|Year : 2022 | Volume
| Issue : 2 | Page : 138-142
Relationship between Helicobacter Pylori and colon cancer
Batool Ali Khorsheed1, Raghdah Maythem Hameed2, Zahraa Hussein Khorsheed1
1 Department of Microbiology, Habboubi Teaching Hospital, Nasiriyah, Iraq
2 Department of Microbiology, Al-Sader Teaching Hospital, Najaf, Iraq
|Date of Submission||06-Apr-2022|
|Date of Decision||20-May-2022|
|Date of Acceptance||28-May-2022|
|Date of Web Publication||15-Jun-2022|
Dr. Raghdah Maythem Hameed
Department of Microbiology, Al-Sader Teaching Hospital, Najaf
Source of Support: None, Conflict of Interest: None
BACKGROUND: Helicobacter pylori is a Gram-negative bacteria found in the gastric epithelia of around half of the world's population. Chronic gastritis, peptic ulcers, gastric mucosa-associated lymphoid tissue, and stomach cancer are all known to be caused by this illness. Furthermore, there is evidence that bacteria are linked to a number of extragastric disorders. Since it was initially hypothesized that the link between extragastric illnesses and colon cancer.
OBJECTIVE: The objective of this study was to obtain the correlation between colon cancer and H. pylori infection.
METHODS: In this study, we tested blood samples were collected from the patients with colon cancer to assess the presence of anti-H. pylori infection antibodies in 10 patients with colorectal cancer and 10 with no specific pathologies as a control group.
RESULTS: There was a statistically significant difference (P > 0.05) and a highly significant difference (P > 0.001) in H. pylori infection and colon cancer between patients and control, respectively. A significant correlation between H. pylori infection and colon cancer (P > 0.05) was noted. It was found to be a positive linear correlation with H. pylori infection (r = 0.436) and significant (P = 0.027). The study showed a significant correlation between age and H. pylori and colon cancer (P = 0.013 and P = 0.034, respectively).
CONCLUSION: H. pylori infection is one of the risk factors that develop colon cancer. The old age correlates with increased colon cancer and H. pylori infection.
Keywords: Colorectal cancer, gastritis, Helicobacter pylori
|How to cite this article:|
Khorsheed BA, Hameed RM, Khorsheed ZH. Relationship between Helicobacter Pylori and colon cancer. J Prev Diagn Treat Strategies Med 2022;1:138-42
|How to cite this URL:|
Khorsheed BA, Hameed RM, Khorsheed ZH. Relationship between Helicobacter Pylori and colon cancer. J Prev Diagn Treat Strategies Med [serial online] 2022 [cited 2022 Jun 26];1:138-42. Available from: http://www.jpdtsm.com/text.asp?2022/1/2/138/347544
| Introduction|| |
Colorectal cancer is the third most common cancer in the world. Colon cancer incidence is increasing in developing countries. It is a heterogeneous tumor made up of a variety of cells with varied characteristics. This cancer results from the proliferation of cancer cells in the colon, rectum, and appendix.
Helicobacter pylori is the most common Helicobacter species seen in humans. Helicobacter species are classified into gastric, enteric, or enterohepatic. H. pylori is a Gram-negative bacterium that lives on the stomach mucosa. It produces urea enzymes, vacuoles toxins, and cytotoxin-related genes.,
Many studies demonstrate that gastric H. pylori infection is linked to stomach cancer. It is also linked to an elevated risk of colorectal cancer. Adenomas are precancerous tumors that can progress to malignancy, which consider the most common cause of colorectal cancer. Numerous studies detected that H. pylori infection is linked to increased serum gastrin. Hypergastrinemia is linked to rectal cell proliferation and increases the growth of colorectal cancer cells. Furthermore, hypergastrinemia causes the formation of colon adenoma and the adenoma-cancer sequence. These findings suggest that infection with H. pylori may raise the risk of colorectal cancer.
