Beyond gastric adenocarcinoma: Multimodality assessment of common and uncommon gastric neoplasms

Abstract

Despite advances in molecular biology, imaging, and treatment, gastric neoplasms remain a significant cause of morbidity and mortality; gastric adenocarcinoma is the fifth most common malignancy and third most common cause of death worldwide (Brenner et al., Methods Mol Biol 472:467-477, 2009; Howson et al. Epidemiol Rev 8:1-27, 1986; Roder, Gastric Cancer 5(Suppl 1):5-11, 2002; Ferlay et al., GLOBOCAN 2012 v1.0, Cancer Incidence and Mortality Worldwide: IARC CancerBase No. 11 [Internet]. International Agency for Research on Cancer, 2013). Because of both the frequency at which malignant gastric tumors occur as well as the worldwide impact, gastric neoplasms remain important lesions to identify and characterize on all imaging modalities. Despite the varied histologies and behaviors of these neoplasms, many have similar imaging features. Nonetheless, the treatment, management, and prognosis of gastric neoplasms vary by pathology, so it is essential for the radiologist to make every effort to differentiate between these lesions and raise the less common entities as differential diagnostic considerations when appropriate.

Keywords: Benign gastric neoplasms; Gastric cancer; Malignant gastric neoplasms; Metastasis.

Conflict of interest statement

None of the other authors have declared any conflicts of interest.

Figures

Fig. 1

Fundic gland polyp. A CT images demonstrating multiple polypoid lesions in the fundus of the stomach (arrow). B Endoscopic images of the fundic gland polyps (arrow).

Fig. 2

Glomus tumor. A CT image demonstrating hyper-enhancing glomus tumor in the antrum and pylorus of the stomach (arrow).

Fig. 3

Gastric Lipoma. A Polypoid fat-attenuating lesion (arrow). B In- (arrow) and out-of-phase (arrowhead) imaging demonstrating loss of signal consistent with fat.

Fig. 4

Heterotopic Pancreas. A CT demonstrating nodular focus within the stomach with similar enhancement characteristics as the pancreas (arrow).

Fig. 5

Pathology of gastric tumors. A Papillary adenocarcinoma. The tumor is composed of papillary structures lined by large tumors cells with prominent nucleoli (arrow). Note the intestinal metaplasia in the background gastric mucosa (arrowhead). B Well-differentiated neuroendocrine tumor (car-cinoid tumor). The tumor shows a nested growth pattern and consists of relatively uniform cells with hyperchromatic nuclei and moderate amounts of cytoplasm (arrow). This tumor arose in a background of chronic atrophic autoimmune gastritis (type I carcinoid). C Gastrointestinal stromal tumor, spindle cell type. The tumor is composed of fascicles of elongated spindle cells with tapering nuclei and palely eosinophilic cytoplasm. D Extranodal marginal zone lymphoma (MALT lymphoma). The tumor is composed of sheets of small lym-phoid cells with variably clear cytoplasm, infiltrating gastric glands (arrow).

Fig. 6

Gastric adenocarcinoma. A Linitis plastica with diffuse gastric wall thickening (arrow). B Coronal image of gastric adenocarcinoma with marked gastric wall thickening at the gastric fundus and tumor extension to the gastrohepatic ligament. C T1 post-contrast images demonstrating enhancing gastric adenocarcinoma in the fundus extending to the gastrohepatic ligament. An associated liver metastasis causes a right-sided perfusion abnormality (arrowhead) and mild intrahepatic biliary ductal dilatation. D T1 post-contrast subtraction MR image from the same patient in Fig. 6C showing an enhancing lesion at the bifurcation of the right hepatic vein (arrow). E Ulcerated gastric adenocarcinoma (arrow) with hepatic (arrowhead) and peritoneal metastases (dashed arrow). F CT demonstrating thickening and calcification in the antrum of the stomach consistent with signet ring gastric cancer.

Fig. 7

Neuroendocrine tumors (carcinoid tumors). A Hyper-vascular gastric neuroendocrine tumor in the fundus, unclassified subtype (arrow). B Hyperenhancing gastrinoma (arrow) in the pancreatic body in a patient with MEN1. C The same patient as in Fig. 2 with resultant hypertrophic gastritis (arrow) in Zollinger–Ellison syndrome and gas-trinomas. This is the substrate for type II neuroendocrine tumors.

Fig. 8

Gastrointestinal stromal tumors (GISTs). A Gastric GIST with endoluminal and exophytic components and calcification (arrow). B Pretreatment appearance of another gastric GIST with associated ulceration (arrow). C Post-treatment appearance of the tumor from B showing marked response to imatinib. D GIST metastasis to the liver showing central hypodensity on CT (arrow). E Post-treatment contrast-enhanced CT demonstrates decreased attenuation of GIST liver metastasis (arrow) measuring 37 Hounsfield Units (HU); pretreatment liver metastasis measured 64 HU.

Fig. 9

Leiomyosarcoma. A Axial CT demonstrating asymmetrical thickening in the body of the stomach (arrow).

Fig. 10

Lymphomas. A CT with oral contrast demonstrating MALT (marginal zone) lymphoma with marked gastric wall thickening (arrow) before treatment. B MALT lymphoma from A shows decreased gastric wall thickening after treatment. C Ulcerated diffuse large B-cell lymphoma (arrow) with peritoneal dissemination (arrowhead). D Diffuse large B-cell lymphoma (arrow) with local spread to the spleen and pancreas (dashed arrow).

Fig. 11

Gastric metastases. Metastases from tabular breast cancer cause diffuse wall thickening on CT (arrow) (A) and marked FDG avidity on PET–CT (arrow) (B). Melanoma metastasis in the stomach shows deep ulceration on CT (arrowhead) (C).

Fig. 12

Gastric seminoma. FDG-PET–CT (A–B) shows diffusely increased FDG uptake in the thickened gastric fundus and body (arrow). Biopsy demonstrated seminoma. Testicular ultrasound showed no primary tumor.