Extended Data Fig. 2: Assessment of glucose and glutamine fate and amino acid levels in primary pancreatic tumors and liver metastases. | Nature Metabolism

Extended Data Fig. 2: Assessment of glucose and glutamine fate and amino acid levels in primary pancreatic tumors and liver metastases.

From: Cancer tissue of origin constrains the growth and metabolism of metastases

Extended Data Fig. 2

(a) Plasma enrichment of U13C-glucose as determined by GC-MS after a 6-hour U13C-glucose infusion at a rate of 0.4 mg/min29 in mice with a primary pancreatic tumor (pancreas; n=2 female mice) or with a liver metastatic pancreatic tumor (liver; n=4 female mice). (b-i) Fractional labeling of each indicated metabolite in the indicated tissue harvested from aged-matched control mice (pancreas, liver) or from mice harboring a primary pancreatic tumor, a subcutaneous pancreatic tumor, or a liver metastatic tumor that was infused with U13C-glucose as measured by GC-MS. In all cases tumors were generated by implanting pancreatic cancer cells derived from a primary tumor arising in the KP−/−C model. Mean +/− stdev; **p= 0.0088, *p=0.0224 (panel b); *p=0.0237; n.s.- not significant. Comparisons between groups were made using a two-tailed Student’s t-test (b and c). n=6 mice were used for the normal tissues (both pancreas and liver), n=4 mice were used for the pancreatic tumor, n=5 mice were used for the liver tumor, and n=5 mice were used for the subcutaneous tumors. (j-o) Fractional labeling of each indicated metabolite in pancreatic cancer primary or liver metastasis tumors as measured by GC-MS following a 6-hour infusion of U13C-glutamine at a rate of 3.7 mg/kg/min into mice. In all cases tumors were generated by implanting pancreatic cancer cells derived from a primary tumor arising in the KP−/−C mouse model. Mean +/− stdev; n=4 mice/group. (p) Levels of amino acids measured by LC-MS from primary pancreatic tumors and matched liver metastases arising in KPC mice; Mean +/− stdev (n=4 mice/condition).

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