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Neuron Specific Enolase (NSE)

Neuron Specific Enolase (NSE)

Test Highlight

Neuron Specific Enolase (NSE)

  

Clinical Use

  • Monitor disease progression and therapy in individuals with small cell lung cancer (SCLC)

  • Monitor therapy in various other cancers

Clinical Background

NSE is a glycolytic enzyme that catalyzes the conversion of phosphoglycerate to phosphoenol pyruvate. It is present in neurons, neuroendocrine cells, and amine precursor uptake and decarboxylation (APUD) cells. Elevated NSE concentrations are observed in patients with neuroblastoma, pancreatic islet cell carcinoma, medullary thyroid carcinoma, pheochromocytoma, and other neuroendocrine tumors as well as in certain benign conditions. NSE levels are frequently increased in patients with SCLC and infrequently in patients with non-SCLC. NSE has therefore been used to monitor disease progression and management in SCLC.

Method

Enzyme immunoassay

Interpretive Information

Distribution of NSE concentrations in healthy subjects and various benign and malignant disorders is provided in the table.

Table. Distribution of NSE
Patient Groups

No. of Patients

Studied

% with NSE in Indicated Range

<13

ng/mL

13-25

ng/mL

25-50

ng/mL

>50

ng/mL

Blood Donors 33 94 6 0 0

Benign Disorders

Bronchopneumonia

Lung lesions

Gastrointestinal & liver

20

11

45

65

91

84

30

9

16

5

0

0

0

0

0

Malignant Disorders

         

SCLC pre-treatment:

Limited disease

Extensive disease

Non SCLC

Lung metastases

Breast & gastrointestinal

with hepatic metastasis

Prostate

38

39

94

10

20

 42

34

12

83

80

85

 74

24

10

10

20

15

19

29

31

3

0

0

7

13

46

4

0

0

0

Reference: Cooper et al. Br J Cancer. 1985;52:333-338.

This test is performed using a kit that has not been approved or cleared by the FDA. The analytical performance characteristics of this test have been determined by Quest Diagnostics Nichols Institute. This test should not be used for diagnosis without confirmation by other medically established means.

Content reviewed 12/2012

 
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