scholarly journals Types of Gastric Carcinomas

2018 ◽  
Vol 19 (12) ◽  
pp. 4109 ◽  
Author(s):  
Helge Waldum ◽  
Reidar Fossmark
Keyword(s):  
Gastric Cancer ◽  
Stem Cell ◽  
Gastric Carcinogenesis ◽  
Cell Of Origin ◽  
Gastric Carcinomas ◽  
Ecl Cell ◽  
Cells Of Origin ◽  
Increased Risk

Gastric cancer has reduced prevalence, but poor prognoses. To improve treatment, better knowledge of carcinogenesis and cells of origin should be sought. Stomach cancers are typically localized to one of the three mucosae; cardial, oxyntic and antral. Moreover, not only the stem cell, but the ECL cell may proliferate and give rise to tumours. According to Laurén, the classification of gastric carcinomas seems to reflect biological important differences and possible different cell of origin since the two subtypes, intestinal and diffuse, do not transform into the other and show different epidemiology. The stem cell probably gives rise to the intestinal type, whereas the ECL cell may be important in the diffuse type. Elevation of gastrin may be the carcinogenic factor for Helicobacter pylori as well as the recently described increased risk of gastric cancer due to proton pump inhibitor treatment. Therefore, it is essential to determine the role of the gastrin target cell, the ECL cell, in gastric carcinogenesis. Clinical trials with gastrin antagonists could improve prognoses in those with gastrin receptor positive tumours. However, further studies on gastric carcinomas applying relative available methods and with the highest sensitivity are warranted to improve our knowledge of gastric carcinogenesis.

scholarly journals Loss of CDC4/FBXW7 in Gastric Carinoma

2010 ◽  
Vol 32 (5-6) ◽  
pp. 347-359
Author(s):  
A. N. Milne ◽  
R. Leguit ◽  
W. E. Corver ◽  
F. H. M. Morsink ◽  
M. Polak ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Loss Of Heterozygosity ◽  
Tissue Microarrays ◽  
Suppressor Gene ◽  
Gastric Carcinogenesis ◽  
Gastric Carcinoma Cell ◽  
Gastric Carcinomas ◽  
Gastric Cancers ◽  
Tumor Types

Background: CDC4/FBXW7, encoding a ubiquitin ligase, maps to 4q32 and has been implicated as a tumor suppressor gene and therapeutic target in many tumor types. Mutations in colonic adenomas, and the frequent losses on 4q described in gastric cancer prompt speculation about the role of CDC4/FBXW7 in gastric carcinogenesis.Methods: We assessed the role of CDC4/FBXW7 in gastric cancer, through loss of heterozygosity (LOH) and multiplex ligation-dependent probe amplification (MLPA) on 47 flow-sorted gastric carcinomas including early-onset gastric cancers (EOGC) and xenografted conventional gastric carcinomas. Ploidy analysis was carried out on 39 EOGCs and immunohistochemistry of CDC4/FBXW7 and its substrates c-myc, c-jun, Notch and cyclin E was performed on 204 gastric carcinomas using tissue microarrays (TMAs). Sequence analysis of CDC4/FBXW7 was carried out on gastric carcinoma cell lines and xenografts.Results: Loss of heterozygosity of CDC4/FBXW7 occurred in 32% of EOGCs, and correlated with loss of expression in 26%. Loss of expression was frequent in both EOGC and conventional gastric cancers. No CDC4/FBXW7 mutations were found and loss of CDC4/FBXW7 did not correlate with ploidy status. There was a significant correlation between loss of CDC4/FBXW7 expression and upregulation of c-myc.Conclusions: Loss of CDC4/FBXW7 appears to play a role in both EOGC and conventional gastric carcinogenesis, and c-myc overexpression is likely to be an important oncogenic consequence of CDC4/FBXW7 loss.

scholarly journals Tumor Classification Should Be Based on Biology and Not Consensus: Re-Defining Tumors Based on Biology May Accelerate Progress, An Experience of Gastric Cancer

Cancers ◽  
2021 ◽  
Vol 13 (13) ◽  
pp. 3159
Author(s):  
Helge Waldum
Keyword(s):  
Gastric Cancer ◽  
Malignant Tumors ◽  
Growth Control ◽  
Neuroendocrine Differentiation ◽  
Diffuse Type ◽  
Cell Of Origin ◽  
Genetic Changes ◽  
Ecl Cell ◽  
Neuroendocrine Carcinomas ◽  
Complete Carcinogens

