tbuckley/cabot-search huggingface dataset:
Results of a global phase II study with crizotinib in advanced <i>ALK</i>-positive non-small cell lung cancer (NSCLC).
Authors: Dong-Wan Kim, Myung-Ju Ahn, Yuankai Shi, Tommaso Martino De Pas, Pan-Chyr Yang, Gregory J. Riely, Lucio Crinò, Tracey L. Evans, Xiaoqing Liu, Ji-Youn Han, Ravi Salgia, Denis Moro-Sibilot, Sai-Hong Ignatius Ou, Scott N. Gettinger, Yi Long Wu, Silvana Lanzalone, Anna Polli, Shrividya Iyer, Alice Tsang Shaw
Journal: Journal of Clinical Oncology (2012)

7533 Background: Approximately 3–5% of NSCLC harbors ALK gene rearrangements. Crizotinib is a first-in-class, oral, small-molecule competitive ALK inhibitor with anti-MET activity. Methods: PROFILE 1005 is an ongoing global, multicenter, open-label, single-arm, phase II study evaluating the safety and efficacy of crizotinib (250 mg BID in 3-week cycles) in patients with advanced ALK-positive NSCLC who progressed after ≥1 chemotherapy for recurrent/advanced/metastatic disease. Tumor response was evaluated by RECIST 1.1 every 6 weeks. Patient-reported symptoms and global quality of life (QOL) were assessed using the EORTC QLQ-C30 and LC-13 at baseline, day 1 each cycle and at end of treatment. Results: As of June 2011, 439 patients were evaluable for safety and 255 patients for tumor response. Median age was 53 years. The majority of patients were female (53%), never smokers (65%), and had adenocarcinoma (92%), ECOG PS 0–1 (83%) and ≥2 prior chemotherapy regimens (85%). Among patients evaluable for efficacy, median treatment duration was 25 weeks (77% of patients still ongoing). ORR was 53% (95% CI: 47–60), disease control rate at 12 weeks was 85% (95% CI: 80–89), median duration of response was 43 weeks (96% CI 36–50) and median PFS was 8.5 months (95% CI: 6.2–9.9). The most frequent treatment-related AEs were visual effects (50%), nausea (46%), vomiting (39%), and diarrhea (35%), mostly grade 1–2. 29 patients (6.6%) had treatment-related SAEs, including dyspnea and pneumonitis (4 patients each; 0.9%), and febrile neutropenia and renal cyst (2 patients each; 0.5%). A statistically significant (p&lt;0.05) and clinically meaningful (≥ 10 points) improvement from baseline was observed for patient-reported overall pain, pain in chest, cough, dyspnea, insomnia, fatigue and global QOL. Conclusions: Crizotinib demonstrated a high response rate and PFS, favorable tolerability profile and improvement in patient-reported symptoms. These results provide strong evidence for crizotinib as a standard of care for advanced ALK-positive NSCLC.
Abstract P2-09-03: Long-term comparison of anastrozole versus tamoxifen: Results from LATTE/ATAC
Authors: J Cuzick, I Sestak, A Bianco, L Strobbe, J Bergh, C Hanusch, P Neven, M Dowsett, JF Forbes, A Buzdar, R Smith, A Howell
Journal: Cancer Research (2017)

Abstract Background: Previous reports from the Anastrozole Tamoxifen Alone or in Combination (ATAC) trial have shown significantly prolonged disease-free survival, lower rates of recurrence and distant recurrence, and reduced contralateral breast cancer in patients treated with anastrozole compared to tamoxifen (Cuzick et al., Lancet, 2010). Here, we compare the long-term effects of anastrozole versus tamoxifen in patients randomised to either monotherapy arm in the ATAC trial. Methods: Postmenopausal women with hormone receptor positive breast cancer randomised to anastrozole or tamoxifen in the main ATAC trial were eligible for the LATTE observational study. The primary objective was to compare the long-term effects of tamoxifen and anastrozole on time to recurrence and death beyond 10 years after randomisation. Secondary objectives included time to distant recurrence, cancer-specific survival, new breast primaries, other cancers, fractures, and cardiac/cerebrovascular events. Cox proportional hazard methods were used to compute hazard ratios (95% CI) for recurrence from the time of last publication (10 years median follow-up). Results: 2452 women from 11 countries were entered into the LATTE study. 