Infection with H. pylori is one of the most common chronic bacterial infections worldwide, particularly in developing countries. This bacterium causes many diseases, including lymphoma, gastritis, peptic ulcers, and stomach cancer. Infection with H. pylori strains that produce the CagA protein raises the chance of developing stomach adenocarcinoma. Only a few previous studies have looked into the link between H. pylori infection and colorectal cancer. H. pylori infection is linked to hypergastrinemia and colorectal mucosa proliferation. This link occurs through direct stimulation, dysbiosis of the gut microbiota, and alterations in the gut microbiome, all of which cause the production of colorectal polyps. However, there is no consensus on whether H. pylori infection is related to colorectal polyps independently or whether the connection varies depending on the histological type of colorectal polyps. Although most of the research mentioned H. pylori's role in gastric cancer, some studies look into its role in cancers of the esophagus, pancreas, colon, rectum, and biliary tract,, including extra-digestive organs such as the lungs and larynx.
The study protocol was approved by the Ethical Committee in the Nasiriyah Health Directorate. In addition, verbal approval was obtained from the patients before taking the sample. Health measures and safety were taken when sampling.
| Methods|| |
In this study, we tested blood samples were collected from the patients with colon cancer to assess the presence of anti-H. pylori infection antibodies in 10 patients with colorectal cancer and 10 with no specific pathologies as a control group was compared to each control group using simple and adjusted analyses.
Data were introduced into a specific software Statistical Package for the Social Sciences version 21 for Windows (GraphPad Software, San Diego, California, USA) to do the statistical analysis. The results were expressed as mean ± standard deviation. Comparisons between two means were performed using the t-test. The Chi-square test was used to compare the two categorical variables. In addition, the Pearson correlation was used to explain the relationship between colon cancer with H. pylori infection. P < 0.05 was considered to indicate the statistical significance and is highly significant if P < 0.001.
| Results|| |
[Table 1] shows a comparison of characteristics according to sex, H. pylori infection, and colon cancer between patients and control. The correlation between H. pylori infection and colon cancer is presented in [Table 2]. The correlation between age and H. pylori and colon cancer is shown in [Table 3]. Further, [Figure 1] shows a correlation between H. pylori infection and colon cancer.
|Table 1: Comparison of characteristics according to sex, Helicobacter pylori infection, and colon cancer between patients and control|
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|Table 2: Correlation between Helicobacter pylori infection and colon cancer|
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|Figure 1: Pearson correlation coefficient: r = 0.436 (P = 0.027), the results of the colon cancer were found to be a positive linear correlation with Helicobacter pylori infection and significant at the 0.05 level (one-tailed)|
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|Table 3: Correlation between age and Helicobacter pylori and colon cancer|
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It is observed that there is no significant difference (P > 0.05) in sex between patients and controls. On the other hand, there was a statistically significant difference (P > 0.05) and a highly significant difference (P > 0.001) in H. pylori infection and colon cancer between patients and control, respectively, as shown in [Table 1].
A significant correlation between H. pylori infection and colon cancer (P > 0.05) is shown in [Table 2]. [Figure 1] shows the results of colon cancer. It was found to be a positive linear correlation with H. pylori infection (r = 0.436) and significant (P = 0.027). The study showed a significant correlation between age and H. pylori and colon cancer (P = 0.013, 0.034, respectively), as presented in [Table 3].
| Discussion|| |
Colon cancer, known as colorectal cancer, bowel cancer, or rectal cancer, is any cancer that affects the colon and rectum. Colorectal cancer is heterogeneous cancer, made up of a variety of cells with varied characteristics. Many studies demonstrate that gastric H. pylori infection (linked to stomach cancer) is linked to a somewhat elevated risk of colon cancer.
The present study showed that there is a significant correlation between H. pylori infection and colon cancer [Table 2], and there was a positive linear correlation with H. pylori infection [Figure 1]. This result agrees with Teimoorian et al., who mentioned that H. pylori infection can be considered a risk factor for colon cancer. Further, Butt and Epplein said that there is growing evidence for H. pylori infection increasing colon cancer risk. The previous meta-analysis of Yuling et al. also demonstrates a positive association between H. pylori infection and the risk of colon cancer. Moreover, José et al. detected that H. pylori might well be one of the factors in the complex multifactorial process that leads to the development of colon cancer.
