GLUT1 glucose transporter expression in colorectal carcinoma: a marker for poor prognosis.

Abstract:

BACKGROUND:Malignant cells exhibit increased glycolytic metabolism, and in many cases increased glucose transporter gene expression. The authors hypothesized that GLUT1 glucose transporter expression is increased in colorectal carcinoma, and that the degree of expression might have prognostic significance. METHODS:GLUT1 glucose transporter immunostaining was studied in normal colon and benign colon adenomas and in 112 colorectal carcinomas from patients for whom long term clinical outcome was known. RESULTS:GLUT1 immunostaining was absent in normal colorectal epithelium and tubular adenomas, and absent or only weakly apparent in tubulovillous adenomas. The majority of carcinomas (101 of 112; 90%) had GLUT1 immunostaining. Tumors from 92 patients had low GLUT1 expression (< 50% of cells were GLUT1 positive) and 19 of these patients (21%) died of disease during follow-up. In contrast, tumors from 20 patients had high GLUT1 expression (> 50% of cells were GLUT1 positive) and 9 of these patients (45%) died of disease during follow-up. Disease specific mortality was greater in patients with high GLUT1 tumors (relative risk of 2.4; P=0.02). In a multivariate analysis to assess whether high GLUT1 staining correlated with increased mortality independently of Dukes stage, the risk of death from colon carcinoma in the group with high GLUT1 staining was 2.3 times that in the group with low GLUT1 staining, a difference that approached statistical significance (P=0.07). CONCLUSIONS:GLUT1 glucose transporter expression is associated strongly with neoplastic progression in the colon, and assessment of the extent of GLUT1 immunostaining in colorectal carcinoma identifies patients with a poorer prognosis.

journal_name

Cancer

journal_title

Cancer

authors

Haber RS,Rathan A,Weiser KR,Pritsker A,Itzkowitz SH,Bodian C,Slater G,Weiss A,Burstein DE

doi

10.1002/(sici)1097-0142(19980701)83:1<34::aid-cncr

subject

Has Abstract

pub_date

1998-07-01 00:00:00

pages

34-40

issue

1

eissn

0008-543X

issn

1097-0142

pii

10.1002/(SICI)1097-0142(19980701)83:1<34::AID-CNCR

journal_volume

83

pub_type

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