Table 2 Correlation between CDKN2A homozygous deletion and MTAP or p16 immunohistochemistry.

From: Utility of methylthioadenosine phosphorylase immunohistochemical deficiency as a surrogate for CDKN2A homozygous deletion in the assessment of adult-type infiltrating astrocytoma

 

All (n = 178)

IDH-mutant astrocytoma (n = 77)

IDH-mutant oligodendroglioma (n = 13)

IDH-wildtype glioblastoma (n = 88)

CDKN2A

CDKN2A

CDKN2A

CDKN2A

CDKN2A

CDKN2A

CDKN2A

CDKN2A

HD

Non-HD

HD

Non-HD

HD

Non-HD

HD

Non-HD

MTAP_lost

68

4

15

1c

4

3

49

0

MTAP_retained

10

96

2

59

2

4

6

33

  Sensitivity (%)

87.2

88.2

66.7

89.1

  Specificity (%)

96.0

98.3

57.1

100

p16 nuca_lost

70

32

16

16

4

6

50

10

p16 nuc_retained

8

68

1

44

2

1

5

23

  Sensitivity (%)

89.7

 

94.1

 

66.7

 

90.9

 

  Specificity (%)

68.0

 

73.3

 

14.3

 

69.7

 

p16 cytob_lost

63

27

16

15

4

6

43

6

p16 cyto_retained

15

73

1

45

2

1

12

27

  Sensitivity (%)

80.8

94.1

66.7

78.2

  Specificity (%)

73.0

75.0

14.3

81.8

  1. ap16 nuclear expression.
  2. bp16 cytoplasmic expression.
  3. cThis tumor was anaplastic astrocytoma, IDH-mutant and harbored 9p21 homozygous deletion by FISH, although CDKN2A was intact by MLPA.
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