Malignant tumors are a consequence of genetic changes mainly occurring during cell division, sometimes with a congenital component. Therefore, accelerated cell divisions will necessarily predispose individuals, whether due to conditions of chronic cell destruction or hormonal overstimulation. It has been postulated that two genetic hits are necessary for the development of malignancy (Knudson). The correct view is probably that the number of genetic changes needed depends on the role the mutated genes have in proliferation and growth control. Hormones should accordingly be regarded as complete carcinogens. In this review based upon experience of gastric cancer where gastrin is central in the pathogenesis, it is argued that oxyntic atrophy—and not metaplasia as postulated by Correa—is the central precancer change in gastric mucosa. Moreover, the target cell of gastrin, the enterochromaffin-like (ECL) cell, is central in gastric carcinogenesis and most probably the cell of origin of gastric carcinomas of the diffuse type according to Lauren (a classification probable in accordance with biology). The distinction between adenocarcinomas and neuroendocrine carcinomas based upon a certain percentage of cancer cells with neuroendocrine differentiation is questioned. To make progress in the treatment of cancer, a correct classification system and knowledge of the pathogenesis are necessary.

scholarly journals Role of Bacterial Overgrowth in the Stomach as an Additional Risk Factor for Gastritis

2003 ◽  
Vol 17 (suppl b) ◽  
pp. 13B-17B ◽  
Author(s):  
Gregory Naylor ◽  
Anthony Axon
Keyword(s):  
Gastric Cancer ◽  
Cell Mass ◽  
Bacterial Overgrowth ◽  
Nitroso Compounds ◽  
Current Evidence ◽  
Additional Risk Factor ◽  
Proximal Small Bowel ◽  
Increased Risk ◽  
H Pylori

Gastric bacteria can either be ingested or ascend from the distal bowel; however, their survival is usually limited by gastric acidity and motility. A reduction in gastric acid can result in bacterial overgrowth in the stomach and proximal small bowel, and the number of organisms rises as the intragastric pH rises.The increased risk of noncardia gastric cancer seen in patients with hypochlorhydria may be explained by an excess of nitrites and N-nitroso compounds (NOCs). These compounds are found in the diet of populations with a high gastric cancer risk, but can also be produced by the organisms that exist in the hypochlorhydria stomach. It has long been hypothsized that nitrites and NOCs act as one of the triggers in the atrophy-metaplasia-dysplasia-carcinoma path. However, although indirect data have linked the premalignant changes of metaplasia and dysplasia to NOCs, direct measurement of gastric nitrites and NOCs has not confirmed such a link.The role ofHelicobacter pyloriin bacterial overgrowth is mainly as a cause of hypochlorhydria resulting from atrophic gastritis, leading to a reduction in the parietal cell mass.Acid-suppressing drugs can result in bacterial overgrowth and increased nitrites and NOCs, although there is no current evidence for an increased risk of gastric cancer in patients taking them. One explanation is that the stomach appears to be colonized by different organisms than those in patients with hypochlorhydria for other reasons. There is some evidence that bacterial overgrowth per se can cause gastric inflammation in mice; however, although in humans the degree of gastric inflammation is greater when overgrowth is more prominant this may simply reflect the greater degree of hypochlorhydria in patients with a more severe H pylori-induced inflammation.

Brain tumor-initiating cells and cells of origin in glioblastoma

2011 ◽  
Vol 2 (4) ◽  
Author(s):  
Sameer Agnihotri ◽  
Diana Munoz ◽  
Gelareh Zadeh ◽  
Abhijit Guha
Keyword(s):  
Brain Tumour ◽  
Large Scale ◽  
Recent Literature ◽  
Cell Of Origin ◽  
Tumor Initiating Cells ◽  
Primary Brain Tumour ◽  
Cells Of Origin ◽  
Brain Tumor Initiating Cells ◽  
Candidate Regions

