Gastric amphicrine carcinoma with leptomeningeal metastases: A case report

Figure 1 Variation curve of tumor markers throughout the course of treatment. CA724: Carbohydrate antigen 72-4; CA199: Carbohydrate antigen 19-9; CEA: Carcinoembryonic antigen; NSE: Neuron-specific enolase; Pro-GRP: Pro-gastrin-releasing peptide.

Figure 2 Computed tomography manifestations during the first-line treatment. A and B: Before first-line treatment; C and D: After two cycles of first-line treatment; E and F: After four cycles of first-line treatment; G and H: After six cycles of first-line treatment.

Figure 3 Gastroscopy examination. A and B: Before first-line treatment; C and D: After three cycles of second-line treatment.

Figure 4 Positron emission tomography-computed tomography examination. A-C: Hypermetabolic lesions in the gastric wall of the antrum (A and B), the liver (B and C), and lymph nodes around the portal vein and along the lesser curvature of the stomach (B and C).

Figure 5 Pathology of the gastric antrum lesion. A: Tumor cells arranged in clusters with a micropapillary pattern (hematoxylin and eosin [H&E], 200 ×); B: Tumor cells exhibiting cord-like or linear arrangements (H&E, 200 ×); C: In certain regions, tumor cells appeared in cord-like or linear patterns, with scattered signet ring cells present within a mucinous background (H&E, 100 ×); D: The majority of tumor cells were moderately large, displaying fine chromatin, inconspicuous nucleoli, and readily identifiable mitotic figures; Some nuclei were eccentrically displaced (H&E, 400 ×); E: Signet ring cells within the mucinous background showed marked atypia, with visible nucleoli (H&E, 400 ×).

Figure 6 Immunohistochemistry of the gastric antrum lesion. A: Chromogranin A (CgA) expression was diffusely positive (EnVision, 200 ×); B: Synaptophysin (Syn) showed diffuse positive expression (EnVision, 200 ×); C: Insulinoma-associated protein 1 (INSM1) demonstrated diffuse positivity (EnVision, 200 ×); D and E: Mucin 1 (MUC1) and MUC2 expression were both positive (EnVision, 200 ×); F: Diastase-Periodic Acid-Schiff (D-PAS) staining revealed intracellular mucin within the cytoplasm of tumor cells (Special stain, 400 ×); G: Cytokeratin 7 (CK7) expression was diffusely positive (EnVision, 200 ×); H: Ki-67 proliferation index (EnVision, 200 ×); I: Dual staining showing combined positivity of D-PAS special staining and INSM1 immunohistochemistry (400 ×).

Figure 7 Pathological findings of the liver lesion and cerebrospinal fluid. A: Tumor cells exhibited marked atypia with nuclear displacement and a morphology resembling signet ring cells (hematoxylin and eosin [H&E], 400 ×); B and C: Insulinoma-associated protein 1 (INSM1) showed diffuse positive expression (EnVision, 200 ×); D and E: Diastase-Periodic Acid-Schiff (D-PAS) staining demonstrated the presence of mucin within the cytoplasm of tumor cells (Special stain, 400 ×); F: Tumor cells were relatively uniform in size, with inconspicuous nucleoli and eccentrically located nuclei, resembling signet ring cells; occasional tumor giant cells were noted (H&E, 400 ×); G: Tumor cells displayed features similar to those in panel D, with identifiable mitotic figures (H&E, 400 ×). CSF: Cerebrospinal fluid.

Figure 8 Computed tomography manifestations during the second-line and third-line treatment. A: Before the second-line treatment; B: After three cycles of second-line treatment; C: After two cycles of third-line treatment.

Figure 9 Process of diagnosis and treatment. PD: Progressive disease; PFS: Progression-free survival.

Figure 10  Schematic diagram of four types of mixed carcinomas. MiNEN: Mixed neuroendocrine–non-neuroendocrine neoplasms.