Developmental Therapeutics Program
Drug discovery and development research
Doctors who treat cancer face a critical need for new anticancer drugs. Relatively few available medications effectively eliminate the major solid tumors in people.
At the Henry Ford Cancer Institute, researchers in the drug discovery and development program are working to solve this challenge. We are identifying and testing anticancer therapies that will stop or shrink tumors. Our program focuses primarily on the niche of developing new leads (promising compounds) from natural products.
Our discovery process relies on a tissue-culture model to study the effects of compounds on human tumor cells and compare those to the effects on normal cells. Through this process, we can move the most promising compounds into clinical evaluation.
Our drug discovery and development research
The drug discovery and drug development process incorporates two closely related disciplines:
- Experimental therapeutics describes the process of applying science, from tissue cultures and molecular biology to animal models, to develop new treatments.
- Clinical therapeutics focuses on translating an experimental finding into human cancer trials.
Recently, our work has emphasized the search for new agents to treat pancreatic, ovarian, liver and brain cancer. These types of tumors are increasing in number and are especially difficult to treat. Some of our leads have moved into clinical trials (testing in humans). These leads include compounds at the experimental and clinical stages for gynecological cancer and glioblastoma (brain tumors).
Spotlight: Drug discovery and development
About 75 percent of all anticancer drugs come from natural sources, and that’s where we focus in our research. We explore the possibilities of microorganisms, marine organisms and even plants to fight cancer.
This work has important applications, including:
- Finding new resources for hard-to-treat cancers and cases where doctors already have exhausted some potential treatments.
- Supporting new frontiers of personalized medicine. We are seeking additional agents to work on different targets within tumors, so that oncologists can compile a drug cocktail tailored for an individual’s unique needs. Learn more about Henry Ford’s work with precision medicine.
- Discovering treatments that modify side effects. We have published our discoveries of molecules that increase the effect of radiation or drugs on tumor cells but don’t affect normal cells.
Henry Ford pharmacokinetics research core
The drug discovery and development lab hosts the Henry Ford pharmacokinetics research core. Researchers can use pharmacokinetics to help them develop compounds that require analysis on a molecular level.
We provide assistance from sample preparation to data analysis. Find out more about Henry Ford’s cancer research cores and shared resources.
Clinical therapeutics and radiation oncology research
Our radiation oncology studies examine which drugs could potentially help make tumor cells more sensitive to radiation. If cells become more sensitive, radiation treatment can have a greater effect.
Our radiation oncology research includes:
- Radiosensitizing using a novel three-pronged gene therapy approach that incorporates gene therapy using adenovirus (a common cold virus); suicide genes (gene therapy that causes cancer cells to self-destruct) and chemotherapy; and radiation
- Mitigating damage to normal tissue (noncancerous cells) by minimizing reactive oxygen species using drugs such as angiotensin-converting enzyme (ACE) inhibitors
- Improving radiation therapy by optimally implementing three-dimensional conformal radiotherapy (3-D CRT), where radiology oncologists shape beams of radiation to fit the tumor and avoid nearby healthy tissue
It might sound like science fiction: a doctor injects a specialized cell into a cancerous tumor, and when the cell reproduces, it helps the body eradicate the cancer. In fact, this is science, not sci-fi, and the Henry Ford Cancer Institute’s cutting-edge gene therapy program is among the first to use this treatment.
Gene therapy is an investigational technology (still being studied) in which a doctor introduces genes into a patient with the goal of curing or lessening a disease. Genes are tiny packets of DNA (genetic material) inside the cells of all living organisms.
Genes tell our cells -- the body’s building blocks -- how to do things. By adjusting those “instructions,” researchers hope to help the body fight off diseases, including cancer. Henry Ford researchers have made several significant advances in gene therapy to treat prostate, pancreatic and now lung cancer.
Gene therapy remains experimental, but researchers know that it works. In fact, the first gene therapy products are making their way to market. Commercially available gene therapies can treat melanoma and herpes.