The exact mechanism of H. pylori infection and colon cancer remains controversial. H. pylori infection of the stomach may promote colon cancer indirectly in a variety of ways. H. pylori upregulates the expression of matrix metalloproteinases (MMPs). MMPs may take part in not only colon cancer but also colorectal tumor invasion and initiation of a metastatic cascade.
H. pylori modulates intestinal microflora. H. pylori infection is associated with reduced acid production, which permits a greater number and variety of microbial species to enter and colonize the intestinal tract. It is proposed that shifts in the composition of colorectal microflora resulting from H. pylori atrophic gastritis may facilitate the selective growth of bacteria such as Bacteroides fragilis, Enterococcus faecalis, and others that are linked to the development of colon cancer.,,,,,
H. pylori infection can lead to abnormal secretion of ghrelin secreted by the gastric mucosa, and ghrelin can prevent the occurrence of colorectal cancer. Further, infection by cagA-positive H. pylori strains is associated with higher levels of gastrin than that by cagA-negative strains., In addition, cagA-positive strains cause overproduction of interleukin (IL-8). IL-8 is known to be a growth factor for human colon carcinoma cells.,,,
H. pylori affects the inflammatory state of the intestine through the release of lipopolysaccharide, cytotoxins, and other toxic substances, which are involved in the formation of colorectal cancer.
The study found a significant correlation between old age and colon cancer [Table 3]. The result agrees with other previous results, who mentioned that the risk of colon cancer increases as people get older. Further, Okamoto et al. showed that the frequency of colon cancer increases with patient age. With age, there is more time for damage in cells to build up and so there is more chance that some of this damage might eventually lead to cancer. This damage in the body can happen by chance when cells are dividing as usual. It may be caused by things from outside the body as chemicals from cigarette smoke or ultrasound rays from the sun. Sometimes, the damage builds up and can cause cells to grow and multiply more than usual, causing cancer.
The present study showed a significant correlation between old age and H. pylori infection, this result agrees with the previous study., This bacterium could be caused by lifestyle choices, such as smoking and diet.
| Conclusion|| |
Current evidence suggested that H. pylori infection was associated with colorectal cancer. These findings suggested that H. pylori infection may be a possible risk factor for colorectal cancer, which is important for the prevention of colorectal cancer in the adult population.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Ferlay J, Shin HR, Bray F, Forman D, Mathers C, Parkin DM. Estimates of worldwide burden of cancer in 2008: GLOBOCAN 2008. Int J Cancer 2010;127:2893-917.
Gutman M, Fidler IJ. Biology of human colon cancer metastasis. World J Surg 1995;19:226-34.
Rickert RR, Auerbach O, Garfinkel L, Hammond EC, Frasca JM. Adenomatous lesions of the large bowel: An autopsy survey. Cancer 1979;43:1847-57.
Kienesberger S, Cox L, Livanos A, Zhang XS, Chung J, Perez-Perez G, et al
. Gastric Helicobacter pylori
infection affects local and distant microbial populations and host responses. Cell Rep 2016;14:1395-407.
Santos ML, De Brito BB, Da Silva FA, Sampaio MM, Marques HS, Silva E, et al. Helicobacter pylori
infection: Beyond gastric manifestations. World Journal of Gastroenterology 2020;26:4076.
Wroblewski LE, Peek RM Jr. Helicobacter pylori
, Cancer, and the Gastric Microbiota. Adv Exp Med Biol 2016;908:393-408. doi:10.1007/978-3-319-41388-4_19.
Limburg PJ, Stolzenberg-Solomon RZ, Colbert LH, Perez-Perez GI, Blaser MJ, Taylor PR, et al
. Helicobacter pylori
seropositivity and colorectal cancer risk: A prospective study of male smokers. Cancer Epidemiol Prev Biomark 2002;11:1095-9.
