Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UMLS:C0476089 (
endometrial cancer
)
11,379
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Glucose is provided to cells by a family of glucose transport facilitators known as GLUTs. These transporters are expressed in a tissue specific manner and are overexpressed in many primary tumors of these tissues. Regulation of glucose transport facilitator expression has been demonstrated in endometrial tissue and endometrial adenocarcinoma. The following experiments were conducted to quantify and localize the expression of GLUT1 and
GLUT8
in benign endometrium and compare this expression to
endometrial cancer
. Endometrial tissue samples were obtained from random hysterectomy specimens of patients with benign indications for surgery and
endometrial cancer
. Immunoblot and immunolocatization studies were performed using GLUT1 and
GLUT8
specific antisera. Endometrial samples from 65 women who had undergone hysterectomy were examined (n=38 benign, n=27 malignant). A 44 and a 35.4 kDa immunoreacive species was demonstrated in endometrium and
endometrial cancer
for GLUT1 and
GLUT8
, respectively. Upregulation of GLUT1 expression was demonstrated with increasing grade of tumors (P<0.002).
GLUT8
expression was increased in all tumor subtypes compared to atrophic endometrium (P<0.001). Apical localization by GLUT1 and
GLUT8
was demonstrated in endometrial glands. GLUT1 and
GLUT8
demonstrated diffuse intracellular localization in the cancer subtypes. GLUT1 and
GLUT8
are expressed in both human endometrium and
endometrial cancer
. There appears to be a step-wise progression in GLUT1 and
GLUT8
expression as tumor histopathology worsens. GLUT1 and
GLUT8
may be important markers in tumor differentiation, as well as providing energy to rapidly dividing tumor cells.
...
PMID:GLUT1 and GLUT8 in endometrium and endometrial adenocarcinoma. 1689 13