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Ofer Reizes Laboratory

❮Cardiovascular & Metabolic Sciences Ofer Reizes Laboratory
  • Ofer Reizes Laboratory
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Principal Investigator

Ofer Reizes Headshot

Ofer Reizes, PhD

Staff
The Laura J. Fogarty Endowed Chair for Uterine Cancer Research
Email: [email protected]
Location: Cleveland Clinic Main Campus

Research

There is a dearth of targeted therapies for women’s cancers and our projects seek to address this shortage by a focused approach on novel new pathways that we recently discovered. We focus on the most therapeutically challenging triple negative breast and gynecologic cancers. Due to limited available therapies, less than 50% of women survive more than 5 years with these cancers.


Biography

Ofer Reizes, PhD is professor and staff in the Department of Cardiovascular and Metabolic Sciences at the Cleveland Clinic Lerner Research Institute (LRI) and the inaugural holder of The Laura J. Fogarty Endowed Chair for Uterine Cancer Research. Dr. Reizes earned a Bachelor of Arts in Molecular and Cellular Biology from the University of Maryland – Baltimore County and a PhD in molecular pharmacology from the University of Texas Southwestern Medical Center – Dallas. He subsequently pursued a post-doctoral fellowship in developmental biology and metabolic disease from The Children’s Hospital Boston/Harvard Medical Center. In 2001, Dr. Reizes was recruited to Procter & Gamble Pharmaceuticals where he led drug discovery efforts in metabolic diseases for 5 years. In 2006, he moved from industry to academia to investigate the mechanistic links between metabolic disease and cancer.

His lab at the Cleveland Clinic focuses on unmasking chemoresistance mechanisms in breast and gynecologic cancers to identify strategies to improve patient outcomes. The research includes investigation of cancer stem cells, hyperthermic intraperitoneal chemotherapy and the impact of the microbiome on tumor growth and chemosensitivity. Dr. Reizes applies his previous drug discovery and development expertise to identification and approaches for cancer therapeutics. His research is published in multiple high impact journals including Cell, Journal of Clinical Investigation, Journal of Experimental Medicine, Nature Communications, Cancer Research and Molecular Cancer. 


Education & Professional Highlights

Post-doctoral Fellowship, Developmental Biology and Endocrinology

The Children’s Hospital Boston – Harvard Medical School

1999  

PhD, Molecular Pharmacology

University of Texas – Southwestern Medical Center at Dallas

1993  

BA, Molecular and Cellular Biology

University of Maryland – Baltimore County

1987  

 

Professional appointments         

Cleveland Clinic Lerner Research Institute             

Staff                                                                                  

present                                                                                                    

The Laura J. Fogarty Endowed Chair for Uterine Cancer Research

Holder                                                                                  

Present  

Cleveland Clinic Lerner Research Institute             

Associate Staff                                                  

2006 - 2014  

Procter & Gamble Pharmaceutical, Metabolic Diseases Discovery

Senior Scientist                                                 

2001 - 2006  

The Children’s Hospital Boston -- Harvard Medical School

Research Instructor                                                        

1999 - 2001   

Research

Research

Complement independent signaling in ovarian cancer.
In the U.S., ovarian cancer is the second most common gynecologic malignancy, but the top cause of gynecologic cancer death, and is responsible for 5% of all cancer deaths in women. In 2017, 22,440 new cases and 14,080 deaths are estimated to occur.  Of these, 10% of ovarian cancers demonstrate an appearance of endometrioid tumor (ET) subtype. 

Treatment for gynecologic malignancy is traditionally comprised of debulking surgery and platinum/taxane-based chemotherapy. Patients initially respond to cytotoxic chemotherapy, however for many the tumor recurs and becomes resistant to platinum. As such, there is a significant unmet medical need to treat ETs. An underlying cause of this resistance is the presence of a cancer stem cell population that contributes to tumor growth, recurrence, and treatment resistance and has been observed in ETs. CSCs offer a potential target population for therapeutic intervention. In published studies, we identified the cell surface protein CD55 as a therapeutic target for ET cancer stem cells and platinum-resistant disease. Our studies focus on defining mechanisms for overcoming resistance and targeting cancer stem cells.


