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NASHVILLE, Tenn.--(BUSINESS WIRE)--Sarah Cannon announced today that it will present cancer research insights through more than 90 presentations selected by the American Society of Clinical Oncology (ASCO®) at the 2017 Annual Meeting. Hosted in Chicago, June 2-6, the meeting brings together more than 30,000 cancer experts from around the world to review the latest research to improve the diagnosis and treatment of cancer. “2017 marks the 20th anniversary of our community-based drug development program, which was the first of its kind,” said Howard A. “Skip” Burris III, MD, President of Clinical Operations and Chief Medical Officer at Sarah Cannon. “Since our program’s inception, we have conducted more than 260 first-in-human clinical trials and made countless contributions to the advancement of cancer therapies. As we look to the future, the team at Sarah Cannon remains excited about our clinical research into how novel agents can provide an even greater benefit to patients and looks forward to sharing insights with our colleagues participating in the Annual Meeting.” Highlights of Sarah Cannon’s research include a presentation in a Clinical Science Symposium by Dr. Burris, who will discuss a study of combined inhibition of IDO1 and PD-L1 in patients with locally-advanced or metastatic solid tumors. Dr. Burris’ presentation, in the symposium titled "Check" This Out: The Step Beyond PD-1 Blockade, will take place on Sunday, June 4 during the session from 9:45-11:15 a.m. in Hall D1. Dr. Burris will also participate as a discussant in a Clinical Science Symposium, Hitting the Target: Antibody-Drug Conjugates, on Monday, June 5 from 9:45-11:15 a.m. in Hall D1, at which David Spigel, MD, Chief Scientific Officer and Director, Lung Cancer Research Program, Sarah Cannon Research Institute, will moderate the discussion. Additionally, Ian Flinn, MD, PhD, Director, Blood Cancer Research Program, Sarah Cannon Research Institute, will present an Oral Abstract on results of the BRIGHT 5-year follow-up study, a first-line treatment of iNHL or MCL patients with BR or R-CHOP/R-CVP, on Saturday, June 3 in the session from 3-6 p.m. in room S100BC. This abstract has also been selected as part of the Best of ASCO® program, which will be held this summer following the meeting, and highlights significant data impacting oncology research and care. Several other Sarah Cannon investigators are presenting noteworthy studies and insights at ASCO®: For a full listing of all presentations authored by Sarah Cannon investigators, visit sarahcannon.com/asco. Additional authors presenting for Sarah Cannon at the conference include: Hendrik-Tobias Arkenau, MD, PhD, FRCP, Raid Aljumaily, MD, Todd Bauer, MD, Johanna Bendell, MD, William Donnellan, MD, Professor Paul Ellis, MD, FRACP, Gerald Falchook, MD, MS, Carol Greenlees, PhD, Camille Gunderson, MD, Erika Hamilton, MD, John Hainsworth, MD, Lowell Hart, MD, Maen Hussein, MD, Jeffrey Infante, MD, Suzanne Jones, PharmD, Kathleen Moore, MD, Manish Patel, MD, DK Strickland, MD, Professor Charles Swanton, FRCP, BSc, PhD, Judy Wang, MD and Denise Yardley, MD. The researchers represent Sarah Cannon’s global network of strategic sites: Sarah Cannon Research Institute at Tennessee Oncology, Sarah Cannon Research Institute at HealthONE, Sarah Cannon Research Institute - United Kingdom, Colorado Blood Cancer Institute, The Center for Cancer and Blood Disorders - Ft. Worth, Sarah Cannon Research Institute at Florida Cancer Specialists, Sarah Cannon Research Institute at HCA Midwest Health and The Stephenson Cancer Center at the University of Oklahoma. Sarah Cannon Research Institute is the research arm of HCA Healthcare’s global cancer institute, Sarah Cannon. Focused on advancing therapies for patients, it is one of the world’s leading clinical research organizations conducting community-based clinical trials throughout the United States and United Kingdom. Sarah Cannon’s network of strategic sites includes more than 275 physicians who engage in research. The organization has led more than 260 first-in-man clinical trials since its inception in 1993, and has been a clinical trial leader in the majority of approved cancer therapies over the last 10 years. Additionally, Sarah Cannon offers management, regulatory, and other research support services for drug development and industry sponsors as well as strategic investigator sites through its contract research organization (CRO), Sarah Cannon Development Innovations. For more information, visit sarahcannon.com.


Kennedy A.S.,Sarah Cannon Research Institute
Current oncology reports | Year: 2014

The most common non-surgical approaches for the treatment of localized hepatocellular carcinoma remain hepatic artery-delivered particles laden with chemotherapy (TACE), or radioactive microparticles (TARE). External beam radiotherapy has been an effective option in many parts of the world for selected HCC patients, but now has an expanded role with stereotactic and proton beam technologies. This review focuses on existing evidence and current guidance for utilizing these modalities for localized, but unresectable, non-transplantable HCC patients.x.