40 women withdrew consent and 759 women died or had a recurrence within 10 years, which left 1653 women for analysis (838 anastrozole vs. 815 tamoxifen). A total of 118 breast events (69 anastrozole (8.2%) vs. 49 tamoxifen (6.0%)) were reported. No significant difference between the two treatment arms were observed (HR=1.36 (0.94-1.97), P=0.098). 57 women had a distant recurrence (33 (3.9%) vs. 24 (2.9%)), 41 reported a loco-regional recurrence (23 (2.7%) vs. 18 (2.2%)), and 26 contra-lateral breast cancer were recorded (17 (2.0%) vs. 9 (1.1%)). None of the treatment comparisons were statistically significant. 305 deaths were recorded (147 (17.5%) vs. 158 (19.4%)), of which 31 were due to breast cancer. Significantly fewer gynaecological cancers were recorded with anastrozole (7 vs. 16; OR=0.42 (0.15-1.09), P=0.05), but overall the effect on other cancers was not significant (54 (6.4%) vs. 64 (7.9%). Fractures, cardiovascular, and cerebrovascular events were evenly distributed between the treatment arms. Conclusions: Although anastrozole was associated with significant fewer recurrences compared to tamoxifen in the first 10 years of follow-up, in this analysis, with limited number of patients, we could not find a significant difference between the two treatment arms. Citation Format: Cuzick J, Sestak I, Bianco A, Strobbe L, Bergh J, Hanusch C, Neven P, Dowsett M, Forbes JF, Buzdar A, Smith R, Howell A. Long-term comparison of anastrozole versus tamoxifen: Results from LATTE/ATAC [abstract]. In: Proceedings of the 2016 San Antonio Breast Cancer Symposium; 2016 Dec 6-10; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2017;77(4 Suppl):Abstract nr P2-09-03.
<i>BRCA2</i> Hypomorphic Missense Variants Confer Moderate Risks of Breast Cancer
Authors: Hermela Shimelis, Romy L.S. Mesman, Catharina Von Nicolai, Asa Ehlen, Lucia Guidugli, Charlotte Martin, Fabienne M.G.R. Calléja, Huong Meeks, Emily Hallberg, Jamie Hinton, Jenna Lilyquist, Chunling Hu, Cora M. Aalfs, Kristiina Aittomäki, Irene Andrulis, Hoda Anton-Culver, Volker Arndt, Matthias W. Beckmann, Javier Benitez, Natalia V. Bogdanova, Stig E. Bojesen, Manjeet K. Bolla, Anne-Lise Borresen-Dale, Hiltrud Brauch, Paul Brennan, Hermann Brenner, Annegien Broeks, Barbara Brouwers, Thomas Brüning, Barbara Burwinkel, Jenny Chang-Claude, Georgia Chenevix-Trench, Ching-Yu Cheng, Ji-Yeob Choi, J. Margriet Collée, Angela Cox, Simon S. Cross, Kamila Czene, Hatef Darabi, Joe Dennis, Thilo Dörk, Isabel dos-Santos-Silva, Alison M. Dunning, Peter A. Fasching, Jonine Figueroa, Henrik Flyger, Montserrat García-Closas, Graham G. Giles, Gord Glendon, Pascal Guénel, Christopher A. Haiman, Per Hall, Ute Hamann, Mikael Hartman, Frans B. Hogervorst, Antoinette Hollestelle, John L. Hopper, Hidemi Ito, Anna Jakubowska, Daehee Kang, Veli-Matti Kosma, Vessela Kristensen, Kah-Nyin Lai, Diether Lambrechts, Loic Le Marchand, Jingmei Li, Annika Lindblom, Artitaya Lophatananon, Jan Lubinski, Eva Machackova, Arto Mannermaa, Sara Margolin, Frederik Marme, Keitaro Matsuo, Hui Miao, Kyriaki Michailidou, Roger L. Milne, Kenneth Muir, Susan L. Neuhausen, Heli Nevanlinna, Janet E. Olson, Curtis Olswold, Jan J.C. Oosterwijk, Ana Osorio, Paolo Peterlongo, Julian Peto, Paul D.P. Pharoah, Katri Pylkäs, Paolo Radice, Muhammad Usman Rashid, Valerie Rhenius, Anja Rudolph, Suleeporn Sangrajrang, Elinor J. Sawyer, Marjanka K. Schmidt, Minouk J. Schoemaker, Caroline Seynaeve, Mitul Shah, Chen-Yang Shen, Martha Shrubsole, Xiao-Ou Shu, Susan Slager, Melissa C. Southey, Daniel O. Stram, Anthony Swerdlow, Soo H. Teo, Ian Tomlinson, Diana Torres, Thérèse Truong, Christi J. van Asperen, Lizet E. van der Kolk, Qin Wang, Robert Winqvist, Anna H. Wu, Jyh-Cherng Yu, Wei Zheng, Ying Zheng, Jennifer Leary, Logan Walker, Lenka Foretova, Florentia Fostira, Kathleen B.M. Claes, Liliana Varesco, Setareh Moghadasi, Douglas F. Easton, Amanda Spurdle, Peter Devilee, Harry Vrieling, Alvaro N.A. Monteiro, David E. Goldgar, Aura Carreira, Maaike P.G. Vreeswijk, Fergus J. Couch