AbstractGlioblastoma Multiforme (GBM) is the most malignant and devastating primary brain tumour with a median survival of ∼12–16 months. Although recent large scale sequencing projects have shed considerable light into the complexity of the disease, there remains much to be elucidated in the hopes of generating effective therapeutic strategies. Although these studies investigate the mutations and expression of bulk tumour they have limits with respect to cell of origin and the concept of brain tumour initiating cells (BTIC). Current research has challenged the old paradigm of the stochastic model as recent evidence suggests that a subset of cancer cells within a tumor is responsible for tumor initiation, maintenance, and resistance to therapy. To gain a better understanding of the different compartment of cells that GBM comprise of require careful and elegant experiments. In addition to studying GBM, exploring the role of normal neural stem cells and progenitors cells is essential to partially explain whether these GBM BTIC behave similarly or differently then their non transformed counterparts. Here we discuss the recent literature between the two models, candidate regions of glioma genesis, candidate cells of origin for GBM, and possible therapeutic avenues to explore.

scholarly journals The Role of PPARγinHelicobacter pyloriInfection and Gastric Carcinogenesis

PPAR Research ◽  
2012 ◽  
Vol 2012 ◽  
pp. 1-6 ◽  
Author(s):  
Jong-Min Lee ◽  
Sung Soo Kim ◽  
Young-Seok Cho
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Current Knowledge ◽  
Mucosal Injury ◽  
Gastric Carcinogenesis ◽  
Etiologic Factor ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
H Pylori

Peroxisome proliferator-activated receptorγ(PPARγ) is a nuclear receptor that is important in many physiological and pathological processes, such as lipid metabolism, insulin sensitivity, inflammation, cell proliferation, and carcinogenesis. Several studies have shown that PPARγplays an important role in gastric mucosal injury due toHelicobacter pylori(H. pylori). AsH. pyloriinfection is the main etiologic factor in chronic gastritis and gastric cancer, understanding of the potential roles of PPARγinH. pyloriinfection may lead to the development of a therapeutic target. In this paper, the authors discuss the current knowledge on the role of PPARγinH. pyloriinfection and its related gastric carcinogenesis.

scholarly journals Interdisciplinary insights into the link between gut microbiome and gastric carcinogenesis—what is currently known?

2021 ◽  
Author(s):  
Karolina Kaźmierczak-Siedlecka ◽  
Agnieszka Daca ◽  
Giandomenico Roviello ◽  
Martina Catalano ◽  
Karol Połom
Keyword(s):  
Gastric Cancer ◽  
Gut Microbiome ◽  
Short Chain Fatty Acids ◽  
Gastric Carcinogenesis ◽  
Point Of View ◽  
Molecular Techniques ◽  
Nitroso Compounds ◽  
Gastric Microbiota ◽  
Development Of Gastric Cancer

AbstractCurrently, gastric cancer is one of the leading death-related cancer globally. The etiopathogenesis of gastric cancer is multifactorial and includes among others dysbiotic alterations of gastric microbiota. Molecular techniques revealed that stomach is not a sterile organ and it is resides with ecosystem of microbes. Due to the fact that the role of Helicobacter pylori infection in development of gastric cancer is established and well-studied, this paper is mainly focused on the role of other bacterial as well as viral and fungal gut microbiota imbalance in gastric carcinogenesis. Notably, not only the composition of gastric microbiota may play an important role in development of gastric cancer, but also its activity. Microbial metabolites, such as short-chain fatty acids, polyamines, N-nitroso compounds, and lactate, may significantly affect gastric carcinogenesis. Therefore, this paper discussed aforementioned aspects with the interdisciplinary insights (regarding also immunological point of view) into the association between gut microbiome and gastric carcinogenesis based on up-to-date studies.

Cleft lip and palate in general dental practice: filling in the gaps

Dental Update ◽  
2021 ◽  
Vol 48 (7) ◽  
pp. 547-554
Author(s):  
Sharan Reddy ◽  
Catherine Liu ◽  
Mina Vaidyanathan ◽  
Nabina Bhujel
Keyword(s):  
Oral Health ◽  
Dental Caries ◽  
Cleft Lip ◽  
Cleft Lip And Palate ◽  
Dental Practice ◽  
Craniofacial Anomalies ◽  
Dental Anomalies ◽  
Increased Risk

