Comparison Log
2025-03-23 07:30:27.943671
mwtab Python Library Version: 1.2.5
Source:      https://www.metabolomicsworkbench.org/rest/study/analysis_id/AN005997/mwtab/...
Study ID:    ST003651
Analysis ID: AN005997
Status:      Inconsistent

Sections "PROJECT" contain missmatched items: {('PROJECT_SUMMARY', "The biguanide metformin attenuates mitochondrial oxidation and has been proposed as an anti-cancer therapy. However, recent clinical studies suggested increased proliferation and fatty acid beta-oxidation (FAO) in a subgroup of breast cancer (BC) patients after metformin therapy. Considering that FAO can activate Src kinase in aggressive triple-negative BC (TNBC), we hypothesized that a low-dose biguanides-driven AMPK-ACC-FAO signaling may activate the Src pathway in TNBC. The low bioavailability of metformin in TNBC xenografts mimicked metformin's in vitro low-dose effect. Pharmacological or genetic inhibition of FAO significantly enhanced the anti-tumor properties of biguanides. Lower doses of biguanides induced and higher doses suppressed Src signaling. Dasatinib and metformin synergistically inhibited TNBC patient-derived xenograft growth but not in high-fat diet-fed mice. This combination also suppressed TNBC metastatic progression. A combination of biguanides with Src inhibitors provides synergy to target metastatic TNBC suffering with limited treatment options."), ('PROJECT_SUMMARY', "The biguanide metformin attenuates mitochondrial oxidation and has been proposed as an anti-cancer therapy. However, recent clinical studies suggested increased proliferation and fatty acid beta-oxidation (FAO) in a subgroup of breast cancer (BC) patients after metformin therapy. Considering that FAO can activate Src kinase in aggressive triple-negative BC (TNBC), we hypothesized that a low-dose biguanides-driven AMPK-ACC-FAO signaling may activate the Src pathway in TNBC. The low bioavailability of metformin in TNBC xenografts mimicked metformin''s in vitro low-dose effect. Pharmacological or genetic inhibition of FAO significantly enhanced the anti-tumor properties of biguanides. Lower doses of biguanides induced and higher doses suppressed Src signaling. Dasatinib and metformin synergistically inhibited TNBC patient-derived xenograft growth but not in high-fat diet-fed mice. This combination also suppressed TNBC metastatic progression. A combination of biguanides with Src inhibitors provides synergy to target metastatic TNBC suffering with limited treatment options.")}
Sections "STUDY" contain missmatched items: {('STUDY_SUMMARY', "The biguanide metformin attenuates mitochondrial oxidation and has been proposed as an anti-cancer therapy. However, recent clinical studies suggested increased proliferation and fatty acid beta-oxidation (FAO) in a subgroup of breast cancer (BC) patients after metformin therapy. Considering that FAO can activate Src kinase in aggressive triple-negative BC (TNBC), we hypothesized that a low-dose biguanides-driven AMPK-ACC-FAO signaling may activate the Src pathway in TNBC. The low bioavailability of metformin in TNBC xenografts mimicked metformin's in vitro low-dose effect. Pharmacological or genetic inhibition of FAO significantly enhanced the anti-tumor properties of biguanides. Lower doses of biguanides induced and higher doses suppressed Src signaling. Dasatinib and metformin synergistically inhibited TNBC patient-derived xenograft growth but not in high-fat diet-fed mice. This combination also suppressed TNBC metastatic progression. A combination of biguanides with Src inhibitors provides synergy to target metastatic TNBC suffering with limited treatment options."), ('STUDY_SUMMARY', "The biguanide metformin attenuates mitochondrial oxidation and has been proposed as an anti-cancer therapy. However, recent clinical studies suggested increased proliferation and fatty acid beta-oxidation (FAO) in a subgroup of breast cancer (BC) patients after metformin therapy. Considering that FAO can activate Src kinase in aggressive triple-negative BC (TNBC), we hypothesized that a low-dose biguanides-driven AMPK-ACC-FAO signaling may activate the Src pathway in TNBC. The low bioavailability of metformin in TNBC xenografts mimicked metformin''s in vitro low-dose effect. Pharmacological or genetic inhibition of FAO significantly enhanced the anti-tumor properties of biguanides. Lower doses of biguanides induced and higher doses suppressed Src signaling. Dasatinib and metformin synergistically inhibited TNBC patient-derived xenograft growth but not in high-fat diet-fed mice. This combination also suppressed TNBC metastatic progression. A combination of biguanides with Src inhibitors provides synergy to target metastatic TNBC suffering with limited treatment options.")}
'Metabolite'