Journal: Cancer Research (2017)

Breast cancer risks conferred by many germline missense variants in the
Independent academic Data Monitoring Committees for clinical trials in cardiovascular and cardiometabolic diseases
Authors: Gerasimos S. Filippatos, Pieter de Graeff, Jeroen J. Bax, John‐Joseph Borg, John G.F. Cleland, Henry J. Dargie, Marcus Flather, Ian Ford, Tim Friede, Barry Greenberg, Cécile Henon‐Goburdhun, Richard Holcomb, Bradley Horst, John Lekakis, Guenther Mueller‐Velten, Athanasios G. Papavassiliou, Krishna Prasad, Giuseppe M.C. Rosano, Thomas Severin, Warren Sherman, Wendy Gattis Stough, Karl Swedberg, Luigi Tavazzi, Dimitris Tousoulis, Panagiotis Vardas, Frank Ruschitzka, Stefan D. Anker
Journal: European Journal of Heart Failure (2017)
An evaluation of the drug interaction potential of netupitant with palonosetron, dexamethasone, and oral contraceptives.
Authors: Jan Vouis, Anders Henriksson, Wolfgang Timmer, Selma Calcagnile, Giorgia Rossi
Journal: Journal of Clinical Oncology (2012)

e19532 Background: Netupitant (NETU) is a highly selective neurokinin 1 receptor antagonist (NK 1 RA) developed to provide protection from nausea and vomiting in patients undergoing emetogenic chemotherapy. Three individual studies were aimed at determining NETU effect on the metabolism of the new generation 5-HT 3 RA palonosetron (PALO), dexamethasone (DEX) and oral contraceptives which may be coadministered in clinical practice. Methods: Two 3-way crossover studies to determine the interaction between NETU (450 mg, day 1) and PALO (0.75 mg PO, day 1), and between NETU (100 mg, 300 mg or 450 mg PO, day 1) and DEX (20 mg PO, day 1; 8 mg BID PO, days 2-4), were performed in 18 and 25 healthy subjects, respectively. The study investigating the effect of NETU/PALO (300 mg/0.5 mg PO) as a fixed dose combination on the PK of oral contraceptives ethinylestradiol and levonorgestrel (60 μg/300 μg) was a 2-way crossover trial of 24 healthy women. Serial blood samples were collected over the course of the three studies and pharmacokinetic parameters were determined for all analytes. Results: There were no significant pharmacokinetic interactions between NETU and PALO. DEX mean AUC and C max increased respectively, by 1.7 and 1.1 fold on day 1 and by 2.4 and 1.7 fold on day 4 when coadministered with NETU. NETU was shown to increase exposure to DEX in a dose-dependent manner. The combination of NETU/PALO did not significantly affect exposure to ethinylestradiol; systemic exposure to levonorgestrel increased by 40%, a level that is not considered clinically relevant. Conclusions: A relevant drug interaction was seen between NETU and DEX and therefore dose reductions are recommended for DEX when administered with NETU. This drug interaction is likely due to inhibition of CYP3A4 by NETU. No interaction was clinically relevant between NETU and PALO, or between NETU/PALO and ethinylestradiol and levonorgestrel. Treatments were well-tolerated in all studies.
Hemostatic Factors Support Colitis and Colitis-Associated Colon Cancer
Authors: Kris A. Steinbrecher, Netanel Horowitz, Maureen A. Shaw, Kelley A. Barney, Matthew J. Flick, Eleana Harmel-Laws, David P. Witte, Elizabeth A. Blevins, Joseph S. Palumbo
Journal: Blood (2008)
Prognostic Significance of Minimal Residual Disease (MRD) in Childhood B-Precursor ALL and Its Relation to Other Risk Factors. A Children’s Oncology Group (COG) Study.