Spotlight: Translational gene therapy research using adenovirus
Since 1996, Svend Freytag, Ph.D., has been developing a gene therapy-based approach for cancer treatment at Henry Ford. The process uses a specialized type of common cold virus, called oncolytic adenovirus, to deliver a pair of cytotoxic (toxic to cells) “suicide” genes to the tumor.
The virus acts against the tumor by destroying cancer cells from the inside out. We sometimes use gene therapy on its own to attack the tumor. Often, we use gene therapy along with radiation therapy to deliver the best results.
Here is how our gene therapy approach works:
- Create a virus: In the lab, we develop a virus that replicates (makes copies of itself) better in tumor cells than in normal cells.
- Customize the virus: We arm the virus with therapeutic genes intended to work against cancer cells. These genes “turn on” when the virus reproduces.
- Inject the virus: We introduce the modified virus directly into the tumor, a process called direct intratumoral injection.
- The virus reproduces: The virus damages the tumor cells as it makes copies of itself. At the same time, it turns on the potentially cancer-fighting genes it carries. Over a few days, the virus releases exact copies of itself that reproduce inside additional tumor cells before the body recognizes the virus and begins to fight it.
- Activate “suicide gene therapy”: At this point, the patient takes two inactive drugs that have no effect on their own. But when they combine with the gene that the virus released, they weaken and eliminate nearby tumor cells that have survived the virus. Because this combination of genes and drugs causes the cells to die, researchers may call the treatment suicide gene therapy.
- Add radiation therapy: The suicide gene therapy makes tumor cells more sensitive to radiation treatment. For this reason, for the third prong of gene therapy treatment, we use targeted radiation therapy to eliminate the remaining, weakened tumor cells.
Clinical trials of adenovirus gene therapy
Once researchers have good reason to believe that an emerging therapy is safe and effective, they study it through clinical trials. These investigational studies try out a new drug in human patients to evaluate how well the treatment works.
Our collaborative and patient-focused environment allows researchers and doctors to work hand-in-hand. We have studied the effectiveness of gene therapy and its potential toxicity in clinical trials for prostate and pancreatic cancer.
Our clinical trials have had promising results, including:
- Prostate cancer: We have conducted five prostate cancer trials using four different products.
- Phase 1 trials: We have conducted four phase 1 trials, with small groups of patients, for prostate cancer.
- Phase 2 trial: We took one product through a randomized, controlled, multicenter phase 2 study. In this larger group, half of the patients studied received radiation alone, and half received radiation along with gene therapy. After two years, the gene therapy had significantly reduced the number of tumors in men who participated in the study.
- Phase 3 trial: We’ve received authorization to pursue a phase 3 trial to further examine our adenovirus therapy for prostate cancer.
- Pancreatic cancer: A trial of our gene therapy method in treating pancreatic cancer is ongoing in Korea.
- Lung cancer: We anticipate opening a lung cancer clinical trial in 2017. We’ll conduct this phase 1 trial at Henry Ford with just nine patients.
- Other cancers: When we’ve determined that this treatment is safe, we anticipate that oncologists could use our gene therapy developments in other cancers, including head, neck and brain cancers.
Get involved with developmental therapeutics research
When we’ve discovered a potential new cancer medication or therapy, the next step is to take the drug or treatment to clinical trials (working with human patients to see how the drug works).
We pursue clinical trials for new treatments with pharmaceutical companies, the National Cancer Institute (NCI) or the cooperative Southwest Oncology Group. Henry Ford’s Clinical Trials office provides support throughout the research and development process. Learn more about clinical trials.
We study new drugs and treatment approaches through phase 1 and phase 2 protocols. Phase 1 studies are brief (lasting a few months) and include a small number of patients. Phase 2 studies observe larger numbers of patients over about a two-year period.
We handle some of these studies internally at Henry Ford. We develop others in collaboration with the NCI, cooperative study groups (such as Southwest Oncology Group) and pharmaceutical and small biotech companies.
To participate in our developmental therapeutics research work as a researcher or a patient:
- Find a clinical trial: Henry Ford has hundreds of clinical trials underway. With a clinical trial, you may be able to benefit from new treatments or techniques before they’re widely available. Learn more about clinical trials.
- Become a Henry Ford researcher: We sometimes take on new drug discovery and development researchers. Join our research team.
