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Grading studies of gliomas according to 11C-acetate PET/CT

 Last Update: 2023-01-01
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Dongwoo Kim et al.
of Severance Hospital affiliated to Yonsei University in South Korea detected cerebral glioma-reactive glial cell proliferation by 11C-acetate PET/CT and graded glioma.
The results were published in the October 2022 issue of the journal
Clinical Nuclear Medicine.

- Excerpted from the article chapter

【Ref: Kim D, et al.
Clin Nucl Med.
2022 Oct 1; 47(10):863-868.
doi: 10.
1097/RLU.
0000000000004341.
Epub 2022 Jul 26.
】

Research background

The World Health Organization (WHO) recommends that clinically relevant genetic information such as isocitrate dehydrogenase (IDH) be combined with traditional histopathology for glioma grading, which can improve the objectivity of grading and the accuracy of
prognosis judgment.

However, histopathology-based tumor grading requires at least invasive tissue biopsy and can lead to sampling errors and reading errors
.

Imaging with advanced data analysis can noninvasively characterize
the tumor and adjacent microenvironment before surgery.

The Neuro-Oncology Working Group recommends PET/CT imaging to help grade tumors, determine boundaries, guide treatment, and determine prognosis
.

Of all PET/CT tracers, neurological tumors are best identified by radiolabeled amino acids, have a high tumor-cortical background uptake ratio, and are able to show tumors that are not enhanced on MRI
.

However, oligodendroglioma has as high amino acid uptake as glioblastoma, severely limiting the grading
of gliomas by radiolabeled amino acids.

11C-acetate is an astrocyte-specific energy substrate that is elevated
in reactive astrocytes in response to neuroinflammatory diseases.

11 C-acetate PET/CT can detect increased uptake of 11 C-acetate due to astrocytes in neuroinflammatory animal models, Alzheimer's disease patients, and glioma patients.

Dongwoo Kim et al.
of Severance Hospital affiliated to Yonsei University in South Korea detected cerebral glioma-reactive glial cell proliferation by 11 C-acetate PET/CT and graded glioma.
The results were published in the October 2022 issue of the journal
Clinical Nuclear Medicine.

Research methods

The study retrospectively analyzed 182 patients with histologically confirmed glioma admitted from February 2016 to December 2020; Among them, there were 104 males and 78 females; The mean age was 47 years (range 23-77 years).

MRI-enhanced imaging and 11C-acetate PET/CT were performed
preoperatively in all patients.

All gliomas were classified
according to the 2016 edition of the WHO Central Nervous System Tumor Grading Standard.

Immunohistochemistry detects IDH1 R132H protein expression
.

When immunohistochemistry is negative, IDH1 sequencing
is performed.

Fluorescence in situ hybridization analysis of 1p/19q codeletion state
.

All patients had a brain scan on an empty stomach 6 hours prior to PET/CT examination, 11 minutes intravenous C-acetate for 10 minutes followed by a brain scan for 20 minutes, and the results were jointly evaluated
by two nuclear medicine physicians.

The tumor and the maximum standard uptake value (SUVmax) and the mean standard uptake value of the contralateral choroid plexus (SUVmean) were collected, and the tumor-to-contralateral choroid plexus ratio (TCR) was used as the tumor radiation uptake standard
.

Study results

The results showed that among the 182 patients, 58 had WHO-2 grade tumors, 53 had WHO-3 tumors, and 71 had WHO-4 grade tumors
.

143 cases were astrocytomas and 39 cases were oligodendroglioma
.

100 cases were completely resected and 82 cases were partially resected
.

Ninety-one cases were IDH1 mutant and 91 were IDH1 wild type
.

The mean TCR of 11 C-acetate in IDH1 mutant patients was 1.
3 (interquartile 1.
10-1.
59); IDH1 wild-type patients11 The mean TCR of C-acetate was 2.
38 (quartile 2.
01-3.
38), and there was a significant difference in TCR values between the two groups (P<0.
0001), and ROC curve analysis showed that the area under the curve of IDH1 mutant and wild type was 0.
917 (P<0.
001).
<b20>
In WHO-2 astrocytoma, the mean TCR of IDH1 mutant 11 C-acetate was 1.
10 (0.
99-1.
30), and IDH1 wild type was 1.
50 (1.
43-1.
81) (P=0.
003).

In WHO-3 astrocytoma, the mean TCR of IDH1 mutant 11 C-acetate was 1.
46 (1.
19-1.
70) and IDH1 wild type was 2.
03 (1.
77-2.
28) (P=0.
002).

Among WHO-4 tumors, 1.
70 (1.
26-2.
17) and 2.
77 (2.
27-3.
82) (P=0.
002),
respectively.

Therefore, it is thought that the TCR value of 11C-acetate differs significantly
between IDH1 mutant and wild-type astrocytoma.

The mean TCR of 11C-acetate was 1.
20 (interquartile 1.
00-1.
50) for low-grade gliomas and 2.
25 (interquartile 1.
70-3.
01) for high-grade gliomas (P<0.
0001<b20>).

The TCRs of IDH1 wild-type low-grade glioma and high-grade glioma were 1.
50 (interquartile 1.
43-1.
81) and 2.
50 (quartile 2.
12-3.
53), respectively (P=0.
0001).
The TCRs of IDH1 mutant low-grade glioma and high-grade glioma were 1.
10 (interquartile 1.
00-1.
35) and 1.
48 (interquartile 1.
30-1.
74), respectively (P<0.
0001<b22>).

To distinguish low-grade and high-grade gliomas, the area under the curve of IDH1 mutant glioma was 0.
951, while the area under the curve of all tumors was 0.
898 (P=0.
134).
There was no significant significance, but the area under the IDH1 mutant curve was significantly larger than that under the IDH1 wild type curve (0.
783, P=0.
0202; P=0.
028).
The results showed that the 11C-acetate TCR value was more useful
in the IDH1 wild-type glioma grade than in the IDH1 mutant glioma grade.

Among the 91 cases of IDH1 mutant glioma, there was no significant difference between astrocytoma and oligodendroglioma 11 C-acetate TCR value (P>0.
05); the average was 11 The C-acetate TCR value was 1.
10 in WHO-2 grade IDH1-mutant astrocytoma, 1.
46 in WHO-3 tumors, and 1.
70
in WHO-4 grade tumors.

There was a significant difference between WHO-2 and WHO-4 tumors (P=0.
002); However, there were no significant differences
between WHO-2 and 3 tumors (P=0.
069) and between WHO-3 and 4 tumors (P=0.
533).

The average 11C-acetate TCR value was 1.
30 in WHO-2 IDH1 mutant oligodendroglioma, which was significantly different from WHO-3 grade 1.
46 (P=0.
010).

11C-acetate has a significant advantage over radiation-labeled amino acids in differentiating oligodendroglioma from high-grade glioma, and the mean 11C-acetate TCR value is significantly lower than that of grade 4 IDH1 wild-type glioma
in WHO-3 oligodendroglioma.

Conclusion of the study

The study found that high uptake of 11C-acetate was associated with high-grade IDH1 wild-type gliomas, which was beneficial in distinguishing high-grade IDH1-mutant gliomas from low-grade
gliomas.

In particular, the low uptake rate of 11C-acetate in oligodendroglioma can distinguish oligodendroglioma from high-grade IDH1 wild-type glioma, which is superior
to radiolabeled amino acids.

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