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Molecular & Cellular Oncology Volume 5, 2018 - Issue 4
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Revisiting glucose metabolism in cancer: lessons from a PKM knock-in model

Taku SatoDivision of Cancer Chemotherapy, Miyagi Cancer Center Research Institute, Natori, JapanView further author information
,
Mami MoritaDivision of Cancer Chemotherapy, Miyagi Cancer Center Research Institute, Natori, JapanView further author information
,
Miyuki NomuraDivision of Cancer Chemotherapy, Miyagi Cancer Center Research Institute, Natori, JapanView further author information
&
Nobuhiro TanumaDivision of Cancer Chemotherapy, Miyagi Cancer Center Research Institute, Natori, JapanCorrespondence[email protected]
View further author information
Article: e1472054 | Received 11 Apr 2018, Accepted 20 Apr 2018, Published online: 01 Aug 2018

Figures & data

Figure 1. Tumor cells of origin and pyruvate kinase M (PKM) isoforms.

Both lung neuroendocrine tumors (NETs) and their cells of origin (bronchial neuroendocrine (NE) cells) show high PKM1 expression, whereas other most tumor cells and their cells/tissues of origin express PKM2.

Figure 1. Tumor cells of origin and pyruvate kinase M (PKM) isoforms.Both lung neuroendocrine tumors (NETs) and their cells of origin (bronchial neuroendocrine (NE) cells) show high PKM1 expression, whereas other most tumor cells and their cells/tissues of origin express PKM2.

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