Engin AB, Karahalil B, Engin A, Karakaya AE. Oxidative stress, Helicobacter pylori
, and OGG1 Ser326Cys, XPC Lys939Gln, and XPD Lys751Gln polymorphisms in a Turkish population with colorectal carcinoma. Genet Test Mol Biomarkers 2010;14:559-64.
Atkin WS, Edwards R, Kralj-Hans I, Wooldrage K, Hart AR, Northover JM, et al.
Once-only flexible sigmoidoscopy screening in prevention of colorectal cancer: A multicentre randomised controlled trial. Lancet 2010;375:1624-33.
Fireman Z, Trost L, Kopelman Y, Segal A, Sternberg A. Helicobacter pylori
: Seroprevalence and colorectal cancer. Isr Med Assoc J 2000;2:6-9.
Teimoorian F, Ranaei M, Tilaki, KH, Shirvani JS, Vosough Z. Association of Helicobacter pylori
infection with colon cancer and adenomatous polyps. Iran J Pathol 2018;13:325.
Shmuely H, Passaro D, Figer A, Niv Y, Pitlik S, Samra Z, et al
. Relationship between Helicobacter pylori
CagA status and colorectal cancer. Am J Gastroenterol 2001;96:3406-10.
Lu D, Wang M, Ke X, Wang Q, Wang J, Li D, et al.
Association between H. pylori
infection and colorectal polyps: A meta-analysis of observational studies. Front Med (Lausanne) 2021;8:706036.
Siddheshwar R, Muhammad K, Gray J, Kelly S. Seroprevalence of Helicobacter pylori
in patients with colorectal polyps and colorectal carcinoma. Am J Gastroenterol 2001;96:84-8.
Trikudanathan G, Philip A, Dasanu CA, Baker WL. Association between Helicobacter pylori
infection and pancreatic cancer. A cumulative meta-analysis. JOP 2011;12:26-31.
Mounika P. Helicobacter pylori
infection and risk of lung cancer: A meta-analysis. Lung Cancer Int 2013;2013:131869.
Teimoorian F, Ranaei M, Hajian Tilaki K, Shokri Shirvani J, Vosough Z. Association of Helicobacter pylori
Infection With Colon Cancer and Adenomatous Polyps. Iran J Pathol 2018;13:325-32.
Butt J, Epplein M. Helicobacter pylori
and colorectal cancer-A bacterium going abroad? PLoS Pathog 2019;15:e1007861.
Yuling Z, Zhao J, Mingjiang B, Chunyan X, Xinyu H, Baoning W. Association between Helicobacter pylori
infection and the risk of colorectal cancer. Medicine 2020;99:e21832.
José UD, William OR, Martín GZ. Review of Helicobacter pylori
and colon cancer. Rev Col Gastroenterol 2014;29:255-61.
Yeh YC, Sheu BS, Cheng HC, Wang YL, Yang HB, Wu JJ. Elevated serum matrix metalloproteinase-3 and -7 in H. pylori
-related gastric cancer can be biomarkers correlating with a poor survival. Dig Dis Sci 2010;55:1649-57.
Groblewska M, Mroczko B, Gryko M, Kędra B, Szmitkowski M. Matrix metalloproteinase 2 and tissue inhibitor of matrix metalloproteinases 2 in the diagnosis of colorectal adenoma and cancer patients. Folia Histochem Cytobiol 2010;48:564-71.
Cuevas-Ramos G, Petit CR, Marcq I, Boury M, Oswald E, Nougayrède JP. Escherichia coli
induces DNA damage in vivo
and triggers genomic instability in mammalian cells. Proc Natl Acad Sci U S A 2010;107:11537-42.
Wu S, Morin PJ, Maouyo D, Sears CL. Bacteroides fragilis
enterotoxin induces c-Myc expression and cellular proliferation. Gastroenterology 2003;124:392-400.
Toprak NU, Yagci A, Gulluoglu BM, Akin ML, Demirkalem P, Celenk T, et al.
A possible role of Bacteroides fragilis
enterotoxin in the aetiology of colorectal cancer. Clin Microbiol Infect 2006;12:782-6.
