Gastric cancer: prevention, screening and early diagnosis

Abstract

Gastric cancer continues to be an important healthcare problem from a global perspective. Most of the cases in the Western world are diagnosed at late stages when the treatment is largely ineffective. Helicobacter pylori (H. pylori) infection is a well-established carcinogen for gastric cancer. While lifestyle factors are important, the efficacy of interventions in their modification, as in the use of antioxidant supplements, is unconvincing. No organized screening programs can be found outside Asia (Japan and South Korea). Although several screening approaches have been proposed, including indirect atrophy detection by measuring pepsinogen in the circulation, none of them have so far been implemented, and more study data is required to justify any implementation. Mass eradication of H. pylori in high-risk areas tends to be cost-effective, but its adverse effects and resistance remain a concern. Searches for new screening biomarkers, including microRNA and cancer-autoantibody panels, as well as detection of volatile organic compounds in the breath, are in progress. Endoscopy with a proper biopsy follow-up remains the standard for early detection of cancer and related premalignant lesions. At the same time, new advanced high-resolution endoscopic technologies are showing promising results with respect to diagnosing mucosal lesions visually and targeting each biopsy. New histological risk stratifications (classifications), including OLGA and OLGIM, have recently been developed. This review addresses the current means for gastric cancer primary and secondary prevention, the available and emerging methods for screening, and new developments in endoscopic detection of early lesions of the stomach.

Keywords: Gastric cancer; Helicobacter pylori.

Figure 1

White light endoscopy of the stomach of a 60-year-old man. A: Hyperplastic gastric polyp 40 mm × 20 mm in size is clearly visible in the foreground. The flat lesion in the background has been missed during first outpatient esophagogastroduodenoscopy; B: Pathomorphology after initial biopsy and polypectomy confirmed the hyperplastic nature of the polyp.

Figure 2

Esophagogastroduodenoscopy of the same patient. A: The flat lesion in the background can been viewed more easily when better lit; B: Closer view of the superficial elevated lesion; C: After chromoendoscopy with indigo carmine - a roundish lesion 25 mm in diameter can be seen, with a smooth lobulated surface and a 6-mm, reddish protrusion in the distal part; type 0-IIa+Is according to Paris classification; D: Due to the marked inflammation and presence of intestinal metaplasia the precise proximal margin of the lesion is still unclear, even with the use of chromoendscopy.

Figure 3

Characterization of the surrounding mucosa of the same patient. A-C: WLE + chromoendoscopy: pronounced focal mucosal hyperemia, edema, petechiae, multiply foci of intestinal metaplasia; D: Narrow band imaging (NBI) + magnified endoscopy (zoom). The results, according to VS-classification[138]: the surrounding mucosa is inflamed, with a regular stick-like microsurface pattern, slightly irregular wavy microvascular pattern; E: Confocal laser endomicroscopy (CLE): A cross-section of normal glands; F: CLE: A longitudinal section of normal glands; G: CLE: Marks of intestinal metaplasia - Goblet cells; H: Pathomorphology: Active chronic Нр+ gastritis with incomplete intestinal metaplasia and low grade epithelial dysplasia.

Figure 4

Some patient after 2 wk of Helicobacter pylori eradication therapy. The characterization of the flat (IIa) part of the lesion type 0-IIa+Is is neoplastic: A-D: High definition Video-EGD + chromoendoscopy + Zoom: Shows a clear demarcation line between the lesion and surrounding mucosa; E-G: NBI + zoom: A clear demarcation line between the lesion and the surrounding mucosa; H, I: NBI + zoom: An irregular microsurface pattern - elongated and different in size and shape; J, K: An irregular microvascular pattern - tortuous, different in shape and size of the capillaries, forming an irregular network; L: CLE: Marks of intestinal metaplasia - Goblet cells; M: CLE: Deformed glands; N: CLE: Dark irregular glands; pseudostratified epithelium; O: CLE: Dark irregular glands; pseudostratified epithelium; P: Pathomorphology: Incomplete intestinal metaplasia and high grade dysplasia with foci of well-differentiated adenocarcinoma.

Figure 5

Some patient after 2 wk of Helicobacter pylori eradication therapy. The characterization of the protruded (Is) part of the lesion type 0-IIa+Is is a differentiated adenocarcinoma. A: High definition Video-EGD + chromoendoscopy: A closer view of the protruded part of the lesion; B-D: Barrow-band imaging (NBI) + zoom: Unclear shredded microsurface pattern with an irregular network microvascular pattern - the capillaries differ in shape and diameter and are tortuous; E: Confocal laser endomicroscopy (CLE): Dark irregular glands; pseudostratified epithelium; irregularly shaped nuclei; F: CLE: Dark irregular glands; pseudostratified epithelium; G: Pathomorphology: A well-differentiated adenocarcinoma.

Figure 6

Same patient. Endosonography of the lesion 0-IIa + Is. Area of the lesion (25 mm in size): Thickening of mucosa up to 5-7 mm; submucosal layer is clear under the tumor; lymph nodes are not visualized.

Figure 7

Same patient. A-D: The lesion was removed en-block using triangle and IT-2 knives at endoscopic submucosal dissection without any complications; E: Well-differentiated adenocarcinoma no invasion in submucosa, clear horizontal and vertical margins, absence of vascular and lymphatic invasion.