PMC9905670_01
The multimodal 18F-FDG PET/MR images for evaluating the uterine. (A) MIP image of whole-body PET. (B) Axial T2WI. (C) Axial T1WI+C. (D) Axial DWI. (E) Axial apparent diffusion image (ADC) map. (F) Sagittal PET image. (G) Sagittal fs T2WI. (H) Sagittal PET/T2WI fusion image. On the pelvic sagittal MRI, there was a polypoid mass in the lower segment of the uterine (red arrow). The polypoid lesion showed a slightly high intensity signal on T1WI and fs T2WI, but no restricted diffusion signal in DWI and ADC. A mild enhancement of the lesion was observed on T1WI+C. The PET and PET/MR fusion images showed slight hypermetabolism in the lesion (SUVmax = 5.7g/ml). Unexpectedly, the MIP image of whole-body PET revealed an abnormal hypermetabolism in the left lower abdomen (red arrow, SUVmax = 17.68 g/ml).
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On the pelvic sagittal MRI, there was no significant thickened endometrium and no high FDG uptake in the uterine corpus, but only a polypoid mass stretching from the lower segment of the uterine endometrium to the cervical canal ( Figures 1B, G ). Figure 1 ). Following gadolinium administration, a mild enhancement of the lesion was observed on contrast enhanced T1WI (T1WI+C) ( Figure 1C ). The PET and PET/MR fusion images showed slight hypermetabolism in the lesion ( Figures 1F, H ). Unexpectedly, the maximum intensity projection (MIP) images of whole-body PET revealed an abnormal hypermetabolism in the left lower abdomen (SUVmax = 17.68 g/ml) ( Figure 1A ).
The multimodal 18F-FDG PET/MR images for evaluating the descending colon mass. (A) Coronal whole-body T2WI. (B) Coronal PET/T2WI fusion image. (C) Axial DWI. (D) Axial T1WI+C. (E) Axial PET PET/T2WI fusion image. The coronal whole-body T2WI and PET/MR fusion images showed that the abnormal hypermetabolism on PET images was a mass in the intestinal wall of the descending colon (red arrow). The thickened descending colon wall that showed markedly high signal intensity on either DWI (ADCmean = 0.75*10^-3 mm2/s) or T1WI+C and hypermetabolism on axial PET/MR fusion images was observed (red arrow).
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T2WI and PET/MR fusion images showed that the abnormal hypermetabolism on PET images was a mass in the intestinal wall of the descending colon ( Figures 2A, B ). The thickened descending colon wall that showed markedly high signal intensity on either DWI (ADCmean = 0.75*10^-3 mm2/s) ( Figure 2C ) or T1WI+C ( Figure 2D ) and hypermetabolism on axial PET/MR fusion images ( Figure 2E ) was observed.
Histopathological images of endometrial and colon carcinomas. (A) The HE staining of colonic mass tissue in the descended colon (the microscope magnifyingx400). (B) The HE staining of polypoid tissue in the lower uterine segment (the microscope magnifyingx400). (C-D) The IHC staining of polypoid tissue in the lower uterine segment (the microscope magnifyingx400). MLH1 and PMS2 proteins were negative expression in the IHC staining.
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And the endometrial carcinoma (G2) ( Figure 3B ) categorized as superficial myometrial invasion and the poor-differentiated tubular adenocarcinoma ( Figure 3A ) invading the muscularis propria without serosa invasion were demonstrated by histologic analysis. MLH1 and PMS2 proteins were negative expression in the resected tumor tissues derived from uterus ( Figures 3C, D ).
Gene analysis of endometrial and colon carcinomas. (A-D) The outcomes of DNA mismatch repair gene analysis in endometrial adenocarcinoma tissue. (E-F) The outcomes of DNA mismatch repair gene analysis in colon adenocarcinoma tissue. Endometrial adenocarcinoma tissue genetic testing revealed deletion mutations of exons 16 and 17, replacement mutations of exon 16 in MSH2, and duplication mutation of exon 5 in MSH6. Exon 10 and 17 mutations in MLH1 were also discovered during genetic testing of the colon adenocarcinoma sample.
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The results of endometrial carcinoma gene analysis included deletion mutations in exon 15 and exon 17 of MLH1 ( Figures 4A, B ), replacement mutation in exon 16 of MSH-2 ( Figure 4C ) and duplication mutation in exon 5 of MSH-6 ( Figure 4D ). And deletion mutation and replacement mutation of MLH-1 derived from the colon tumor were also confirmed ( Figures 4E, F ).