Expression of hexokinase II and Glut-1 in untreated human breast cancer

Brown, Raya S.; Goodman, Tonya M.; Zasadny, Kenneth R.; Greenson, Joel K.; Wahl, Richard L.

doi:10.1016/s0969-8051(02)00288-3

Cited by 133 publications

(90 citation statements)

References 26 publications

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“…GLUT-1 expression was lower in central differentiated areas of WDSCC, i.e. a prostromal pattern, which could be inversely related to the glycogen content, as discussed previously (14,15,19,20).…”

Section: Discussionsupporting

confidence: 66%

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GLUT-1 immunoexpression in oral epithelial dysplasia, oral squamous cell carcinoma, and verrucous carcinoma

Angadi¹,

Angadi²

2015

Journal of Oral Science

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Section: Discussionsupporting

confidence: 66%

“…In the present study, most oral carcinomas demonstrated strong GLUT-1 expression in comparison to NOM and dysplasia. Furthermore, a progressive increase in staining intensity with histologic grade was observed, PDSCC showing the highest intensity (14,15,19,20).…”

Section: Discussionmentioning

confidence: 95%

GLUT-1 immunoexpression in oral epithelial dysplasia, oral squamous cell carcinoma, and verrucous carcinoma

Angadi¹,

Angadi²

2015

Journal of Oral Science

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“…This includes upregulation of hypoxia-inducible factor (HIF) and related proteins such as carbonic anhydrase IX and GLUT-1 (Wykoff et al, 2001;Brown et al, 2002 Figure 1 (A) (from Gatenby and Gillies (2004) with permission). The evolution of breast cancer over time is shown left to right.…”

mentioning

confidence: 99%

“…The diffusion reaction kinetics of spheroids mimics those of intraductal tumour. To detect evolution of constitutive upregulation of glycolysis, we stained specimens for GLUT-1 since prior studies have demonstrated a direct correlation between GLUT-1 expression and increased glucose flux as measured by FdG PET (Brown et al, 1996(Brown et al, , 2002. The presence of regional acidosis was defined by increased expression of NHE-1, which is primarily responsible for extrusion of H þ ions in MCF-7 and other breast cancer-derived populations (Bischof et al, 1996;Turturro et al, 2004).…”

mentioning

confidence: 99%

Cellular adaptations to hypoxia and acidosis during somatic evolution of breast cancer

et al. 2007

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Conceptual models of carcinogenesis typically consist of an evolutionary sequence of heritable changes in genes controlling proliferation, apoptosis, and senescence. We propose that these steps are necessary but not sufficient to produce invasive breast cancer because intraductal tumour growth is also constrained by hypoxia and acidosis that develop as cells proliferate into the lumen and away from the underlying vessels. This requires evolution of glycolytic and acid-resistant phenotypes that, we hypothesise, is critical for emergence of invasive cancer. Mathematical models demonstrate severe hypoxia and acidosis in regions of intraductal tumours more than 100 mm from the basement membrane. Subsequent evolution of glycolytic and acid-resistant phenotypes leads to invasive proliferation. Multicellular spheroids recapitulating ductal carcinoma in situ (DCIS) microenvironmental conditions demonstrate upregulated glucose transporter 1 (GLUT1) as adaptation to hypoxia followed by growth into normoxic regions in qualitative agreement with model predictions. Clinical specimens of DCIS exhibit periluminal distribution of GLUT-1 and Na þ /H þ exchanger (NHE) indicating transcriptional activation by hypoxia and clusters of the same phenotype in the peripheral, presumably normoxic regions similar to the pattern predicted by the models and observed in spheroids. Upregulated GLUT-1 and NHE-1 were observed in microinvasive foci and adjacent intraductal cells. Adaptation to hypoxia and acidosis may represent key events in transition from in situ to invasive cancer.

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“…The primary mechanism of enhanced FDG uptake in tumors is via up-regulation of glucose transporters, although other factors related to the in vivo tumor microenvironment have also been implicated (19)(20)(21)(22).…”

Section: Methodsmentioning

confidence: 99%

In vivopositron-emission tomography imaging of progression and transformation in a mouse model of mammary neoplasia

Abbey¹,

Borowsky²,

McGoldrick³

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

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Expression of hexokinase II and Glut-1 in untreated human breast cancer

Cited by 133 publications

References 26 publications

GLUT-1 immunoexpression in oral epithelial dysplasia, oral squamous cell carcinoma, and verrucous carcinoma

GLUT-1 immunoexpression in oral epithelial dysplasia, oral squamous cell carcinoma, and verrucous carcinoma

Cellular adaptations to hypoxia and acidosis during somatic evolution of breast cancer

In vivopositron-emission tomography imaging of progression and transformation in a mouse model of mammary neoplasia

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