Summary of Study ST000438

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 PR000338. The data can be accessed directly via it's Project DOI: 10.21228/M8X01N This work is supported by NIH grant, U2C- DK119886.

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Study IDST000438
Study TitleCharacterizing commonalities and differences between the breast and prostate cancer metabotypes in African-American cohorts (part I)
Study TypeIdentify Breast Cancer Progression and Prostate Cancer correlative Metabolite Markers
Study SummaryThus, we aimed to 1) understand mechanisms related to the onset and progression of BCa, 2) identify precursors and targets for prevention and therapy for each stage, grade and subtype which may contribute to the disparate impact of BCa in African American women, and 3) Identify common and different BCa metabolite markers versus PCa markers.
Institute
University of North Carolina
DepartmentNIH Eastern Regional Comprehensive Metabolomics Resource Core (RTI RCMRC)
LaboratorySumner Lab
Last NameSumner
First NameSusan
AddressEastern Regional Comprehensive Metabolomics Resource Core, UNC Nutrition Research Institute, 500 Laureate Way, Kannapolis, NC, 28081
Emailsusan_sumner @unc.edu
Phone704-250-5066
Submit Date2016-08-02
Num Groups2
Total Subjects48
Num Females48
Raw Data AvailableYes
Analysis Type DetailNMR
Release Date2016-09-23
Release Version1
Susan Sumner Susan Sumner
https://dx.doi.org/10.21228/M8X01N
ftp://www.metabolomicsworkbench.org/Studies/ application/zip

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Project:

Project ID:PR000338
Project DOI:doi: 10.21228/M8X01N
Project Title:Characterizing commonalities and differences between the breast and prostate cancer metabotypes in African-American cohorts
Project Type:Identify Breast Cancer Progression and Prostate Cancer correlative Metabolite Markers
Project Summary:Many attempts have been made to identify critical events responsible for the development and progression of breast cancer (BCa). In spite of this, the mechanisms underlying notably tumor invasion and BCa dissemination remain largely unclear. The pathological features of BCa follow a sequential progression from the transformation of a normal cell to benign proliferation, hyperplasia, atypical ductal hyperplasia (ADH), ductal carcinoma in-situ (DCIS) to invasive ductal carcinoma (IDC) and metastatic diseases. It has been reported that the disease phenotype is distinguishable in ADH and progresses along distinct pathways for each subtype. The genetic signature for disease heterogeneity across subtypes is greater than the heterogeneity of progression from DCIS to IDC within a subtype, suggesting that the disease subtypes have distinct progression pathways. Even so, genetics does not fully explain etiology nor progression. Additionally, a large population based study reported an increased risk of male BCa after prostate cancer (PCa). The two cancers share similarities with a wide heterogeneity of both phenotype and biology. A unique feature of PCa and BCa is that at least in the initial stages, they are hormone-dependent and have remarkable underlying biological similarities. Our recent study and others showed an increased level of common metabolites in BCa and PCa. Thus, understanding the metabolic profiles of breast and prostate cancer would pave the way for new biomarkers to improve diagnosis and treatment strategies.
Institute:Howard University
Department:Department of Microbiology and Cancer Center
Last Name:Kanaan
First Name:Yasmine
Address:1840 Seventh Street, NW Suite 309, Washington, DC 20001
Email:ymkanaan@Howard.edu
Phone:202 806 9540
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