- Support cancer research: Henry Ford’s Cancer Research Advisory Group (CRAG) provides funding and resources to help advance our research. Learn how you can support cancer research.
Our drug discovery and development researchers work closely with other cancer investigators.
Below, you can learn more about our researchers and their interests. You also can read more about how to join our research team.
Developmental therapeutics research leader and clinical co-leader
Developmental therapeutics scientific members
- Ali, Meser, Ph.D.
- Brown, Stephen, Ph.D.
- Buller, Benjamin, Ph.D.
- Devpura, Suneetha, Ph.D.
- Freytag, Svend, Ph.D.
- Giri, Shailendra, Ph.D.
- Glide-Hurst, Carri, Ph.D.
- Katakowski, Mark, Ph.D.
- Mi, Qing-Sheng, Ph.D.
- Valeriote, Fred, Ph.D.
- Wang, Ding, M.D., Ph.D.
- Zhong, Hualiang, Ph.D.
Developmental therapeutics clinical members
- Ajlouni, Munther, M.D.
- Chapman, Robert, M.D.
- Craig, Joseph, M.D.
- Doemer, Anthony, M.S.
- Dragovic, Jadranka, M.D.
- Gordon, J. James
- Huang, Yimei, Ph.D.
- Kim, Jae Ho, M.D.
- Kim, Jinkoo
- Lindholm, Jamie
- Loutfi, Randa, M.D.
- Mayyas, Essa
- Movsas, Benjamin, M.D.
- Ormsby, Adrian, M.D.
- Rank, Aaron
- Rybkin, Igor, M.D.
- Siddiqui, Farzan, M.D.
- Smith, Chadd, Ph.D.
- Steffes, Christopher, M.D.
- Szilagy, Eric, M.D.
Publications in developmental therapeutics research
We regularly publish work in scientific journals to share our findings with the oncology community. Search the publications below for topics that interest you.
Publications by Henry Ford developmental therapeutics researchers
Al Feghali KA, Kolozsvary A, Lapanowski K, Isrow D, Brown SL and Kim JH. A novel mechanism of radiosensitization by metformin. International journal of radiation oncology, biology, physics. 2016; 96(2s):E574.
Apolo AB, Infante JR, Hamid O, Patel MR, Wang D, Kelly K, Mega AE, Britten CD, Mita AC, Ravaud A, Cuillerot JM, von Heydebreck A and Gulley JL. Safety, clinical activity, and PD-L1 expression of avelumab (MSB0010718C), an anti-PD-L1 antibody, in patients with metastatic urothelial carcinoma from the JAVELIN Solid Tumor phase Ib trial. J Clin Oncol. 2016; 34(2):1.
Apolo AB, Infante JR, Hamid O, Patel MR, Wang D, Kelly K, Mega AE, Britten CD, Ravaud A, Mita AC, Safran H, Stinchcombe T, Grote HJ, V on Heydebreck A, Cuillerot JM and Gulley JL. Avelumab (MSB0010718C; anti-PD-L1) in patients with metastatic urothelial carcinoma from the JAVELIN solid tumor phase 1b trial: Analysis of safety, clinical activity, and PD-L1 expression. J Clin Oncol. 2016; 34.
Bagher-Ebadian H, Siddiqui F, Liu C, Movsas B and Chetty IJ. Prediction of response to radiation therapy treatment of head and neck cancers using an artificial neural network developed from cone beam computed tomography image textural information. International journal of radiation oncology, biology, physics. 2016; 96(2s):S98.
Berman AT, Rosenthal SA, Moghanaki D, Woodhouse KD, Movsas B and Vapiwala N. Focusing on the "person" in personalized medicine: The future of patient-centered care in radiation oncology. Journal of the American College of Radiology : JACR. 2016; 13(12 Pt B):1571–1578.
Bertin MJ, Demirkiran O, Navarro G, Moss NA, Lee J, Goldgof GM, Vigil E, Winzeler EA, Valeriote FA and Gerwick WH. Kalkipyrone B, a marine cyanobacterial gamma-pyrone possessing cytotoxic and anti-fungal activities. Phytochemistry. 2016; 122:113–118.
