PMC9755197_01
Treatment timeline. (A) Gastroscopy report at first visit: A large annular mass was observed in the duodenal bulb, extending to the upper part of the descending part. (B, C) Positron emission tomography/computed tomography (PET/CT) before the first-line treatment: a significant uneven thickening of the intestinal wall of duodenal bulb (47 x 40 mm) and multiple lymph node metastases. (D) Computed tomography after four sessions of XELOX treatment. The tumor progressed and fused with surrounding lymph nodes after four cycles of XELOX (65 x 63 mm). (E, F) Computed tomography after two and 19 sessions of tislelizumab in combination with irinotecan.
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Electronic gastroscopy found a huge ring-shaped mass ( Figure 1A ) in the duodenal bulb, and a poorly differentiated adenocarcinoma was confirmed by biopsy. Positron emission tomography/computed tomography (PET/CT) indicated a significant uneven thickening of the duodenal bulb's intestinal wall (47 x 40 mm) and multiple lymph node metastases ( Figures 1B, C ). After two XELOX cycles, the tumor shrank slightly (35 x 28 mm,  Supplementary Figures S1A, B ), and the response evaluation criteria in solid tumors 1.1 (RECIST 1.1) indicated stable disease. On April 6, 2021, a chest and abdominal contrast-enhanced CT suggested that the tumor progressed and fused with surrounding lymph nodes (65 x 63 mm,  Figure 1D ). The giant nodules in the intestinal wall and the lymph nodes shrunk significantly after two sessions of tislelizumab in combination with irinotecan ( Supplementary Figures S1C, D ). After 19 therapy sessions, the giant nodules in the intestinal wall disappeared, and the lymph nodes shrunk significantly ( Figures 1E, F ).
Immune cell infiltration among different TP53/KRAS mutation groups in gastrointestinal tumors. (A) T cell CD8+. (B) T cell regulatory (Tregs). P-values represented TP53/KRAS mutation groups compared to non-mutant group. (Wilcox test. *, P < 0.05; **, P < 0.01; ***, P < 0.001).
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(A, B) Expression of CD8A and PD-L1 among STAD'sTP53/ KRAS mutation groups. (C) Expression of PD-L1 protein among different TP53/ KRAS mutation groups in STAD. (D, E) Expression of CD8A and PD-L1 among different TP53/ KRAS mutation groups in COAD. (F) Expression of PD-L1 protein among different TP53/ KRAS mutation groups in COAD. (Wilcox test. *, P<0.05; ***, P<0.001).
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B ), and the expression of CD8A and PL-L1 was lower than in the wild-type TP53/KRAS group ( Figure 3 ). Besides, reduced PD-L1 protein expression was also associated with TP53 mutation in STAD.