Cleft lip and palate (CLP) is the most common of craniofacial anomalies in humans. CLP results from disruption of embryonic processes during orofacial development; while syndromic clefts may have clearer aetiology, non-syndromic clefts are heterogeneous in aetiology. It is important for GDPs to understand the classification of CLP and the structure of centralized cleft centres in order to communicate with cleft teams. This article aims to clarify the role of GDPs within cleft management and discusses challenges in maintaining oral health in this group of patients, including increased risk of dental caries and periodontal disease, dental anomalies and psychosocial considerations. CPD/Clinical Relevance: The GDP should be responsible for maintaining good oral health for the patient with cleft lip and palate, focusing on prevention from a young age and restorative work if needed.

scholarly journals The Updated World Health Organization Glioma Classification: Cellular and Molecular Origins of Adult Infiltrating Gliomas

2017 ◽  
Vol 141 (12) ◽  
pp. 1633-1645 ◽  
Author(s):  
David J. Pisapia
Keyword(s):  
Central Nervous System ◽  
Animal Models ◽  
Who Classification ◽  
World Health ◽  
Central Nervous System Tumors ◽  
Nervous System Tumors ◽  
Cells Of Origin ◽  
Health Organization

Context.— In the recently updated World Health Organization (WHO) classification of central nervous system tumors, our concept of infiltrating gliomas as a molecular dichotomy between oligodendroglial and astrocytic tumors has been codified. Advances in animal models of glioma and a wealth of sophisticated molecular analyses of human glioma tissue have led to a greater understanding of some of the biologic underpinnings of gliomagenesis. Objective.— To review our understanding of gliomagenesis in the setting of the recently updated WHO classification of central nervous system tumors. Topics addressed include a summary of an updated diagnostic schema for infiltrating gliomas, the crucial importance of isocitrate dehydrogenase mutations, candidate cells of origin for gliomas, environmental and other posited contributing factors to gliomagenesis, and the possible role of chromatin topology in setting the stage for gliomagenesis. Data Sources.— We conducted a primary literature search using PubMed. Conclusions.— With multidimensional molecular data sets spanning increasingly larger numbers of patients with infiltrating gliomas, our understanding of the disease at the point of surgical resection has improved dramatically and this understanding is reflected in the updated WHO classification. Animal models have demonstrated a diversity of candidates for glioma cells of origin, but crucial questions remain, including the role of neural stem cells, more differentiated progenitor cells, and glioma stem cells. At this stage the increase in data generated from human samples will hopefully inform the creation of newer animal models that will recapitulate more accurately the diversity of gliomas and provide novel insights into the biologic mechanisms underlying tumor initiation and progression.

scholarly journals Molecular characterization of the stomach microbiota in patients with gastric cancer and in controls

2009 ◽  
Vol 58 (4) ◽  
pp. 509-516 ◽  
Author(s):  
Johan Dicksved ◽  
Mathilda Lindberg ◽  
Magnus Rosenquist ◽  
Helena Enroth ◽  
Janet K. Jansson ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Gastric Acid ◽  
Rflp Analysis ◽  
Rrna Gene ◽  
Bacterial Phyla ◽  
Increased Risk ◽  
H Pylori ◽  
Development Of Gastric Cancer

Persistent infection of the gastric mucosa by Helicobacter pylori can initiate an inflammatory cascade that progresses into atrophic gastritis, a condition associated with reduced capacity for secretion of gastric acid and an increased risk of developing gastric cancer. The role of H. pylori as an initiator of inflammation is evident but the mechanism for development into gastric cancer has not yet been proven. A reduced capacity for gastric acid secretion allows survival and proliferation of other microbes that normally are killed by the acidic environment. It has been postulated that some of these species may be involved in the development of gastric cancer; however, their identities are poorly defined. In this study, the gastric microbiota from ten patients with gastric cancer was characterized and compared with that from five dyspeptic controls using the molecular profiling approach terminal restriction fragment length polymorphism (T-RFLP), in combination with 16S rRNA gene cloning and sequencing. T-RFLP analysis revealed a complex bacterial community in the cancer patients that was not significantly different from that in the controls. Sequencing of 140 clones revealed 102 phylotypes, with representatives from five bacterial phyla (Firmicutes, Bacteroidetes, Proteobacteria, Actinobacteria and Fusobacteria). The data revealed a relatively low abundance of H. pylori and showed that the gastric cancer microbiota was instead dominated by different species of the genera Streptococcus, Lactobacillus, Veillonella and Prevotella. The respective role of these species in development of gastric cancer remains to be determined.

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