Spigel D.R.,Sarah Cannon Research Institute
Journal of clinical oncology : official journal of the American Society of Clinical Oncology | Year: 2013

Increased hepatocyte growth factor/MET signaling is associated with poor prognosis and acquired resistance to epidermal growth factor receptor (EGFR) -targeted drugs in patients with non-small-cell lung cancer (NSCLC). We investigated whether dual inhibition of MET/EGFR results in clinical benefit in patients with NSCLC. Patients with recurrent NSCLC were randomly assigned at a ratio of one to one to receive onartuzumab plus erlotinib or placebo plus erlotinib; crossover was allowed at progression. Tumor tissue was required to assess MET status by immunohistochemistry (IHC). Coprimary end points were progression-free survival (PFS) in the intent-to-treat (ITT) and MET-positive (MET IHC diagnostic positive) populations; additional end points included overall survival (OS), objective response rate, and safety. There was no improvement in PFS or OS in the ITT population (n = 137; PFS hazard ratio [HR], 1.09; P = .69; OS HR, 0.80; P = .34). MET-positive patients (n = 66) treated with erlotinib plus onartuzumab showed improvement in both PFS (HR, .53; P = .04) and OS (HR, .37; P = .002). Conversely, clinical outcomes were worse in MET-negative patients treated with onartuzumab plus erlotinib (n = 62; PFS HR, 1.82; P = .05; OS HR, 1.78; P = .16). MET-positive control patients had worse outcomes versus MET-negative control patients (n = 62; PFS HR, 1.71; P = .06; OS HR, 2.61; P = .004). Incidence of peripheral edema was increased in onartuzumab-treated patients. Onartuzumab plus erlotinib was associated with improved PFS and OS in the MET-positive population. These results combined with the worse outcomes observed in MET-negative patients treated with onartuzumab highlight the importance of diagnostic testing in drug development.


Yardley D.A.,Sarah Cannon Research Institute
Breast Cancer: Basic and Clinical Research | Year: 2013

Improvements in survival of patients with breast cancer have been attributed to the development of agents that target key components of dysregulated pathways involved in oncogenesis and progression of breast cancer. Aberrant mammalian target of rapamycin (mTOR) activation has been implicated in oncogenesis, angiogenesis, and the development of estrogen independence and resistance to chemotherapy in breast tumors. Several mTOR inhibitors (sirolimus, everolimus, temsirolimus, and ridaforolimus) have demonstrated antitumor activity in breast cancer cells. Combining mTOR inhibitors with endocrine therapies has demonstrated clinical antitumor activity in patients with metastatic breast cancer. In addition, mTOR inhibitor combinations with various targeted biologic agents or cytotoxic chemotherapeutic agents are being examined in more than 40 clinical trials with some early promising results. Combination therapies targeting multiple components of these central signaling pathways may be an optimal treatment strategy for patients with advanced breast cancer. © the author(s), publisher and licensee Libertas Academica Ltd.


Berdeja J.G.,Sarah Cannon Research Institute
Frontiers in Bioscience - Landmark | Year: 2014

Lorvotuzumab mertansine (LM) is an ADC composed of an anti CD56 humanized N901 monoclonal antibody conjugated via a stable disulfide linker to the maytansinoid DM1. CD56 is expressed in up to 78% of multiple myelomas. LM displays antitumor activity in preclinical models of multiple myeloma. In a phase I study of MM, the MTD of single-agent LM was 112 mg/m2. The dose-limiting toxicities were grade 3 fatigue and grade 3 acute, reversible, renal failure. 2 PRs and 4 MRs were observed at various dose levels starting at 60 mg/m2. Building on the single agent experience, a phase II study of LM in combination with lenalidomide and dexamethasone was conducted. The optimal dose of LM was 75 mg/m2 in the combination. The ORR was 56.4%. The most common treatment-related AE was peripheral neuropathy (PN), mostly grade 2 or less, with the majority of patients having a grade 1 PN at baseline. Continued evaluation of optimal dosing levels and schedules will be important to better define the utility of this promising treatment.


Burris III H.A.,Sarah Cannon Research Institute
Expert Opinion on Biological Therapy | Year: 2011

Introduction: Trastuzumab emtansine (T-DM1) is an antibody-drug conjugate (ADC) that combines intracellular delivery of the potent cytotoxic agent, DM1 (a derivative of maytansine) with the antitumor activity of trastuzumab. While there are several ADCs in Phase III development, T-DM1 is the only one in which the targeting antibody has antitumor properties. T-DM1 is also the only ADC that is directed toward the human EGFR 2 (HER2). Effective therapies are limited in HER2-positive advanced or metastatic breast cancer (MBC), particularly following progression on available HER2-targeted therapies. Areas covered: The mechanisms of action, preclinical efficacy and clinical profile of T-DM1 are reported. The latest preclinical and clinical data for T-DM1 are examined. Expert opinion: T-DM1 has significant antitumor potency in vitro and in vivo, which is maintained in tumors resistant to trastuzumab or lapatinib. In Phase I and II trials, T-DM1 provided objective tumor responses and was well tolerated across various lines of therapy in patients with HER2-positive MBC. In addition, it showed similar efficacy to trastuzumab plus docetaxel in first-line MBC. Ongoing trials (including two Phase III studies) are investigating T-DM1 as single-agent therapy or combined with other chemotherapeutic or biologic agents, and the results should help to define the place of T-DM1 within current treatment algorithms for HER2-positive disease. © Informa UK, Ltd.


