [56] | Graeter, L., Hertenstein, E., Accurso, C. and Labiner, G. (2014) Elsevier’s Medical Laboratory Science Review (e-Book). Elsevier Health Sciences. P. 30. ISBN: 9780323292412. |
| [57] | Fredlund, H., Falk, L., Jurstrand, M. and Unemo, M. (2004) Molecular Genetics Methods for Diagnosis and Characterisation of Chlamydia trachomatis and Neisseria gonorrhoeae Impact on Epidemiological Surveillance and Interventions. APMIS: Acta Pathologica Microbiologica et Immunologica Scandinavica. 112 (11-12): Pp 771-84. DOI: http://doi.org/10.1111/j.1600-0463.2004.apm11211-1205.x. PMID: 15638837. |
| [58] | World Health Organization Media Centre (2017c) Trachoma. Available: http://www.who.int/mediacentre/factsheets/fs382/en/. Accessed 04-02-2018. |
| [59] | Joseph, S. J., Didelot, X., Rothschild, J., de Vries, H. J. C., Morré, Read, T. D. and Dean, D. (2012) Population Genomics of Chlamydia trachomatis: Insights on Drift, Selection, Recombination, and Population Structure. Molecular Biology and Evolution. 29 (12): Pp 3933-3946. DOI: http://doi.org/10.1093/molbev/mss198. |
| [60] | Paavonen, J. (2001) Chlamydia trachomatis and Cancer. Sexually Transmitted Infections. 77: Pp 154-156. |
| [61] | Rosin, M. P., Anwar, W. A. and Ward, J. A. (2001) Inflammation, Chromosomal Instability and Cancer: the Schistosomiasis Model. Cancer Research. 54 (Suppl 7): Pp 1929-33. |
| [62] | Paavonen, J., Miettinen, A. and Heinonen, P. K. (1989) Serum CA 125 in Acute Pelvic Inflammatory Disease. British Journal of Obstetrics and Gynecology. 96: Pp 574-9. |
| [63] | Paavonen, J., Kiviat, N. and Wölner-Hanssen, P. (1988) Colposcopic Manifestations of Cervical and Vaginal Infections. Obstetrical and Gynecological Survey. 43: Pp 373-81. |
| [64] | Herzog, S. A., Althaus, C. L., Heijne, J. C. M., Oakeshott, P., Kerry, S., Hay, P. and Low, N. (2012) Timing of Progression from Chlamydia trachomatis Infection to Pelvic Inflammatory Disease: A Mathematical Modelling Study. BMC Infectious Diseases. 12: Pp 187. DOI: https://doi.org/10.1186/1471-2334-12-187. |
| [65] | Risch, H. A., Marrett, L. D. and Howe, G. R. (1994) Parity, Contraception, Infertility, and Risk of Epithelial Ovarian Cancer. American Journal of Epidemiology. 140: Pp 585-97. |
| [66] | Anttila, T., Saikku, P. and Koskela, P. (2001) Serotypes of Chlamydia trachomatis and the Risk for the Development of Cervical Squamous Cell Carcinoma. JAMA. 285: Pp 47-51. |
| [67] | Smelov, V., Sundstom, K., Ploner, A., McKay-Chopin, S., Eklund, C., Tommasino, M. and Dillner, J., (2016) Lack of Significant Effects of Chlamydia trachomatis Infection on Cervical Adenocarcinoma Risk: Nested Case-Control Study. Plos One. DOI: https://doi.org/10.1371/journal.pone.0156215. |
| [68] | Kiviat N., Paavonen J. and Brockway J. (1985) Cytologic Manifestations of Vaginal and Cervical Infections: Epithelial and Inflammatory Cellular Changes. JAMA. 253: P989. |
| [69] | Fan, T., Lu, H., Hu H., Shi, L., McClarty, G. A., Nance, D. M. et al. (1998) Inhibiton of Apoptosis in Chlamydia-Infected Cells: Blockade of Mitochondrial Cytochrome c Release and Caspase Activation. The Journal of Experimental Medicine. 187: Pp 487-96. DOI: http://dx.doi.org/10.1084/jem.187.4.487. |
| [70] | Henkart, P. A. (1996) ICE Family Proteases: Mediators of All Apoptotic Cell Death? Immunity 4: Pp 195-201, PMID: 8624810. |
| [71] | Zou, H., Henzel, W. J., Liu, X., Lutsch, A. and Wang, X. (1997) Apaf-1, a Human Protein Homologous to C. elegans CED-4, Participates in Cytochrome c-Dependent Activation of Acaspase-3. Cell. 90: 405-413. |
| [72] | Shi, L., Chen, G., MacDonald, G., Bergeron, L., Li, H., Miura, M. et al. (1996) Activation of an Interleukin 1 Converting Enzyme-Dependent Apoptosis Pathway by Granzyme B. Proceedings of the National Academy of Sciences of the United States of America. 93: 11002-11007. |
| [73] | Kroemer, G., Zamzami, N. and Susin, S. A. (1997) Mitochondrial Control of Apoptosis. Immunology Today. 18: Pp 44-51, PMID: 9018974. |