Connexin/Focal Adhesion Kinase/NANOG complex in Triple Negative Breast Cancer.
Triple-negative breast cancer is the most aggressive breast cancer subtype and is resistant to therapies. Our objective is to identify unique, targetable mechanisms to neutralize cancer stem cells, which are thought to underlie resistance to chemotherapeutics, as well as recurrence and metastasis, and minimize collateral damage to surrounding cells. To identify key processes that are important for cancer stem cell function, we developed a reporter system to track and study these cells in real time. With this reporter, we identified that the protein connexin 26 (Cx26) is necessary and sufficient for the survival of cancer stem cells in triple-negative breast cancer models. While Cx26 was previously proposed to be a tumor suppressor, epidemiological studies suggest otherwise, as patients with high Cx26 had a poorer prognosis. Our studies indicate that Cx26 promotes cancer stem cell survival by forming a protein complex with the transcription factor NANOG, a master regulator of cancer stem cell function, and focal adhesion kinase in triple-negative breast cancer but not in other breast cancers. Our objective is to prevent this complex from forming and thereby inhibit cancer stem cell survival and growth.

Our Team

Our Team

Publications

Selected Publications

Reizes, O., Lincecum, J., Wang, Z., et al. Transgenic expression of syndecan-1 uncovers a novel control of feeding behavior by hypothalamic syndecan-3. Cell 2001, 106: 105-116

Strader, A.D*, Reizes, O.* et al. Syndecan-3 null mice are resistant to diet induced obesity. J. Clin. Invest. 2004, 114: 1354-1360.

Thiagarajan PS, Sinyuk M, Turaga SM, Mulkearns-Hubert EE, Hale JS, Rao V, Demelash A, Saygin C, China A, Alban TJ2, Hitomi M, Torre-Healy LA, Alvarado AG, Jarrar A, Wiechert A, Adorno-Cruz V, Fox PL, Calhoun BC, Guan JL, Liu H, Reizes O, Lathia JD. Cx26 drives self-renewal in triple-negative breast cancer via interaction with NANOG and focal adhesion kinase. Nat Commun. 2018 Feb 8;9(1):578. doi: 10.1038/s41467-018-02938-1.

Saygin C, Wiechert A, Rao VS, Alluri R, Connor E, Thiagarajan PS, Hale JS, Li Y, Chumakova A, Jarrar A, Parker Y, Lindner DJ, Nagaraj AB, Kim JJ, DiFeo A, Abdul-Karim FW, Michener C, Rose PG, DeBernardo R, Mahdi H, McCrae KR, Lin F, Lathia JD, Reizes O. CD55 regulates self-renewal and cisplatin resistance in endometrioid tumors. J Exp Med. 2017 Sep 4;214(9):2715-2732. doi: 10.1084/jem.20170438. Epub 2017 Aug 24.

Careers

Careers

Training at Lerner Research Institute

Our education and training programs offer hands-on experience at one of the nationʼs top hospitals. Travel, publish in high impact journals and collaborate with investigators to solve real-world biomedical research questions.

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Research News

Research News

...
New findings remove roadblock to targeted treatment for chemo-resistant ovarian cancer

Discovering a new way a protein behaves in ovarian cancer led to new research, potential treatments.



...
New research highlights unprecedented targeted approach to treating triple-negative breast cancer

A peptide drug candidate based on a Cleveland Clinic discovery disrupted cancer growth and self-renewal.



...
Restoring the gut biome after antibiotics could lead to better outcomes for ovarian cancer patients

Reassessing antibiotic dosage and type could improve survival rates in deadliest gynecologic malignancy, Cleveland Clinic research finds.



...
How Cancer Stem Cells Drive Triple-Negative Breast Cancer

Triple-negative breast cancer (TNBC) cells lack the receptors needed to bind to hormones and growth factors, meaning typical cancer treatments that target these areas are ineffective.



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