Brown SL, Elmghirbi R, Nagaraja T, Keenan KA, Lapanowski K, Panda S, Inder P, Cabral G, Liu L, Kim JH, Movsas B, Chetty IJ, Ewing JR and Parry R. Toward a noninvasive measurement of cancer stem cells and tumor aggressiveness. International journal of radiation oncology, biology, physics. 2016; 96(2s):E592.
Buller B, Moore T, Zhang Y, Pikula E, Martin C, Mortazavi F, Rosene D, Chopp M and Zhang Z. Exosomes from rhesus monkey MSCs promote neuronal growth and myelination. Stroke. 2016; 47.
Burmeister J, Chen Z, Chetty IJ, Dieterich S, Doemer A, Dominello MM, Howell RM, McDermott P, Nalichowski A, Prisciandaro J, Ritter T, Smith C, Schreiber E, Shafman T, Sutlief S and Xiao Y. The american society for radiation oncology's 2015 core physics curriculum for radiation oncology residents. International journal of radiation oncology, biology, physics. 2016; 95(4):1298–1303.
Chen RC, Hoffman KE, Sher DJ, Showalter TN, Morrell R, Chen AB, Benda R, Nguyen PL, Movsas B and Hardenbergh P. Development of a standard survivorship care plan template for radiation oncologists. Pract Radiat Oncol. 2016; 6(1):57–65.
Chen WB, Gao L, Wang J, Wang YG, Dong Z, Zhao J, Mi QS and Zhou L. Conditional ablation of HDAC3 in islet beta cells results in glucose intolerance and enhanced susceptibility to STZ-induced diabetes. Oncotarget. 2016.
Chetvertkov MA, Siddiqui F, Kim J, Chetty I, Kumarasiri A, Liu C and Gordon JJ. Use of regularized principal component analysis to model anatomical changes during head and neck radiation therapy for treatment adaptation and response assessment. Med Phys. 2016; 43(10):5307–5319.
Chow LQ, Smith DC, Tan AR, Denlinger CS, Wang D, Shepard DR, Chaudhary A, Lin Y and Gao L. Lack of pharmacokinetic drug-drug interaction between ramucirumab and paclitaxel in a phase II study of patients with advanced malignant solid tumors. Cancer chemotherapy and pharmacology. 2016; 78(2):433–441.
Craig JR, Petrov D, Khalili S, Brooks SG, Lee JY, Adappa ND and Palmer JN. The nasofrontal beak: A consistent landmark for superior septectomy during Draf III drill out. American journal of rhinology & allergy. 2016; 30(3):230–234.
Craig JR, Zhao K, Doan N, Khalili S, Lee JY, Adappa ND and Palmer JN. Cadaveric validation study of computational fluid dynamics model of sinus irrigations before and after sinus surgery. International forum of allergy & rhinology. 2016.
Cristea MC, Miao J, Argiris A, Chen AM, Daly ME, Decker RH, Garland LL, Wang D, Koczywas M, Moon J, Kelly K and Gandara DR. SWOG S1206: A dose-finding study of veliparib (ABT-888) added to chemoradiotherapy (CRT) with carboplatin (C) and paclitaxel (P) for unresectable stage III non-small cell lung cancer (NSCLC). J Clin Oncol. 2016; 34.
Davis BJ, Taira AV, Nguyen PL, Assimos DG, D'Amico AV, Gottschalk AR, Gustafson GS, Keole SR, Liauw SL, Lloyd S, McLaughlin PW, Movsas B, Prestidge BR, Showalter TN and Vapiwala N. ACR appropriateness criteria permanent source brachytherapy for prostate cancer. Brachytherapy. 2016.
Deeb D, Gao X, Liu Y, Zhang Y, Shaw J, Valeriote FA and Gautam SC. The inhibition of cell proliferation and induction of apoptosis in pancreatic ductal adenocarcinoma cells by verrucarin A, a macrocyclic trichothecene, is associated with the inhibition of Akt/NF-small ka, CyrillicB/mTOR prosurvival signaling. International journal of oncology. 2016; 49(3):1139–1147.