| [74] | Rasmussen, S. J., Eckmann, L., Quayle, A. J., Shen, L., Zhang, Y. X., Anderson. et al. (1997) Secretion of Proinflammatory Cytokines by Epithelial Cells in Response to Chlamydia Infection Suggests a Central Role for Epithelial Cells in Chlamydial Pathogenesis. Journal of Clinical Investigation. 99: Pp 77-87. |
| [75] | Strasser, A., Harris, A. W., Huang, D. C, Krammer, P. H. and Cory, S. (1995) Bcl-2 and Fas/APO-1 Regulate Distinct Pathways to Lymphocyte Apoptosis. European Molecular Biology Organisation. 14: 6136-6147, PMID: 8557033. |
| [76] | Chiu, V. K., Walsh, C. M., Liu, C. C., Reed, J. C. and Clark W. R. (1995) Bcl-2 Blocks Degranulation but Not Fas-Based Cell-Mediated Cytotoxicity. The Journal of Immunology. 154: Pp 2023-2032. PMID: 7532659. |
| [77] | Erhardt, P. and Cooper, G. M. (1996) Activation of CPP32 Apoptotic Protease by Distinct Sgnaling Pathways with Differential Sensitivity to Bcl-Xl. The Journal of Biological Chemistry. 271: Pp 17601-4. |
| [78] | Centres for Disease Control and Prevention (2017b) Fungal Diseases. Available online: http://www.cdc.gov/fungal/diseases/candidiasis/index.html. Accessed 20-01-2019, 23: 04 hours. |
| [79] | Kurzai, O., Schmitt, C., Frosch, M. and Kolb-Maurer, A. (2005) Polymorphism of Candida albicans is a Major Factor in the Interaction With Human Dendritic cells. International Journal of Medical Microbiology. 295 (2): Pp 121-7. |
| [80] | Villar, C. C., Kashleva, H. and Dongari-Bagtzoglou, A. (2004) Role of Candida albicans Polymorphism in Interactions with Oral Epithelial Cells. Oral Microbiology and Immunology. 19 (4): Pp 262-9. |
| [81] | Sudbery, P., Gow, N. and Berman, J. (2004) The Distinct Morphogenic States of Candida albicans. Trends in Microbiology. 12 (7): Pp 317-24. |
| [82] | Bakri, M. M., Hussaini, H. M., Holmes, A. R., Cannon, R. D. and Rich, A. M. (2010) Revisiting the Association Between Candidal Infection and Carcinoma, Particularly Oral Squamous Cell Carcinoma. Journal of Oral Microbiology. 2 (1): Pp 5780. DOI: http://dx.doi.org/10.3402/jom.v2i0.5780. |
| [83] | Ramirez-Garcia, A., Rementeria, A., Aguirre-Urizar, J. M., Moragues, M. D., Antoran, A., Pellon, A. et al. (2016) Candida albicans and Cancer: Can this Yeast Induce Cancer Development or Progression? Critical Review in Microbiology. 42 (2): Pp 181-93. DOI: https://doi.org/10.3109/1040841X.2014.913004. |
| [84] | Ji, S. (2016) Yeast is a Cause of Cancer and Turmeric Can Kill Both, Research Confirms. Green MedInfo. Available: http://www.greenmedinfo.com/blog/yeast-cause-cancer-and-turmeric-can-kill-both-research-confirms. Accessed 06-03-2018. |
| [85] | Hostetter, M. K. (2008) The iC3b Receptor of Candida albicans and its Roles in Pathogenesis. Vaccine. 26 (Suppl. 8): I108-I112. DOI: https://doi.org/10.16/j.vaccine.2008.11.056. |
| [86] | Reed-Guy, L. and Jewell, T. (2016) Trichomoniasis. Healthline. Available online: www.healthline.com/health/trichomonas-infection. |
| [87] | Centres for Disease Control and Prevention. STD Facts- Trichomoniasis. Available online: www.cdc.gov/std/trichomonas/stdfact-trichomoniasis.htm. Accessed 08-10-2018. |
| [88] | Soper, D. (2004) Trichomoniasis: Under Control or Undercontrolled? American Journal of Obstetrics in Gynaecology. 190 (1): Pp 281-90. |
| [89] | Sutcliffe, S., Neace, C., Magnuson, Reeves, R., Alderete, J. F. (2012) Trichomoniasis, a Common Curable STI, and Prostate Carcinogenesis—A Proposed Molecular Mechanism. Plos Pathogens. 8 (8): e1002801. DOI: http://doi.org/10.1371/journal post.ppat.1002801. |
| [90] | Bachmann, M. and Möröy, T. (2005) The Serine/Threonine Kinase Pim1. The International Journal of Biochemistry and Cell Biology. 37 (4): Pp 726-30. |
| [91] | Roh, M. Franco, O. E., Hayward, S. W., van der Meer, R. and Abdulkadir, S. A. (2008) A Role for Polyploidy in Tumorigenicity of Pim-1 Expressing Human Prostate and Mammary Epithelial Cells. Plos One. 3: c2572. |
