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Paulina Helisz
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Helisz, P.; Gwioździk, W.; Krupa-Kotara, K.; Grajek, M.; Głogowska-Ligus, J.; Słowiński, J. Characteristics and General Classification of Gastric Cancer. Encyclopedia. Available online: https://encyclopedia.pub/entry/41773 (accessed on 20 May 2024).
Helisz P, Gwioździk W, Krupa-Kotara K, Grajek M, Głogowska-Ligus J, Słowiński J. Characteristics and General Classification of Gastric Cancer. Encyclopedia. Available at: https://encyclopedia.pub/entry/41773. Accessed May 20, 2024.
Helisz, Paulina, Weronika Gwioździk, Karolina Krupa-Kotara, Mateusz Grajek, Joanna Głogowska-Ligus, Jerzy Słowiński. "Characteristics and General Classification of Gastric Cancer" Encyclopedia, https://encyclopedia.pub/entry/41773 (accessed May 20, 2024).
Helisz, P., Gwioździk, W., Krupa-Kotara, K., Grajek, M., Głogowska-Ligus, J., & Słowiński, J. (2023, March 01). Characteristics and General Classification of Gastric Cancer. In Encyclopedia. https://encyclopedia.pub/entry/41773
Helisz, Paulina, et al. "Characteristics and General Classification of Gastric Cancer." Encyclopedia. Web. 01 March, 2023.
Characteristics and General Classification of Gastric Cancer
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This entry is adapted from the peer-reviewed paper 10.3390/onco3010003

Gastric tumors have been divided based on their location—cardiac and distal. The former refers to the small paracardial area, while the latter refers to the rest of it. The most popular classification in terms of histology is the Laurén classification, which distinguishes between two types of gastric cancer (GC)—intestinal and diffuse. The first GC subtype is often associated with Helicobacter Pylori and lifestyle, which includes a high intake of table salt and alcohol, a low supply of fruits and vegetables, or smoking. It is estimated that about 15–20% of tumors do not fall under Laurén’s classification and are, therefore, considered intermediate tumors. Clinically, GC can also be divided according to its early or advanced stage. Early gastric cancers refer to small tumors (2–5 cm) that take the form of invasive carcinoma of the gastric mucosa or submucosa. Detection of lesions at their early stage is associated with relatively good survival.

gastric cancer nutraceuticals cancer microbiota

1. Helicobacter Pylori as a Carcinogen

A constant object of research by scientists is the link between bacterial infections and cancer. Although the topic is quite controversial, at this point, it is known that Helicobacter pylori promote the development of GC. The cancer process is a multi-year, multi-stage process that most often begins with chronic gastritis. The vast majority of GC cases are associated with Helicobacter pylori infection (about 60%) [1][2], which is classified as a Gram-negative bacterium, and its natural site of occurrence is the surface of gastric mucosal epithelial cells. Infection with the bacterium of the Helicobacteraceae family is believed to occur as early as childhood, which explains the reduced ability of gastric mucosal lining cells to produce hydrochloric acid with age. Moreover, it is estimated that more than 50% of people worldwide are infected. Undoubtedly, a peculiar feature of Helicobacter pylori is its ability to colonize the stomach for decades, as well as its ability to provide appropriate adaptive conditions surrounding the pathogen by producing large amounts of urease. This enzyme contributes to the degradation of urea to carbon dioxide and ammonia, which, in turn, increases the pH in the stomach due to a previous reduction in hydrochloric acid secretion [1][2][3][4].
The International Agency for Research on Cancer (IARC) and the World Health Organization (WHO) have recognized Helicobacter pylori infection as an important type I carcinogen in the development of GC, but the pathomechanism of the bacterium’s effect on gastric cancer progression is not fully understood, due to the multilevel impact of the pathogen. However, it is known that Helicobacter pylori is associated with superficial gastritis and associated inflammation, and this, in turn, promotes a predisposition to gastric ulcers and adenocarcinoma. The literature data indicate that the bacterium of the genus Helicobacteraceae contributes to structural changes in the gastric epithelium, thereby causing abnormalities in its function. The above course appears to be crucial in the initial stages of carcinogenesis. The process of progression of gastric and duodenal ulceration is initiated by inflammation caused by Helicobacter pylori followed by a decrease in the number of D cells responsible for the production of somatostatin, which, in turn, acts as a somatoliberin antagonist. As a result, there is an increased secretion of hydrochloric acid, which is induced by the hormone produced by G-cells in the gastric body—gastrin [2][3][4][5].
This is because it is emphasized that gastric cancer of the intestinal type is the domain of people of the African race. In contrast, GC with the proximal location of the tumor is the domain of people of the Caucasian race. In addition, it has been proven that environmental factors, as well as lifestyle, play key roles. Helicobacter pylori is an important factor in increasing the risk of developing GC, and a meta-analysis conducted by Hooi et al. in 2017 [6] stresses that the highest incidence of the carcinogenic pathogen is found in Africa, Latin America, the Caribbean, and Asia. The lowest incidence, on the other hand, was attributed to North America and Oceania. The reasons for the above geographical distribution in terms of Helicobacter pylori incidence are attributed to socioeconomic factors, such as the level of urbanization, access to clean water, sanitation, professional education, and environmental awareness. Analyses of the prevalence of infection with the pathogenic bacterium should take into account the fact that populations are sometimes mixed, which can affect the statistics. Nevertheless, Helicobacter pylori infection is often transmitted via the fecal-oral route, so in developing countries without access to clean water, failure to practice proper hygiene, as well as limited access to medical care, may contribute to a higher incidence of infection compared to developed countries [6][7].