Sobhani I, Tap J, Roudot-Thoraval F, Roperch JP, Letulle S, Langella P, et al.
Microbial dysbiosis in colorectal cancer (CRC) patients. PLoS One 2011;6:e16393.
Wang X, Allen TD, May RJ, Lightfoot S, Houchen CW, Huycke MM. Enterococcus faecalis
induces aneuploidy and tetraploidy in colonic epithelial cells through a bystander effect. Cancer Res 2008;68:9909-17.
Moore WE, Moore LH. Intestinal floras of populations that have a high risk of colon cancer. Appl Environ Microbiol 1995;61:3202-7.
Romo-González C, Mendoza E, Mera RM, Coria-Jiménez R, Chico-Aldama P, Gomez-Diaz R, et al. Helicobacter pylori
infection and serum leptin, obestatin, and ghrelin levels in Mexican schoolchildren. Pediatr Res 2017;82:607-13.
Murphy G, Cross AJ, Dawsey SM, Stanczyk FZ, Kamangar F, Weinstein SJ, et al.
Serum ghrelin is associated with risk of colorectal adenocarcinomas in the ATBC study. Gut 2018;67:1646-51.
Parente F, Imbesi V, Maconi G, Cucino C, Sangaletti O, Vago L, et al.
Influence of bacterial CagA status on gastritis, gastric function indices, and pattern of symptoms in H. pylori
-positive dyspeptic patients. Am J Gastroenterol 1998;93:1073-9.
Konturek PC, Konturek SJ, Bielanski W, Karczewska E, Pierzchalski P, Duda A, et al.
Role of gastrin in gastric cancerogenesis in Helicobacter pylori
infected humans. J Physiol Pharmacol 1999;50:857-73.
Li A, Varney ML, Singh RK. Expression of interleukin 8 and its receptors in human colon carcinoma cells with different metastatic potentials. Clin Cancer Res 2001;7:3298-304.
Lee YS, Choi I, Ning Y, Kim NY, Khatchadourian V, Yang D, et al.
Interleukin-8 and its receptor CXCR2 in the tumour microenvironment promote colon cancer growth, progression and metastasis. Br J Cancer 2012;106:1833-41.
Fox SH, Whalen GF, Sanders MM, Burleson JA, Jennings K, Kurtzman S, et al.
Angiogenesis in normal tissue adjacent to colon cancer. J Surg Oncol 1998;69:230-4.
Brew R, Erikson JS, West DC, Kinsella AR, Slavin J, Christmas SE. Interleukin-8 as an autocrine growth factor for human colon carcinoma cells in vitro
. Cytokine 2000;12:78-85.
Yokota S, Ohnishi T, Muroi M, Tanamoto K, Fujii N, Amano K. Highly-purified Helicobacter pylori
LPS preparations induce weak inflammatory reactions and utilize Toll-like receptor 2 complex but not Toll-like receptor 4 complex. FEMS Immunol Med Microbiol 2007;51:140-8.
Guo Q, Shen S, Li X, Tang K, Zhou W. Inflammatory factors promote the development of colorectal cancer. Zhong Nan Da Xue Xue Bao Yi Xue Ban 2011;36:646-9.
Efremidou EI, Liratzopoulos N, Papageorgiou SM, Romanidis K, Tourlis T, Kouklakis G, et al.
Colorectal carcinoma: Correlation between age, gender and subsite distribution. Chirurgia (Bucur) 2008;103:659-63.
Okamoto M, Shiratori Y, Yamaji Y, Kato J, Ikenoue T, Togo G, et al.
Relationship between age and site of colorectal cancer based on colonoscopy findings. Gastrointest Endosc 2002;55:548-51.
Pilotto A, Franceschi M. Helicobacter pylori
infection in older people. World J Gastroenterol 2014;20:6364-73.
Safe AF, Warren B, Corfield A, McNulty CA, Watson B, Mountford RA, Read A. Helicobacter pylori Infection in elderly people: Correlation between histology and serology. Age Ageing 1993;22:215-20.
[Table 1], [Table 2], [Table 3]