| [92] | Reeves R. and Beckerbauer, L. (2001) HMG1/Y Proteins: Flexible Regulators of Transcription and Chromatin Structure. Biochimica et Biophysica Acta. 1519: Pp 13-29. |
| [93] | Hawksworth, D., Ravindranath, L., Chen, Y., Furusato, B., Sesterhenn, I. A., McLeod, D. G. et al. (2010) Overexpression of C-MYC Oncogene in Prostate Cancer Predicts Biochemical Recurrence. Prostate Cancer and Prostatic Diseases. 13 (4): Pp 311-5. DOI: http://doi.org/10.1038/pcan.2010.31. |
| [94] | Wolfer, A. and Ramaswamy, S. (2011) MYC and Metastasis. Cancer Research. 71 (6): Pp 2034-2037. DOI: http://doi.org/10.1158/0008-5472. |
| [95] | Pegoraro, S., Ros, G., Piazza, S., Sommaggio, R., Ciani, Y., Rosato, A. et al. (2013) HMGA1 Promotes Metastatic Processes in Basal-Like Breast Cancer Regulating EMT and Stemness. Oncotarget. 14 (8): Pp 1293-1308. |
| [96] | Schuldenfrei, A., Belton, A., Kowalski, J., Talbot, C. C. Jr., Di Cello, F., Poh, W. et al. (2011) HMGA1 Drives Stem Cell, Inflammatory Pathway, and Cell Cycle Progression Genes During Lymphoid Tumorigenesis. BMC Genomics. 12: Pp 549. |
| [97] | Resar, L., Dhara, S., Sumter, T. F., Mukherjee, M., Turkson, J., Jove, R. et al. (2006) STAT3: A Direct HMGA1 Gene Target Important in Lymphoid Malignancy. Blood Advances. 108: P2222. |
| [98] | Zhang, Y, Wang, Z., Li, X. and Magnuson, N. S. (2008) Pim Kinase-Dependent Inhibition of c-Myc Degradation. Oncogene. 27: Pp 4809-4819. |
| [99] | Tesfaye, A., Di Celso, F., Hillion, J., Ronnett, B. M., Elbahloul, O., Ashfaq, R. et al. (2007) The High Mobility Group A1 Up-regulates Cyclooxygenase 2 Expression in Uterine Tumorigenesis. Cancer Research. 67: Pp3988-4004. |
| [100] | Singh, B., Berry, J. A., Shoher, A., Ramakrishnan, V. and Lucci, A. (2005) COX-2 Overexpression Increases Motility and Invasion of Breast Cancer Cells. International Journal of Oncology. 26 (5): Pp 1393-9. |
| [101] | Garcia, A. F., Benchimol, M. and Alderete, J. F. (2005) Trichomonas vaginalis Polyamine Metabolism is Linked to Host Cell Adherence and Cytotoxcity. Infection and Immunity. 73 (5): Pp 2602-2610. |
| [102] | Cowan, M. J., Coll, T. and Shelhamer, J. H. (2006) Polyamine-Mediated Reduction in Human Airway Epithelial Migration in Response to Wounding is PGE2-Dependent Through Decreases in COX-2 and Cpla2 Protein Levels. Journal of Applied Physiology. DOI: http://doi.org/10.1152/japplphysiol.01287.2005. |
APA Style
Emmanuel Sokefun, Olayemi Akinnola. (2020). Cancer-Inducing Mechanisms of Representative Sexually-Transmitted Infection Pathogens. Cell Biology, 8(1), 12-21. https://doi.org/10.11648/j.cb.20200801.13
ACS Style
Emmanuel Sokefun; Olayemi Akinnola. Cancer-Inducing Mechanisms of Representative Sexually-Transmitted Infection Pathogens. Cell Biol. 2020, 8(1), 12-21. doi: 10.11648/j.cb.20200801.13
AMA Style
Emmanuel Sokefun, Olayemi Akinnola. Cancer-Inducing Mechanisms of Representative Sexually-Transmitted Infection Pathogens. Cell Biol. 2020;8(1):12-21. doi: 10.11648/j.cb.20200801.13
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Download@article{10.11648/j.cb.20200801.13,
author = {Emmanuel Sokefun and Olayemi Akinnola},
title = {Cancer-Inducing Mechanisms of Representative Sexually-Transmitted Infection Pathogens},
journal = {Cell Biology},
volume = {8},
number = {1},
pages = {12-21},
doi = {10.11648/j.cb.20200801.13},
url = {https://doi.org/10.11648/j.cb.20200801.13},
eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.cb.20200801.13},