Dzinic SH, Bernardo MM, Li X, Fernandez-Valdivia R, Ho YS, Mi QS, Bandyopadhyay S, Lonardo F, Vranic S, Oliveira D, Bonfil RD, Dyson G, Chen K, Omerovic A, Sheng X, Han X, et al. An essential role of maspin in embryogenesis and tumor suppression. Cancer Res. 2016.
Elmghirbi R, Nagaraja TN, Brown SL, Panda S, Aryal MP, Keenan KA, Bagher-Ebadian H, Cabral G and Ewing JR. Acute temporal changes of mri-tracked tumor vascular parameters after combined anti-angiogenic and radiation treatments in a rat glioma model: Identifying signatures of synergism. Radiation research. 2016.
Fahs F, Bi XL, Yu FS, Zhou L and Mi QS. Small rnas play big roles: Micrornas in diabetic wound healing. Current molecular medicine. 2016.
Feng M, Matuszak MM, Boike TP, Grills IS, Kestin LL, Movsas B, Paximadis PA, Griffith KA, Gustafson GS, Moran JM, Nurushev TS, Radawski JD, Pierce LJ, Hayman JA and Schipper M. Predictors of heart dose from lung radiation therapy in a large consortium of community and academic practices. International journal of radiation oncology, biology, physics. 2016; 96(2s):E482.
Freytag SO, Movsas B and Stricker H. Clinical trials of oncolytic adenovirus-mediated gene therapy. Mol Ther. 2016; 24:S205–S205.
Freytag SO, Zhang Y and Siddiqui F. Preclinical toxicology of oncolytic adenovirus-mediated cytotoxic and interleukin-12 gene therapy for prostate cancer. Molecular therapy oncolytics. 2015; 2.
Gerber DE, Urbanic JJ, Langer C, Hu C, Chang IF, Lu B, Movsas B, Jeraj R, Curran WJ and Bradley JD. Treatment design and rationale for a randomized trial of cisplatin and etoposide plus thoracic radiotherapy followed by nivolumab or placebo for locally advanced non-small-cell lung cancer (rtog 3505). Clinical lung cancer. 2016.
Glide-Hurst C, Price R, Kim JP, Zheng W and Chetty IJ. Validation of synthetic CTs for MR-only planning of brain cancer. Radiother Oncol. 2016; 119:S870.
Glide-Hurst CK, Miller BM, Kim JP, Siddiqui MS and Movsas B. Potential failure modes for magnetic resonance-only treatment planning in the pelvis. International journal of radiation oncology, biology, physics. 2016; 96(2s):S233–S234.
Gordon JJ. On the feasibility of extracting dose-response curves from clinical DVH data using correlation and regression analysis. Biomedical physics and engineering express. 2016; 2(1).
Harvey RD, Gore L, Wang D, Mita A, Sharma S, Nemunaitis J, Papadopoulos K, Pinchasik D, Ou Y, Demirhan E, Cutler RE and Tsimberidou AM. A phase I study to assess food effect on oprozomib in patients with advanced malignancies. Clin Pharmacol Ther. 2016; 99:S98–S99.
Hijaz M, Das S, Mert I, Gupta A, Al-Wahab Z, Tebbe C, Dar S, Chhina J, Giri S, Munkarah A, Seal S and Rattan R. Folic acid tagged nanoceria as a novel therapeutic agent in ovarian cancer. BMC cancer. 2016; 16(1):220.
Isaacs SR, Wang J, Kim KW, Yin C, Zhou L, Mi QS and Craig ME. MicroRNAs in type 1 diabetes: Complex interregulation of the immune system, beta cell function and viral infections. Current diabetes reports. 2016; 16(12):133.
Isrow D, Kolozsvary A, Lapanowski K, Brown SL and Kim JH. Metformin's preferential cytotoxic effect on cancer stem/non-stem cell populations is (glucose) dependent and correlated with intracellular levels of reactive oxygen species. International journal of radiation oncology, biology, physics. 2016; 96(2s):E565.
