<p>The linitis plastica (LP) phenotype is characterized by diffuse infiltrative mural thickening, reduced distensibility, and absent or subtle mucosal abnormality. It creates a diagnostic paradox in which cross-sectional imaging may suggest advanced malignancy while superficial endoscopic biopsies remain nondiagnostic. This review addresses three key radiologic tasks: recognizing the infiltrative, non-polypoid pattern on cross-sectional imaging; distinguishing it from malignant, benign, and technical mimics; and identifying when persistent imaging suspicion should prompt recommendation of EUS-guided deep tissue sampling after nondiagnostic mucosal biopsy. In the stomach, LP most commonly reflects primary gastric signet ring cell carcinoma (SRCC), but metastatic invasive lobular carcinoma (ILC) of the breast is its most important mimic and may present as delayed gastric involvement years after the initial breast cancer diagnosis. These entities share convergent discohesive tumor biology linked to loss of E-cadherin function encoded by <i>CDH1</i>, a relationship also reflected in the combined gastric and lobular breast cancer risk recognized in Hereditary Diffuse Gastric Cancer syndrome. Beyond the stomach, the linitis pattern may occur as primary or metastatic disease in the rectum, colon, esophagus, duodenum, and urinary bladder. Metastatic spread may also involve the biliary tract, ureters, and gallbladder, where mural thickening or stricturing can mimic inflammatory disease or an alternative primary neoplasm. Recognition of this metastatic hollow-viscus pattern, particularly in patients with known or remote ILC or SRCC, may reduce diagnostic delay and prompt appropriate tissue sampling and pathologic work-up.</p> Graphical abstract <p></p>

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Stomach and beyond: imaging the linitis plastica phenotype in signet ring cell carcinoma

  • Edward McDermott,
  • Korosh Khalili,
  • Tae Kyoung Kim,
  • Vanessa Murad,
  • Chloe Sew Hee,
  • Khaled Y. Elbanna

摘要

The linitis plastica (LP) phenotype is characterized by diffuse infiltrative mural thickening, reduced distensibility, and absent or subtle mucosal abnormality. It creates a diagnostic paradox in which cross-sectional imaging may suggest advanced malignancy while superficial endoscopic biopsies remain nondiagnostic. This review addresses three key radiologic tasks: recognizing the infiltrative, non-polypoid pattern on cross-sectional imaging; distinguishing it from malignant, benign, and technical mimics; and identifying when persistent imaging suspicion should prompt recommendation of EUS-guided deep tissue sampling after nondiagnostic mucosal biopsy. In the stomach, LP most commonly reflects primary gastric signet ring cell carcinoma (SRCC), but metastatic invasive lobular carcinoma (ILC) of the breast is its most important mimic and may present as delayed gastric involvement years after the initial breast cancer diagnosis. These entities share convergent discohesive tumor biology linked to loss of E-cadherin function encoded by CDH1, a relationship also reflected in the combined gastric and lobular breast cancer risk recognized in Hereditary Diffuse Gastric Cancer syndrome. Beyond the stomach, the linitis pattern may occur as primary or metastatic disease in the rectum, colon, esophagus, duodenum, and urinary bladder. Metastatic spread may also involve the biliary tract, ureters, and gallbladder, where mural thickening or stricturing can mimic inflammatory disease or an alternative primary neoplasm. Recognition of this metastatic hollow-viscus pattern, particularly in patients with known or remote ILC or SRCC, may reduce diagnostic delay and prompt appropriate tissue sampling and pathologic work-up.

Graphical abstract