Greco F.A.,Sarah Cannon Research Institute
Nature Reviews Cancer | Year: 2014

Cancer of unknown primary site (CUP) has frustrated patients, their families and physicians for decades because appropriate therapies for patients with metastatic cancers are determined by the primary site or the tissue of origin. Now that we have methods to identify the tissue of origin for the majority of these patients, additional clinical and biological questions are being asked and addressed.


Burris III H.A.,Sarah Cannon Research Institute
Cancer Chemotherapy and Pharmacology | Year: 2013

Background: Most targeted anticancer therapies, as well as cytotoxic and radiation therapies, are encumbered by the development of secondary resistance by cancer cells. Resistance is a complex phenomenon involving multiple mechanisms, including activation of signaling pathways such as phosphatidylinositol 3-kinase (PI3K)/AKT/mammalian target of rapamycin (mTOR). Novel strategies to overcome resistance by targeting these signaling pathways are being evaluated. Methods: PubMed and key cancer congress abstracts were searched until July 2012 for preclinical and clinical data relating to the PI3K/AKT/mTOR pathway and anticancer treatment resistance, and use of PI3K/AKT/mTOR inhibitors in resistant cancer cell lines and patient populations. Results: Activation of the PI3K/AKT/mTOR pathway is frequently implicated in resistance to anticancer therapies, including biologics, tyrosine kinase inhibitors, radiation, and cytotoxics. As such, inhibitors of the PI3K/AKT/mTOR pathway are being rapidly evaluated in preclinical models and in clinical studies to determine whether they can restore therapeutic sensitivity when given in combination. In breast cancer, non-small-cell lung cancer, and glioblastoma, we find compelling preclinical evidence to show that inhibitors of PI3K or mTOR can restore sensitivity in resistant cells. Although clinical evidence is less mature, a recent Phase III study with the mTORC1 inhibitor everolimus in patients with advanced breast cancer resistant to aromatase inhibition and several Phase I/II studies with PI3K inhibitors demonstrate proof-of-concept, warranting future clinical evaluation. Conclusion: Current preclinical and clinical evidence suggest that inhibitors of the PI3K/AKT/mTOR pathway could have utility in combination with other anticancer therapies to circumvent resistance by cancer cells. Multiple clinical studies are ongoing. © 2013 Springer-Verlag Berlin Heidelberg.


Bauer T.M.,Sarah Cannon Research Institute | Patel M.R.,Sarah Cannon Research Institute | Infante J.R.,Sarah Cannon Research Institute
Pharmacology & therapeutics | Year: 2015

The PI3K/Akt/mTOR pathway is the most frequently known activated aberrant pathway in human cancers. Pathologic activation can occur at multiple levels along the signaling pathway by a variety of mechanisms, including point mutations, amplifications, and inactivation of tumor suppressor genes. This pathway is also a known resistance pathway, as it can be activated by both receptor tyrosine kinases and other oncogenes. mTOR inhibitors were the first targeted molecules in this pathway, and have already been FDA-approved in multiple indications. Because of the broad potential applications of inhibiting this pathway upstream of mTOR, multiple compounds targeting PI3K are in development. In this review, we discuss the clinical development of these inhibitors, including dual PI3K/mTOR inhibitors, pan-PI3K inhibitors, and isoform-selective PI3K inhibitors. Common adverse events, including rash, nausea, vomiting, diarrhea, and hyperglycemia, have created a narrow therapeutic window for all classes of PI3K inhibitors. Furthermore, single agent clinical activity has also been limited, with the exception of isoform-selective inhibitors, particularly the PI3Kδ and PI3Kγ inhibitors in hematologic malignancies. The future role of inhibitors of the PI3K/Akt/mTOR pathway in the clinical practice of oncology likely depends on the development of patient selection strategies and the results of combination trials that are currently ongoing. Copyright © 2014 Elsevier Inc. All rights reserved.


Breast cancer (BC) is diagnosed in nearly 1 in 3 women with cancer in the United States; one third of these patients have regional lymph node metastases at the time of diagnosis. The 5-year survival rate of patients with metastatic BC is very low, and approximately 40,000 women were expected to die of the disease in 2013. About 75% of patients with BC have hormone receptorepositive (HR+) disease, which is often managed with endocrine therapy; however, most patients eventually have resistance to these therapies. Recently, the mammalian target of rapamycin (mTOR) inhibitor everolimus, in combination with exemestane, improved progression-free survival (PFS) of patients with advanced BC, leading to its approval by the US Food and Drug Administration. Because adverse events (AEs) associated with everolimus might differ from AEs that oncologists who treat patients with BC are more familiar with, everolimus AEs and their effective management are reviewed in this article. Possible dose adjustments of everolimus for patients with renal or hepatic impairment and strategies for minimizing potential interactions of everolimus with other drugs and food are also discussed. © 2014 Elsevier Inc.

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