Summary of Study ST002527
This data is available at the NIH Common Fund's National Metabolomics Data Repository (NMDR) website, the Metabolomics Workbench, https://www.metabolomicsworkbench.org, where it has been assigned Project ID PR001627. The data can be accessed directly via it's Project DOI: 10.21228/M8D434 This work is supported by NIH grant, U2C- DK119886.
See: https://www.metabolomicsworkbench.org/about/howtocite.php
This study contains a large results data set and is not available in the mwTab file. It is only available for download via FTP as data file(s) here.
| Study ID | ST002527 |
| Study Title | HPLC-MS-MS analysis amino acid levels in PDAC IF samples upon arginase inhibition |
| Study Summary | To test the hypothesis that myeloid arginase-1 activity could be responsible for pancreatic ductal adenocarninoma microenvironmental arginine starvation (PMID: 30990168), we generated orthotopic allograft mPDAC tumors in a mouse model with myeloid specific Arg1 knockout (LysM-Cre+/+-; Arg1fl/fl) and control animals (Arg1fl/fl). We also tested this with pharmacological inhibition of arginase-1 with the small-molecule inhibitor CB-1158. We then isolated IF from these tumors at end-stage and measured the levels of amino acids including arginine and ornithine in these samples. |
| Institute | University of Chicago |
| Last Name | Apiz Saab |
| First Name | Juan |
| Address | 929 E. 57th St. |
| japizsaab@uchicago.edu | |
| Phone | 7738346506 |
| Submit Date | 2022-08-05 |
| Raw Data Available | Yes |
| Raw Data File Type(s) | raw(Thermo) |
| Analysis Type Detail | LC-MS |
| Release Date | 2023-04-13 |
| Release Version | 1 |
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Project:
| Project ID: | PR001627 |
| Project DOI: | doi: 10.21228/M8D434 |
| Project Title: | Pancreatic tumors activate arginine biosynthesis to adapt to myeloid-driven amino acid stress |
| Project Summary: | Nutrient stress in the tumor microenvironment requires cancer cells to adopt adaptive metabolic programs to maintain survival and proliferation. Therefore, knowledge of microenvironmental nutrient levels and how cancer cells cope with such nutrition is critical to understand the metabolism underpinning cancer cell biology. Previously, we performed quantitative metabolomics of the interstitial fluid (the local perfusate) of murine pancreatic ductal adenocarcinoma (PDAC) tumors to comprehensively characterize nutrient availability in the microenvironment of these tumors (Sullivan et al., 2019a). Here, we develop Tumor Interstitial Fluid Medium (TIFM), a cell culture medium that contains nutrient levels representative of the PDAC microenvironment, enabling study of PDAC metabolism under physiological nutrition. We show that PDAC cells cultured in TIFM, compared to standard laboratory models, adopt a cellular state more similar to PDAC cells in tumors. Further, using the TIFM model we identified arginine biosynthesis as a metabolic adaptation PDAC cells engage to cope with microenvironmental arginine starvation driven by myeloid cells in PDAC tumors. Altogether, these data show that nutrient availability in tumors is an important determinant of cancer cell metabolism and behavior, and cell culture models that incorporate physiological nutrient availability have improved fidelity and enable the discovery of novel cancer metabolic phenotypes. |
| Institute: | University of Chicago |
| Last Name: | Apiz Saab |
| First Name: | Juan |
| Address: | 929 E. 57th St. |
| Email: | japizsaab@uchicago.edu |
| Phone: | 7738346506 |