2. Gastric Microbiota

Scientific reports relating to the presence of Helicobacter pylori in the gastrointestinal tract have sparked greater interest in the stomach microbiota as a so-called “ecological niche.” It turns out that the stomach environment is populated by bacteria with a high degree of diversity, and their density is estimated at 101–103 CFU (colony-forming units). Studies of the gastric microbiota are inconclusive. In terms of GC development, the potential role of Lactobacillus and Lactococcus bacteria is highlighted. The theoretical causal relationship is seen in their fermentation end product, lactic acid. Most likely, lactate may contribute to tumor progression and enhance angiogenesis. In addition to Lactobacillus and Lactococcus bacteria, attention is also drawn to Nitrospirae bacteria, which are observed in people with GC. There is no doubt that an inadequate diet plays a key role in cancer progression. Thus, in the case of GC, the carcinogenic importance of nitrates, ubiquitous in smoked and cured products—mainly meat—which can consequently lead to the synthesis of N-nitroso compounds, is emphasized. Bacteria of the Nitrospirae type are involved in the metabolic transformation of nitrates and nitrites, so attention is drawn to the carcinogenic role of N-nitrosamines produced by the described pathogen, which may explain their presence in the stomach of GC patients [4][8][9][10].
On the other hand, it is emphasized that chronic Helicobacter pylori infection provides a friendly environment for the growth of new bacteria, through reduced secretion of hydrochloric acid. A study conducted on mice clearly shows that Helicobacter pylori-infected rodents with concomitant hypergastrinemia have a more complex gastric microbiota in GC compared to healthy animals. A study by Ferreira et al. [5] showed that patients with chronic gastritis were characterized by increased amounts of bacteria such as Helicobacter, Streptococcus, Prevontella, and Neisseria, regardless of the presence of Helicobacter pylori infection. In contrast, Citrobacter, Clostridium, and Lactobacillus were observed in patients with achlorhydria and GC. In addition, the authors of the study highlighted the role of Citrobacter rodentium in the process of epithelial cell proliferation, which, in turn, promotes the development of colon tumors in rodents with a genetic load for CC [5]. A 2016 study by Wang et al. [10], on the other hand, found an increased abundance of Escherichia-Shigella in GC patients. The researchers also highlighted the potential genotoxic effects of E. coli in the development of gastric cancer [10].