Jin Y, Andersen G, Yorgov D, Ferrara TM, Ben S, Brownson KM, Holland PJ, Birlea SA, Siebert J, Hartmann A, Lienert A, van Geel N, Lambert J, Luiten RM, Wolkerstorfer A, Wietze van der Veen JP, et al. Genome-wide association studies of autoimmune vitiligo identify 23 new risk loci and highlight key pathways and regulatory variants. Nature genetics. 2016; 48(11):1418–1424.
Katakowski M and Chopp M. Exosomes as tools to suppress primary brain tumor. Cellular and molecular neurobiology. 2016.
Katakowski M, Charteris N, Chopp M and Khain E. Density-dependent regulation of glioma cell proliferation and invasion mediated by miR-9. Cancer microenvironment: official journal of the International Cancer Microenvironment Society. 2016.
Kelly K, Heery CR, Patel MR, Infante JR, Iannotti N, Leach JW, Wang D, Chandler JC, Arkenau HT, Taylor MH, Gordon MS, Wong DJL, Safran H, Kaufman H, Keilholz U, Bajars M, et al. Avelumab (MSB0010718C; anti-PD-LI) in patients with advanced cancer: Safety data from 1300 patients enrolled in the phase 1b JAVELIN Solid Tumor trial. J Clin Oncol. 2016; 34.
Kim J, Wu Q, Zhao B, Wen N, Ajlouni M, Movsas B and Chetty IJ. To gate or not to gate - dosimetric evaluation comparing Gated vs. ITV-based methodologies in stereotactic ablative body radiotherapy (SABR) treatment of lung cancer. Radiation oncology (London, England). 2016; 11(1):125.
Kim JH, Brown SL and Kolozsvary A. Methods to mitigate injury from radiation exposure by administering cxcr4 antagonist during decisive treatment window. Google patents. 2016.
Kumar A, Giri S and Kumar A. AICAR-mediated AMPK activation induces protective innate responses in bacterial endophthalmitis. Cellular microbiology. 2016.
Kumar N, Nakagawa P, Janic B, Romero CA, Worou ME, Monu SR, Peterson EL, Shaw J, Valeriote F, Ongeri EM, Niyitegeka JV, Rhaleb NE and Carretero OA. The anti-inflammatory peptide Ac-SDKP is released from thymosin beta4 by renal meprin alpha and prolyl oligopeptidase. American journal of physiology Renal physiology. 2016:ajprenal.00562.02015.
Kupsky D, Wang DD, Eng M, Song T, Pantelic M, Nadig J, Greenbaum A and O'Neill W. TCT-621 Left atrial appendage characteristics evaluated by computed tomography following closure with Watchman device. J Am Coll Cardiol. 2016; 68(18s):B253.
Liu LJ, Brown SL, Ewing JR, Ala BD, Schneider KM and Schlesinger M. Estimation of tumor interstitial fluid pressure (tifp) noninvasively. PloS one. 2016; 11(7):e0140892.
Liu Q, Wu D, Han L, Deng J, Zhou L, He R, Lu C and Mi QS. Roles of MicroRNAs in psoriasis: immunological functions and potential biomarkers. Experimental dermatology. 2016.
Liu Y, Gao X, Deeb D, Zhang Y, Shaw J, Valeriote FA and Gautam SC. Mycotoxin verrucarin A inhibits proliferation and induces apoptosis in prostate cancer cells by inhibiting prosurvival Akt/NF-kB/mTOR signaling. Journal of experimental therapeutics & oncology. 2016; 11(4):251–260.
Liu Z, Wang S, Mi QS and Dong Z. MicroRNAs in pathogenesis of acute kidney injury. Nephron. 2016.
Mangalam AK, Rattan R, Suhail H, Singh J, Hoda MN, Deshpande M, Fulzele S, Denic A, Shridhar V, Kumar A, Viollet B, Rodriguez M and Giri S. AMP-activated protein kinase suppresses autoimmune central nervous system disease by regulating m1-type macrophage-th17 axis. Journal of immunology (Baltimore, Md: 1950). 2016.
Mattour AH, Walbert T, Lee I and Wang D. A revisit of the devastating outcome of leptomeningeal disease. J Clin Oncol. 2016; 34.
