Summary of Study ST001984

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 PR001260. The data can be accessed directly via it's Project DOI: 10.21228/M8V401 This work is supported by NIH grant, U2C- DK119886.

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Study IDST001984
Study TitleMetabolic adaptations in an endocrine-related breast cancer mouse model unveil potential markers of tumor response to hormonal therapy
Study Typecase - control study
Study SummaryBreast cancer (BC) is the most common type of cancer in women and, in most cases, it is hormone-dependent (HD), thus relying on ovarian hormone activation of intracellular receptors to stimulate tumor growth. Endocrine therapy (ET) aimed at preventing hormone receptor activation is the primary treatment strategy, however, about half of the patients, develop resistance in time. This involves the development of hormone independent tumors that initially are ET-responsive (HI), which may subsequently become resistant (HIR). The mechanisms that promote the conversion of HI to HIR tumors are varied and not completely understood. The aim of this work was to characterize the metabolic adaptations accompanying this conversion through the analysis of the polar metabolomes of tumor tissue and non-compromised mammary gland from mice implanted subcutaneously with HD, HI and HIR tumors from a medroxyprogesterone acetate (MPA)-induced BC mouse model. This was carried out by nuclear magnetic resonance (NMR) spectroscopy of tissue polar extracts and data mining through multivariate and univariate statistical analysis. Initial results unveiled marked changes between global tumor profiles and non-compromised mammary gland tissues, as expected. More importantly, specific metabolic signatures were found to accompany progression from HD, through HI and to HIR tumors, impacting on amino acids, nucleotides, membrane percursors and metabolites related to oxidative stress protection mechanisms. For each transition, sets of polar metabolites are advanced as potential markers of progression, including acquisition of resistance to ET. Putative biochemical interpretation of such signatures are proposed and discussed.
Institute
University of Aveiro
DepartmentChemistry
LaboratoryMetabolomics
Last NameSilva
First NameAna
AddressCampus Universitário de Santiago, 3810-193
Emailanarita.asilva@ua.pt
Phone234370200
Submit Date2021-10-06
Num Groups8
Total Subjects48
Num Females48
Study CommentsFor this study 48 female 2-month old Balb/c mice were used
Analysis Type DetailNMR
Release Date2021-12-01
Release Version1
Ana Silva Ana Silva
https://dx.doi.org/10.21228/M8V401
ftp://www.metabolomicsworkbench.org/Studies/ application/zip

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Factors:

Subject type: Mammal; Subject species: Mus musculus (Factor headings shown in green)

mb_sample_id local_sample_id Sample type
SA185699B71control
SA185700B77control
SA185701B65control
SA185702B53control
SA185703B47control
SA185704C11control
SA185705B59control
SA185706C17control
SA185707C41control
SA185708A17control
SA185709C35control
SA185710C29control
SA185711C23control
SA185712B41control
SA185713B83control
SA185714A41control
SA185715A53control
SA185716A59control
SA185717A34control
SA185718A29control
SA185719A23control
SA185720B35control
SA185721A65control
SA185722A47control
SA185723B17control
SA185724B29control
SA185725A83control
SA185726B23control
SA185727A77control
SA185728A71control
SA185729C43tumor
SA185730C44tumor
SA185731C45tumor
SA185732B99tumor
SA185733B98tumor
SA185734B97tumor
SA185735C46tumor
SA185736B108tumor
SA185737C54tumor
SA185738C52tumor
SA185739C53tumor
SA185740B107tumor
SA185741C51tumor
SA185742C50tumor
SA185743C48tumor
SA185744C49tumor
SA185745C47tumor
SA185746B88tumor
SA185747B91tumor
SA185748B92tumor
SA185749B93tumor
SA185750B90tumor
SA185751B89tumor
SA185752B85tumor
SA185753B86tumor
SA185754B87tumor
SA185755B94tumor
SA185756B95tumor
SA185757B103tumor
SA185758B104tumor
SA185759B105tumor
SA185760B102tumor
SA185761B101tumor
SA185762B96tumor
SA185763B100tumor
SA185764B106tumor
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