3. Gut Microbiota and Gastric Cancer

Each year, the number of published papers in the field of gut microbiota and its impact on the host body increases. According to current knowledge, the microbiota of the lower gastrointestinal tract is the most complex and dynamic ecosystem in the human body. It is well known that intestinal dysbiosis has a positive correlation in the aspect of colorectal cancer [11][12][13]. At the time of editing this paper, online database search engines displayed access to a few papers relating to the gut microbiota in the aspect of gastric cancer, which may be due to the limitations and analytical difficulties of the microbiome of this section of the gastrointestinal tract. However, there is no doubt that this topic is becoming an increasing object of interest, due to the desire to understand the pathomechanism of the development of malignant neoplasms, which are among the leading causes of death, and to develop chemoprevention methods. Nevertheless, already several years ago, there were the first firm claims that changes in the intestinal microbiome in the gastrointestinal tract may have a significant impact on the development of gastric cancer [14]. It has also been pointed out that a higher abundance of Enterobacteriaceae is associated with all types of gastric cancer, which could potentially be useful as a marker of gastric cancer [15]. It is also worth noting the mechanism by which the microbiota influences carcinogenesis. Chronic inflammation and infections are important causes of gastric cancer development due to carcinogenic mechanisms, such as inducing mutations and altering gene status, promoting angiogenesis and cell proliferation [16]. The dysbiosis microbiota and its metabolites affect carcinogenesis not only by inducing inflammation and immune dysregulation, leading to genetic instability but also by interfering with drugs used in anticancer therapy [17].
One effective method of GC prevention is Helicobacter pylori eradication. Unfortunately, its adverse consequences include an impact on the disruption of the gut microbiota. Individuals with a history of Helicobacter pylori infection showed a decreased abundance of Bacteroidetes and increased Firmicutes and Proteobacteria [11]. In contrast, those infected with Helicobacter pylori and simultaneously suffering from the aggressive gastric disease had markedly lower abundances of several Bifidobacterium species in the lower intestine, indicating a reduced abundance of protective bacteria [18]. Another study noted an association between Helicobacter pylori infection and the abundance of bacteria from the genera Enterococcus, Lachnoclostridium, Tyzzerella, Roseburia, Butyricicoccus, Dorea, Halomonas, and Burkholderiales. Moreover, an association has been observed between intestinal dysbiosis and the incidence of obesity and older age [19]. In turn, other sources indicate that successful eradication of Helicobacter pylori potentially restores the gastric microbiota to a state similar to that found in uninfected individuals and has been shown to have beneficial effects on the gut microbiota [20].
Clinical studies have noted an altered gut microbiota during the perioperative period. In the intestinal microbiota of GC patients, a higher abundance of Escherichia/Shigella, Veillonella, and Clostridium XVIII and a lower abundance of Bacteroides were observed compared to healthy controls. In contrast, the abundances of Akkermansia, Escherichia/Shigella, Lactobacillus, and Dialister genera changed after surgery [21]. This indicates the problem of intestinal dysbiosis not only as a potential risk factor for the development of gastric cancer but also as a consequence of its occurrence, which affects the patient’s quality of life and health consequences. In addition, it is noteworthy that the choice of treatment has an impact on the gut microbiota of patients with gastric cancer—the surgery will result in a significant change in the gut microbiota [22].
Commonly used proton pump inhibitors (PPIs) in the course of H. pylori infection bear their consequences on the patient’s gut microbiota. The effect of PPIs is to raise the pH of the stomach, which has been disturbed via a pathogen of the Helicobacteraceae genus. Proper use of PPIs, as prescribed by the doctor, brings the expected therapeutic results. However, it is worth noting that long-term intake of proton pump inhibitors contributes to the development of intestinal disorders such as small intestinal bacterial overgrowth (SIBO) and C. difficile infections. PPIs are widely available over-the-counter drugs, so statistics on the use of the aforementioned pharmaceuticals may be underestimated. The effect of the discussed group of drugs does not refer only to increasing the pH in the stomach but also to blocking the action of the so-called proton pump or hydrogen-potassium ATPase, which, in turn, contributes to hypochlorhydria, which explains the increased risk of C. difficile infection and SIBO [23][24]. The prevalence of small intestinal bacterial overgrowth among gastric cancer patients is confirmed by clinical studies [21][23][24][25]. A scientific article edited by Liang et al. [21] highlights the prevalence of SIBO in patients with gastric and colorectal malignancies, as nearly 70% of the study’s participants, claiming to have taken PPIs for a long time, struggled with the intestinal condition addressed [21].

