PMC10021297_01
(A) HE (x100); (B) Vimentin(+) (x100); (C) CD68(+) (x100); (D) CK(partial+) (x100).
pore-29-1610983-g001.jpg
PMC10021297_04_pore-29-1610983-g001.jpg
F1
Pathological sections from this patient were subjected to whole genome anslysis by second-generation sequencing (Sidi Precision Medicine, Illumina Nextseq500; 3DMed, Shanghai, China, http://www.3dmedcare.com), and the results demonstrated (Supplementary Table S1; Supplementary Figure S1) that 6 genetic mutations were associated with targeted therapy, prognosis and drug resistance.
PMC10021297_02
(A) HE (x100); (B) Vimentin(+) (x100); (C) CD68(focal +) (x100); (D) CK(focal +) (x100).
pore-29-1610983-g002.jpg
PMC10021297_04_pore-29-1610983-g002.jpg
F2
PARP inhibitor-related genes had no mutations (BRCA1/2 no mutations, HRD score 0 (Supplementary Figure S2)).
PMC10021297_03
(A) HE(x100); (B) Vimentin(+) (x100); (C) CD68(OGC+) (x100); (D) CK(+) (x100).
pore-29-1610983-g003.jpg
PMC10021297_04_pore-29-1610983-g003.jpg
F3
Immunotherapy-related gene mutations were observed negative PD-1 immunohistochemistry results (TPS <1%, CPS = 5) and a low tumor mutational burden (TMB) (Supplementary Figure S3A) at 3.35 Muts/Mb, which occur in less 76% of pancreatic cancer patients. Microsatellite analysis showed microsatellite stability (MSS) (Supplementary Figure S3B) and negative EBV test results.
PMC10021297_04
(A) HE (x100); (B) Vimentin(+) (x100); (C) CD68(+) (x100); (D) CK(partial+) (x100).
pore-29-1610983-g001.jpg
PMC10021297_04_pore-29-1610983-g001.jpg
F1
Pathological sections from this patient were subjected to whole genome anslysis by second-generation sequencing (Sidi Precision Medicine, Illumina Nextseq500; 3DMed, Shanghai, China, http://www.3dmedcare.com), and the results demonstrated (Supplementary Table S1; Supplementary Figure S1) that 6 genetic mutations were associated with targeted therapy, prognosis and drug resistance.
(A) HE (x100); (B) Vimentin(+) (x100); (C) CD68(focal +) (x100); (D) CK(focal +) (x100).
pore-29-1610983-g002.jpg
PMC10021297_04_pore-29-1610983-g002.jpg
F2
PARP inhibitor-related genes had no mutations (BRCA1/2 no mutations, HRD score 0 (Supplementary Figure S2)).
(A) HE(x100); (B) Vimentin(+) (x100); (C) CD68(OGC+) (x100); (D) CK(+) (x100).
pore-29-1610983-g003.jpg
PMC10021297_04_pore-29-1610983-g003.jpg
F3
Immunotherapy-related gene mutations were observed negative PD-1 immunohistochemistry results (TPS <1%, CPS = 5) and a low tumor mutational burden (TMB) (Supplementary Figure S3A) at 3.35 Muts/Mb, which occur in less 76% of pancreatic cancer patients. Microsatellite analysis showed microsatellite stability (MSS) (Supplementary Figure S3B) and negative EBV test results.
(A) HE (x100); (B) Vimentin (intraepithelial carcinoma -, anaplastic +) (x100); (C) CD68(+) (anaplastic +) (x100); (D) CK(intraepithelial carcinoma +, few anaplastic +) (x100).
pore-29-1610983-g004.jpg
PMC10021297_04_pore-29-1610983-g004.jpg
F4
Immunohistochemical staining (as in Figure 4) revealed the following Vim (intraepithelial carcinoma -, anaplastic +), CK (intraepithelial carcinoma +, few anaplastic +), EMA (intraepithelial carcinoma +), CK7 (intraepithelial carcinoma +), CK8/8 (intraepithelial carcinoma +), CD68 (anaplastic +), CK20 (-), CR (subepithelial mesenchymal +), des (subepithelial mesenchymal +), Muc-1 (intraepithelial carcinoma +), Muc-2 (-), P53 (anaplastic +20%), and Ki-67 (intraepithelial carcinoma +80%, anaplastic +70%).