Folate Receptor Alpha Expression Is Associated With Increased Risk of Recurrence in Triple-negative Breast Cancer

2017 ◽  
Vol 17 (7) ◽  
pp. 544-549 ◽  
Author(s):  
Paula S. Ginter ◽  
Patrick J. McIntire ◽  
Xiaoyan Cui ◽  
Lina Irshaid ◽  
Yifang Liu ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Triple Negative Breast Cancer ◽  
Triple Negative ◽  
Folate Receptor ◽  
Folate Receptor Alpha ◽  
Risk Of Recurrence ◽  
Receptor Alpha ◽  
Increased Risk

Triple Negative Breast Cancer: Expression of Folate Receptor Alpha in Indian population

2020 ◽  
Vol 49 ◽  
pp. 151598
Author(s):  
Pooja Gajaria ◽  
Vandana Kadu ◽  
Asawari Patil ◽  
Sangeeta Desai ◽  
Tanuja Shet
Keyword(s):  
Breast Cancer ◽  
Triple Negative Breast Cancer ◽  
Indian Population ◽  
Triple Negative ◽  
Folate Receptor ◽  
Folate Receptor Alpha ◽  
Receptor Alpha

scholarly journals Investigating the Potential of Conjugated Selenium Redox Folic Acid as a Treatment for Triple Negative Breast Cancer

Antioxidants ◽  
2020 ◽  
Vol 9 (2) ◽  
pp. 138 ◽  
Author(s):  
Soni Khandelwal ◽  
Mallory Boylan ◽  
Gilbert Kirsch ◽  
Julian E. Spallholz ◽  
Lauren S. Gollahon
Keyword(s):  
Breast Cancer ◽  
Folic Acid ◽  
Cell Line ◽  
Triple Negative Breast Cancer ◽  
Triple Negative ◽  
Folate Receptor ◽  
Folate Receptor Alpha ◽  
Receptor Alpha ◽  
Redox Active

Previous studies have demonstrated that redox selenium compounds arrest cancer cell viability in vitro through their pro-oxidative activity by generating superoxide (O2•−). Currently, there are no efficacious treatment options for women with Triple Negative Breast Cancer (TNBC). However, the association between the over-expression of the Folate Receptor Alpha (FRA) in TNBC and other cancer cells, has led to the possibility that TNBCs might be treated by targeting the FRA with redox selenium covalent Folic Acid conjugates. The present study reports the synthesis of the redox active vitamer, Selenofolate, generating superoxide. Superoxide (O2•−) catalytic generation by Selenofolate was assessed by an in vitro chemiluminescence (CL) assay and by a Dihydroethidium (DHE) in vivo assay. Cytotoxicity of Selenofolate was assessed against the TNBC cell line MDA-MB-468 and an immortalized, mammary epithelial cell line, HME50-5E. Cytotoxicity of Selenofolate was compared to Folic Acid and sodium selenite, in a time and dose dependent manner. Selenofolate and selenite treatments resulted in greater inhibition of MDA-MB-468 cell proliferation than HME50-5E as evaluated by Trypan Blue exclusion, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) metabolic assay and Annexin V apoptosis assays. Folate receptor alpha (FRA) protein expression was assessed by Western blotting, with the experimental results showing that redox active Selenofolate and selenite, but not Folic Acid, was cytotoxic to MDA-MB-468 cells in vitro, suggesting a possible clinical option for treating TNBC and other cancers over-expressing FRA.

scholarly journals Anti-Folate Receptor Alpha–Directed Antibody Therapies Restrict the Growth of Triple-negative Breast Cancer

2018 ◽  
Vol 24 (20) ◽  
pp. 5098-5111 ◽  
Author(s):  
Anthony Cheung ◽  
James Opzoomer ◽  
Kristina M. Ilieva ◽  
Patrycja Gazinska ◽  
Ricarda M. Hoffmann ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Triple Negative Breast Cancer ◽  
Triple Negative ◽  
Folate Receptor ◽  
Folate Receptor Alpha ◽  
Receptor Alpha

scholarly journals Triple-Negative Breast Cancer: Adjuvant Therapeutic Options

2011 ◽  
Vol 2011 ◽  
pp. 1-13 ◽  
Author(s):  
Ayca Gucalp ◽  
Tiffany A. Traina
Keyword(s):  
Breast Cancer ◽  
Triple Negative Breast Cancer ◽  
Triple Negative ◽  
Growth Factor Receptor ◽  
Progesterone Receptors ◽  
Cytotoxic Chemotherapy ◽  
Breast Cancers ◽  
Targeted Agents ◽  
Increased Risk ◽  
Disproportionate Number

Triple-negative breast cancer (TNBC), a subtype distinguished by negative immunohistochemical assays for expression of the estrogen and progesterone receptors (ER/PR) and human epidermal growth factor receptor-2(HER2) represents 15% of all breast cancers. Patients with TNBC generally experience a more aggressive clinical course with increased risk of disease progression and poorer overall survival. Furthermore, this subtype accounts for a disproportionate number of disease-related mortality in part due to its aggressive natural history and our lack of effective targeted agents beyond conventional cytotoxic chemotherapy. In this paper, we will review the epidemiology, risk factors, prognosis, and the molecular and clinicopathologic features that distinguish TNBC from other subtypes of breast cancer. In addition, we will examine the available data for the use of cytotoxic chemotherapy in the treatment of TNBC in both the neoadjuvant and adjuvant setting and explore the ongoing development of newer targeted agents.

Sign in / Sign up

Export Citation Format

Share Document