References

  1. Alipour, M. Molecular Mechanism of Helicobacter pylori-Induced Gastric Cancer. J. Gastrointest. Cancer 2021, 52, 23–30.
  2. Chiang, T.H.; Chang, W.J.; Chen, S.L.; Yen, A.M.; Fann, J.C.; Chiu, S.Y.; Chen, Y.R.; Chuang, S.L.; Shieh, C.F.; Liu, C.Y.; et al. Mass eradication of Helicobacter pylori to reduce gastric cancer incidence and mortality: A long-term cohort study on Matsu Islands. Gut 2021, 70, 243–250.
  3. Waldum, H.L.; Rehfeld, J.F. Gastric cancer and gastrin: On the interaction of Helicobacter pylori gastritis and acid inhibitory induced hypergastrinemia. Scand. J. Gastroenterol. 2019, 54, 1118–1123.
  4. Stewart, O.A.; Wu, F.; Chen, Y. The role of gastric microbiota in gastric cancer. Gut. Microbes 2020, 11, 1220–1230.
  5. Ferreira, R.M.; Pereira-Marques, J.; Pinto-Ribeiro, I.; Costa, J.; Carneiro, F.; Machado, J.; Figueiredo, C. Gastric microbial community profiling reveals a dysbiotic cancer-associated microbiota. Gut 2018, 67, 226–236.
  6. Hooi, J.K.Y.; Lai, W.Y.; Ng, W.K.; Suen, M.M.Y.; Underwood, F.E.; Tanyingoh, D.; Malfertheiner, P.; Graham, D.Y.; Wong, V.W.S.; Wu, J.C.Y.; et al. Global Prevalence of Helicobacter pylori Infection: Systematic Review and Meta-Analysis. Gastroenterology 2017, 153, 420–429.
  7. Kadar, Z.; Jung, I.; Orlowska, J.; Szentirmay, Z.; Sugimura, H.; Turdean, S.; Simona, G. Geographic particularities in incidence and etiopathogenesis of sporadic gastric cancer. Pol. J. Pathol. 2015, 66, 254–259.
  8. Piscione, M.; Mazzone, M.; Di Marcantonio, M.C.; Muraro, R.; Mincione, G. Eradication of Helicobacter pylori and Gastric Cancer: A Controversial Relationship. Front Microbiol. 2021, 12, 630852.
  9. Dai, D.; Yang, Y.; Yu, J.; Dang, T.; Qin, W.; Teng, L.; Ye, J.; Jiang, H. Interactions between gastric microbiota and metabolites in gastric cancer. Cell Death Dis. 2021, 12, 1104.
  10. Wang, L.; Zhou, J.; Xin, Y.; Geng, C.; Tian, Z.; Yu, X.; Dong, Q. Bacterial overgrowth and diversification of microbiota in gastric cancer. Eur. J. Gastroenterol. Hepatol. 2016, 28, 261–266.
  11. Krupa-Kotara, K.; Helisz, P.; Gwioździk, W.; Grajek, M. The importance of the microbiota in shaping women’s health—The current state of knowledge. Appl. Microbiol. 2022, 3, 11–34.
  12. Chen, C.; Chen, L.; Lin, L.; Jin, D.; Yaoqiang, D.; Lyu, J. Research progress on gut microbiota in patients with gastric cancer, esophageal cancer, and small intestine cancer. Appl. Microbiol. Biotechnol 2021, 105, 4415–4425.
  13. Gao, J.J.; Zhang, Y.; Gerhard, M.; Mejias-Luque, R.; Zhang, L.; Vieth, M.; Ma, J.-L.; Bajbouj, M.; Suchanek, S.; Liu, W.-D.; et al. Association Between Gut Microbiota and Helicobacter pylori-Related Gastric Lesions in a High-Risk Population of Gastric Cancer. Front. Cell Infect. Microbiol. 2018, 8, 202.
  14. Patel, T.; Bhattacharya, P.; Das, S. Gut microbiota: An Indicator to Gastrointestinal Tract Diseases. J. Gastrointest. Canc. 2016, 47, 232–238.