abstract = {The causal organisms of the numerous sexually transmitted infections (STIs) may be bacteria, viruses, fungi or protozoa. Apart from the known STIs these organisms cause, along with their accompanying physical, psychological and social effects, these organisms have also been implicated in oncogenesis. Each pathogen has its unique mechanisms of action, however, one representative organism was examined for each of the groups of microbes that cause STIs, namely: viruses, bacteria, fungi and protozoa, to show their oncogenic association. The human papillomavirus, which causes genital warts, is associated with oropharyngeal, cervical, anogenital, testicular and prostate cancer by the actions of the E5, E6 and E7 oncogenes, which have different functions. Chlamydia trachomatis, the etiological agent of Chlamydia infection, is linked to lymphogranuloma venereum, trachoma, cervical, and ovarian cancers by squamous cell metaplasia, and by the inhibition of apoptosis factors: caspase 3 and mitcochondrial cytochrome c; which consequently inhibits apoptosis. Candida albicans, the causal organism of thrush in the mouth and the vagina, could cause cancer by producing carcinogenic by-products, triggering inflammation, molecular mimicry, and induction of the TH17 response. Trichomonas vaginalis, the protozoon which causes trichomoniasis, is known to cause the influx of pro-inflammatory molecules: chemoattractant protein-1, interleukin-8, and leukotriene B4, d neutrophils, and IL-6, and this may play a role in carcinogenesis. Expression of the oncogenes PIM1, HMGA1, and COX-2 by T. vaginalis has also been associated with the onset of cancer. Vaccination, healthy lifestyles, a mutually-monogamous sexual relationship, completing treatment regimen, use of sterile medical equipment, and not sharing sharp or invasive materials, are recommended in prevention and control of the STI pathogens and consequently, the cancers they cause.},
year = {2020}
}
TY - JOUR T1 - Cancer-Inducing Mechanisms of Representative Sexually-Transmitted Infection Pathogens AU - Emmanuel Sokefun AU - Olayemi Akinnola Y1 - 2020/07/22 PY - 2020 N1 - https://doi.org/10.11648/j.cb.20200801.13 DO - 10.11648/j.cb.20200801.13 T2 - Cell Biology JF - Cell Biology JO - Cell Biology SP - 12 EP - 21 PB - Science Publishing Group SN - 2330-0183 UR - https://doi.org/10.11648/j.cb.20200801.13 AB - The causal organisms of the numerous sexually transmitted infections (STIs) may be bacteria, viruses, fungi or protozoa. Apart from the known STIs these organisms cause, along with their accompanying physical, psychological and social effects, these organisms have also been implicated in oncogenesis. Each pathogen has its unique mechanisms of action, however, one representative organism was examined for each of the groups of microbes that cause STIs, namely: viruses, bacteria, fungi and protozoa, to show their oncogenic association. The human papillomavirus, which causes genital warts, is associated with oropharyngeal, cervical, anogenital, testicular and prostate cancer by the actions of the E5, E6 and E7 oncogenes, which have different functions. Chlamydia trachomatis, the etiological agent of Chlamydia infection, is linked to lymphogranuloma venereum, trachoma, cervical, and ovarian cancers by squamous cell metaplasia, and by the inhibition of apoptosis factors: caspase 3 and mitcochondrial cytochrome c; which consequently inhibits apoptosis. Candida albicans, the causal organism of thrush in the mouth and the vagina, could cause cancer by producing carcinogenic by-products, triggering inflammation, molecular mimicry, and induction of the TH17 response. Trichomonas vaginalis, the protozoon which causes trichomoniasis, is known to cause the influx of pro-inflammatory molecules: chemoattractant protein-1, interleukin-8, and leukotriene B4, d neutrophils, and IL-6, and this may play a role in carcinogenesis. Expression of the oncogenes PIM1, HMGA1, and COX-2 by T. vaginalis has also been associated with the onset of cancer. Vaccination, healthy lifestyles, a mutually-monogamous sexual relationship, completing treatment regimen, use of sterile medical equipment, and not sharing sharp or invasive materials, are recommended in prevention and control of the STI pathogens and consequently, the cancers they cause. VL - 8 IS - 1 ER -
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