Summary of Study ST003479
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 PR002137. The data can be accessed directly via it's Project DOI: 10.21228/M8CZ33 This work is supported by NIH grant, U2C- DK119886. See: https://www.metabolomicsworkbench.org/about/howtocite.php
| Study ID | ST003479 |
| Study Title | Fatty acid analysis of similarly sized MC38 tumors from control-diet- or high-fat-diet-fed C57BL/6 mice revealed an increase in tumoral oleic acid in high-fat-diet-fed mice. |
| Study Summary | Similarly sized MC38 tumors from control-diet- and high-fat-diet-fed mice were subject to fatty acid analysis via GC-FID. These data revealed an increase in oleic acid in tumors from high-fat-diet-fed mice. Oleic acid was the only fatty acid to exhibit this trend. |
| Institute | Stanford University |
| Last Name | Bagchi |
| First Name | Sreya |
| Address | 3373 Hillview Avenue |
| bagchipuja@gmail.com | |
| Phone | 4086214773 |
| Submit Date | 2024-08-12 |
| Analysis Type Detail | Other |
| Release Date | 2024-10-18 |
| Release Version | 1 |
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Project:
| Project ID: | PR002137 |
| Project DOI: | doi: 10.21228/M8CZ33 |
| Project Title: | Acid-sensing receptor, GPR65, on tumor macrophages drives accelerated tumor growth in obesity |
| Project Summary: | Multiple cancers, including colorectal cancer (CRC), are more frequent and often more aggressive in obese individuals. Here, we show that macrophages accumulate within tumors of obese CRC patients and in obese CRC mice and promote accelerated tumor growth. These changes are initiated by oleic acid accumulation and subsequent tumor cell-derived acid production, and driven by signaling through GPR65, an acid-sensing receptor on CRC-associated macrophages. We demonstrate a similar role for GPR65 in hepatocellular carcinoma (HCC) in obese mice. Tumors in obese patients with CRC or HCC also exhibit increased GPR65 expression, suggesting that the mechanism revealed here likely contributes to tumor growth in a range of obesity-associated cancers and represents a potential therapeutic target. |
| Institute: | Stanford University |
| Last Name: | Bagchi |
| First Name: | Sreya |
| Address: | 3373 Hillview Avenue |
| Email: | sbagchi@stanford.edu |
| Phone: | 4086214773 |