Michael Bauer T, Adkins D, Schwartz GK, Werner TL, Alva AS, Hong DS, Carvajal RD, Saleh MN, Bazhenova L, Goel S, Eaton KD, Siegel RD, Wang D, Lauer RC, Neuteboom STC, Faltaos D, et al. A first in human phase I study of receptor tyrosine kinase (RTK) inhibitor MGCD516 in patients with advanced solid tumors. J Clin Oncol. 2016; 34.
Movsas TZ, Yechieli R, Movsas B and Darwish-Yassine M. Partner's perspective on long-term sexual dysfunction after prostate cancer treatment. American journal of clinical oncology. 2016; 39(3):276–279.
Munkarah A, Hamid S, Chhina J, Mert I, Jackson L, Hensley-Alford S, Chitale D, Giri S and Rattan R. Targeting of free fatty acid signaling in ovarian cancer may serve as a potential therapeutic approach. Clin Cancer Res. 2016; 22.
Munkarah A, Mert I, Chhina J, Hamid S, Poisson L, Hensley-Alford S, Giri S and Rattan R. Targeting of free fatty acid receptor 1 in EOC: A novel strategy to restrict the adipocyte-EOC dependence. Gynecol Oncol. 2016; 141(1):72–79.
Munkarah AR, Kim S, Buekers TE, Chhina J, Poisson L, Giri S and Rattan R. Metabolic effects of metformin treatment in ovarian cancer cell lines. Gynecol Oncol. 2016; 141:168.
Patel MR, Fakih M, Olszanski AJ, Lockhart AC, Drilon AE, Fu S, Bazhenova L, Patel R, Oliver JW, Multani PS and Wang D. A phase 1 dose escalation study of RXDX-105, an oral RET and BRAF inhibitor, in patients with advanced solid tumors. J Clin Oncol. 2016; 34.
Paximadis PA, Schipper M, Matuszak MM, Feng M, Boike TP, Grills IS, Kestin L, Movsas B, Griffith KA, Gustafson GS, Moran JM, Nurushev TS, Radawski JD, Pierce LJ and Hayman JA. Dosimetric variables predicting for acute esophagitis during definitive radiation therapy for locally advanced non-small cell lung cancer-results of a large prospective observational study. International journal of radiation oncology, biology, physics. 2016; 96(2s):E447–E448.
Price RG, Kim JP, Zheng W, Chetty IJ and Glide-Hurst C. Image guided radiation therapy using synthetic computed tomography images in brain cancer. International journal of radiation oncology, biology, physics. 2016.
Qin Y, Zhong H, Wen N, Snyder K, Huang Y and Chetty IJ. Deriving detector-specific correction factors for rectangular small fields using a scintillator detector. Journal of applied clinical medical physics. 2016; 17(6):6433.
Rattan R, Mert I, Chhina J, Hamid S, Hijaz M, Poisson L, Hensley Alford S, Giri S and Munkarah AR. Targeting of free fatty acid receptor 1 in EOC: A novel strategy to restrict the adipocyte-EOC dependence. Gynecol Oncol. 2016; 141:47.
Sabry OM, Goeger DE, Valeriote FA and Gerwick WH. Cytotoxic halogenated monoterpenes from Plocamium cartilagineum. Natural product research. 2016:1–7.
Sakr S, Giri S, Rattan R, Abdulfatah E, Pardeshi V, Morris RT, Munkarah AR and Ali-Fehmi R. Expression of alcohol dehydrogenase 5 in ovarian carcinoma: Effect on prognosis and therapeutic potential. Gynecol Oncol. 2016; 141:67.
Santoso AP, Song KH, Qin Y, Gardner SJ, Liu C, Chetty IJ, Movsas B, Ajlouni M and Wen N. Evaluation of gantry speed on image quality and imaging dose for 4D cone-beam CT acquisition. Radiation oncology (London, England). 2016; 11(1):98.
Siebers JV and Gordon JJ. Regarding: "The dosimetric impact of image guided radiation therapy by intratumoral fiducial markers". Pract Radiat Oncol. 2016.