  15. Sarhadi, V.; Mathew, B.; Kokkola, A.; Karla, T.; Tikkanen, M.; Rautelin, H.; Lahti, L.; Puolakkainen, P.; Knuutila, S. Gut microbiota of patients with different subtypes of gastric cancer and gastrointestinal stromal tumors. Gut Pathog. 2021, 13, 11.
  16. Yang, D.; Meng, X.-Y.; Wang, Y.; Zhang, J.; Zhao, Y.; Zheng, Z.C.; Zhang, T. Effects of probiotics on gastric cancer-related inflammation: A systematic review and meta-analysis. J. Food Biochem. 2022, 46, e14034.
  17. Meng, C.; Bai, C.; Brown, T.D.; Hood, L.E.; Tian, Q. Human Gut Microbiota and Gastrointestinal Cancer. Genom. Proteom. Bioinform. 2018, 16, 33–49.
  18. Devi, T.B.; Devadas, K.; George, M.; Gandhimathi, A.; Chouhan, D.; Retnakumar, R.J.; Alexander, S.M.; Varghese, J.; Dharmaseelan, S.; Chandrika, S.K.; et al. Low Bifidobacterium Abundance in the Lower Gut Microbiota Is Associated with Helicobacter pylori-Related Gastric Ulcer and Gastric Cancer. Front. Microbiol. 2021, 12, 631140.
  19. Miao, Y.; Tang, H.; Zhai, Q.; Liu, L.; Xia, L.; Wu, W.; Xu, Y.; Wang, J. Gut Microbiota Dysbiosis in the Development and Progression of Gastric Cancer. J. Oncol. 2022, 2022, 9971619.
  20. Guo, Y.; Zhang, Y.; Gerhard, M.; Gao, J.J.; Mejias-Luque, R.; Zhang, L.; Vieth, M.; Ma, J.L.; Bajbouj, M.; Suchanek, S.; et al. Effect of Helicobacter pylori on gastrointestinal microbiota: A population-based study in Linqu, a high-risk area of gastric cancer. Gut 2020, 69, 1598–1607.
  21. Liang, W.; Yang, Y.; Wang, H.; Wang, H.; Yu, X.; Lu, Y.; Shen, S.; Teng, L. Gut microbiota shifts in patients with gastric cancer in perioperative period. Medicine 2019, 98, e16626.
  22. Chen, C.; Shen, J.; Du, Y.; Shi, X.; Niu, Y.; Jin, G.; Liu, Y.; Shi, Y.; Lyu, J.; Lin, L. Characteristics of gut microbiota in patients with gastric cancer by surgery, chemotherapy and lymph node metastasis. Clin. Transl. Oncol. 2022, 24, 2181–2190.
  23. Hills, R.D., Jr.; Pontefract, B.A.; Mishcon, H.R.; Black, C.A.; Sutton, S.C.; Theberge, C.R. Gut Microbiome: Profound Implications for Diet and Disease. Nutrients 2019, 11, 1613.
  24. Weitsman, S.; Celly, S.; Leite, G.; Mathur, R.; Sedighi, R.; Barlow, G.M.; Morales, W.; Sanchez, M.; Parodi, G.; Villanueva-Millan, M.J.; et al. Effects of Proton Pump Inhibitors on the Small Bowel and Stool Microbiomes. Dig. Dis. Sci. 2022, 67, 224–232.
  25. Jacobs, C.; Coss Adame, E.; Attaluri, A.; Valestin, J.; Rao, S.S. Dysmotility and ppi use are independent risk factors for small intestinal bacterial and/or fungal overgrowth. Aliment. Pharm. Ther. 2013, 37, 1103–1111.
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Subjects: Oncology; Health Policy & Services; Nutrition & Dietetics
Contributors MDPI registered users' name will be linked to their SciProfiles pages. To register with us, please refer to https://encyclopedia.pub/register :
Paulina Helisz
,
Weronika Gwioździk
,
Karolina Krupa-Kotara
,
Mateusz Grajek
,
Joanna Głogowska-Ligus
,
Jerzy Słowiński
View Times: 274
Entry Collection: Gastrointestinal Disease
Revisions: 3 times (View History)
Update Date: 03 Mar 2023
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