Lindsay E. Calderon
- Courses9
- Reviews26
- School: Eastern Kentucky University
- Campus:
- Department: Biology
- Email address: Join to see
- Phone: Join to see
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Location:
521 Lancaster Ave
Richmond, KY - 40475 - Dates at Eastern Kentucky University: November 2013 - May 2020
- Office Hours: Join to see
N/A
Would take again: Yes
For Credit: Yes
0
0
Mandatory
Good
Prof. Lindsay is a better option than my BIO 307 prof.
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Would take again: Yes
For Credit: Yes
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Not Mandatory
Good
Professor Calderon has a good personality. Her exams were very wordy. Also, you need to know the material as your own to do well on this course remotely.
Biography
Eastern Kentucky University - Biology
Associate Professor at Eastern Kentucky University
Lindsay
Calderon
Lexington, Kentucky Area
Lindsay Calderon is currently a tenure track Associate Professor in the Department of Biological Sciences at Eastern Kentucky University. She obtained her Ph.D. in Molecular and Biomedical Pharmacology at the University of Kentucky. She has published 10 peer reviewed articles, five of which deal with the molecular mechanisms of smooth muscle regulation and hypertension. Her current research interest centers on the molecular regulation and inhibition of neoplastic growth. Dr. Calderon has also received numerous grants to fund her research and actively involves her students in her laboratory, which she uses not only as a platform for scientific advancement but also as a platform for post-graduate education. Dr. Calderon has won numerous teaching awards at Eastern Kentucky University, including EKU’s Critical Thinking Teacher of the Year Award and three Golden Apple Awards.
Dr. Calderon is also active in public health issues and donates her time and research expertise to Health Watch USA, a non-profit organization which promotes patient advocacy and healthcare transparency. She was an integral part of the research team which produced several publications on the importance of MRSA Surveillance, and problems with research integrity and its effects on healthcare policy designed to confront the MRSA epidemic. In addition, she has worked on projects dealing with central line bloodstream infections and investigated the effects of malpractice reform on reducing healthcare expenditures. She was the lead investigator on an analysis of the current methodology of reporting catheter associated urinary tract infections and presented evidence that the current method is not only flawed but may also result in the Centers for Medicare and Medicaid Services penalizing higher performing facilities.
Experience
Eastern Kentucky University
Assistant Professor
Lindsay worked at Eastern Kentucky University as a Assistant Professor
Education
University of Kentucky
Doctor of Philosophy (Ph.D.)
Molecular and Biomedical Pharmacology
Degree awarded May 2012Gill Heart Institute Research Conference, Graduate student division
2nd Place
Publications
Bromoenol Lactone Attenuates Nicotine-Induced Breast Cancer Cell Proliferation and Migration.
PLoS One
Objectives: Calcium independent group VIA phospholipase A2 (iPLA2β) and Matrix Metalloproteinase-9 (MMP-9) are upregulated in many disease states; their involvement with cancer cell migration has been a recent subject for study. Further, the molecular mechanisms mediating nicotine-induced breast cancer cell progression have not been fully investigated. This study aims to investigate whether iPLA2β mediates nicotine-induced breast cancer cell proliferation and migration through both in-vitro and in-vivo techniques. Subsequently, the ability of Bromoenol Lactone (BEL) to attenuate the severity of nicotine-induced breast cancer was examined. Method and Results: We found that BEL significantly attenuated both basal and nicotine-induced 4T1 breast cancer cell proliferation, via an MTT proliferation assay. Breast cancer cell migration was examined by both a scratch and transwell assay, in which, BEL was found to significantly decrease both basal and nicotine-induced migration. Additionally, nicotine-induced MMP-9 expression was found to be mediated in an iPLA2β dependent manner. These results suggest that iPLA2β plays a critical role in mediating both basal and nicotine-induced breast cancer cell proliferation and migration in-vitro. In an in-vivo mouse breast cancer model, BEL treatment was found to significantly reduce both basal (p<0.05) and nicotine-induced tumor growth (p<0.01). Immunohistochemical analysis showed BEL decreased nicotine-induced MMP-9, HIF-1alpha, and CD31 tumor tissue expression. Subsequently, BEL was observed to reduce nicotine-induced lung metastasis. Conclusion: The present study indicates that nicotine-induced migration is mediated by MMP-9 production in an iPLA2β dependent manner. Our data suggests that BEL is a possible chemotherapeutic agent as it was found to reduce both nicotine-induced breast cancer tumor growth and lung metastasis.
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