Singh J, Deshpande M, Suhail H, Rattan R and Giri S. Targeted stage-specific inflammatory microrna profiling in urine during disease progression in experimental autoimmune encephalomyelitis: Markers of disease progression and drug response. J Neuroimmune Pharmacol. 2016; 11(1):84–97.
Singh J, Olle B, Suhail H, Felicella MM and Giri S. Metformin-induced mitochondrial function and ABCD2 up regulation in X-linked adrenoleukodystrophy involves AMP activated protein kinase. Journal of neurochemistry. 2016.
Small W, Jr., James JL, Moore TD, Fintel DJ, Lutz ST, Movsas B, Suntharalingam M, Garces YI, Ivker R, Moulder J, Pugh S and Berk LB. Utility of the ace inhibitor captopril in mitigating radiation-associated pulmonary toxicity in lung cancer: Results from nrg oncology rtog 0123. American journal of clinical oncology. 2016.
Snyder KC, Kim J, Reding A, Fraser C, Gordon J, Ajlouni M, Movsas B and Chetty IJ. Development and evaluation of a clinical model for lung cancer patients using stereotactic body radiotherapy (SBRT) within a knowledge-based algorithm for treatment planning. Journal of applied clinical medical physics. 2016; 17(6):6429.
St Louis D, Romero R, Plazyo O, Arenas-Hernandez M, Panaitescu B, Xu Y, Milovic T, Xu Z, Bhatti G, Mi QS, Drewlo S, Tarca AL, Hassan SS and Gomez-Lopez N. Invariant NKT cell activation induces late preterm birth that is attenuated by rosiglitazone. Journal of immunology (Baltimore, Md: 1950). 2016; 196(3):1044–1059.
Stinchcombe T, Zhang YJ, Vokes EE, Schiller JH, Bradley JD, Curran WJ, Movsas B, Schild SE, Clamon GH, Govindan R, Blumenschein GR, Socinski MA, Ready N, Akerley WL, Cohen HJ, Pang H, et al. A pooled analysis of concurrent chemoradiotherapy (CCRT) for patients with stage III non-small cell lung cancer (NSCLC) who participated in U.S. cooperative group trials: Comparing the outcomes of elderly to younger patients (pts). J Clin Oncol. 2016; 34.
Taylor M, Mert I, Hijaz M, Chhina J, Morris RT, Giri S, Rattan R and Munkarah AR. Effects of an olaparib and metformin combination on the AMPK and DNA-damage pathways in ovarian cancer. Gynecol Oncol. 2016; 141:197–198.
To DT, Kim JP, Price RG, Chetty IJ and Glide-Hurst CK. Impact of incorporating visual biofeedback in 4D MRI. Journal of applied clinical medical physics. 2016; 17(3):6017.
Tsimberidou AM, Ou Y, Xu Y, Wang Z, Harvey RD, Mita A, Sharma S, Papadopoulos K, Wang D, Pinchasik D, Demirhan E, Cutler RE and Gore L. A phase I study of oprozomib to assess drug-drug interaction with midazolam in patients with advanced malignancies. Clin Pharmacol Ther. 2016; 99:S100.
Vance S, Al Feghali KA, Taylor A, Kaur M, Neslund-Dudas C, Chetty IJ, Simoff M, Ajlouni M and Movsas B. Do race and income influence quality of life (QoL) or survival outcomes after lung stereotactic body radiation therapy (SBRT)? a prospective study. International journal of radiation oncology, biology, physics. 2016; 96(2s):E534.
Wang D, Braiteh F, Lee JJ, Denlinger CS, Shepard DR, Chaudhary A, Lin Y, Gao L, Asakiewicz C, Nasroulah F and LoRusso P. Lack of pharmacokinetic drug-drug interaction between ramucirumab and irinotecan in patients with advanced solid tumors. Cancer chemotherapy and pharmacology. 2016.
Wang DD, Eng M, Greenbaum A, Myers E, Forbes M, Pantelic M, Song T, Nelson C, Divine G, Taylor A, Wyman J, Guerrero M, Lederman RJ, Paone G and O'Neill W. Predicting LVOT obstruction after TMVR. JACC Cardiovascular imaging. 2016.
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