Authors: Michael J. Borowitz, Meenakshi Devidas, W. Paul Bowman, William L. Carroll, I.-Ming Chen, Richard Harvey, Stephen Hunger, Paul L. Martin, Jeanette Pullen, David Viswanatha, Cheryl L. Willman, Naomi Winick, Bruce Camitta
Journal: Blood (2006)
Long-Term Effects of Budesonide or Nedocromil in Children with Asthma
Authors: Stanley Szefler, Scott Weiss, James Tonascia, N Franklin Adkinson, Bruce Bender, Reuben Cherniack, Michele Donithan, H William Kelly, Joseph Reisman, Gail G Shapiro, Alice L Sternberg, Robert Strunk, Virginia Taggart, Mark Van Natta, Robert Wise, Margaret Wu, Robert Zeiger
Journal: New England Journal of Medicine (2000)

Antiinflammatory therapies, such as inhaled corticosteroids or nedocromil, are recommended for children with asthma, although there is limited information on their long-term use.We randomly assigned 1041 children from 5 through 12 years of age with mild-to-moderate asthma to receive 200 microg of budesonide (311 children), 8 mg of nedocromil (312 children), or placebo (418 children) twice daily. We treated the participants for four to six years. All children used albuterol for asthma symptoms.There was no significant difference between either treatment and placebo in the primary outcome, the degree of change in the forced expiratory volume in one second (FEV1, expressed as a percentage of the predicted value) after the administration of a bronchodilator. As compared with the children assigned to placebo, the children assigned to receive budesonide had a significantly smaller decline in the ratio of FEV1 to forced vital capacity (FVC, expressed as a percentage) before the administration of a bronchodilator (decline in FEV1:FVC, 0.2 percent vs. 1.8 percent). The children given budesonide also had lower airway responsiveness to methacholine, fewer hospitalizations (2.5 vs. 4.4 per 100 person-years), fewer urgent visits to a caregiver (12 vs. 22 per 100 person-years), greater reduction in the need for albuterol for symptoms, fewer courses of prednisone, and a smaller percentage of days on which additional asthma medications were needed. As compared with placebo, nedocromil significantly reduced urgent care visits (16 vs. 22 per 100 person-years) and courses of prednisone. The mean increase in height in the budesonide group was 1.1 cm less than in the placebo group (22.7 vs. 23.8 cm, P=0.005); this difference was evident mostly within the first year. The height increase was similar in the nedocromil and placebo groups.In children with mild-to-moderate asthma, neither budesonide nor nedocromil is better than placebo in terms of lung function, but inhaled budesonide improves airway responsiveness and provides better control of asthma than placebo or nedocromil. The side effects of budesonide are limited to a small, transient reduction in growth velocity.
The Telomerase Inhibitor, Imetelstat, Rapidly Reduces Myeloma Cancer Stem Cells (CSCs) in a Phase II Trial
Authors: Carol Ann Huff, Quiju Wang, Ashraf Z. Badros, Richard J. Jones, Anita Reddy, Kevin Nishimoto, Monic J. Stuart, Stephen M Kelsey, William Matsui
Journal: Blood (2012)
Abstract A28: Challenging new epigenetic vulnerabilities in human metastatic melanoma PDXs
Authors: Daniela Bossi, Angelo Cicalese, Ivan Gaetano Dellino, Lucilla Luzi, Simona Punzi, Carolina D'Alesio, Elena Cavallaro, Saverio Minucci, PierGiuseppe Pelicci, Luisa Lanfrancone
Journal: Clinical Cancer Research (2016)

Abstract Metastatic melanoma is one of the most aggressive cancers, refractory to most of the current therapies in its late stage. Melanoma is characterized by a strong molecular heterogeneity, and patients can be stratified in different subtypes according to genetic alterations. Despite the approval of new targeted drugs, patient treatment produces only partial responses and frequent and rapid relapses, mostly due to increased resistance. Mounting evidence highlights the necessity to better stratify melanomas on the basis of altered molecular pathways and to define new specific and effective tailored therapies. Our main goal is the genetic and functional characterization of metastatic melanomas aimed to generate new predictive and prognostic biomarkers and to identify new potential “druggable” candidates involved in melanoma progression. We have generated a series of human-in-mouse melanoma models, by xeno-transplantation of a cohort of human melanoma samples in immune-compromised mice. Our patient-derived xenografts (PDXs) faithfully recapitulate the heterogeneity of the original tumors at phenotypic and genetic level. Taking advantage of our model, we performed the first in vivo genetic screen on patient-derived tumors, using metastatic NRAS- and BRAF-mutant melanomas and targeting chromatin genes (~240). Our screens revealed unprecedented numerosity of tumor drivers (~50% of tested genes) and unexpected functional heterogeneity among patients (~60 drivers per tumor; &amp;lt;15% in common). Tumor drivers, however, were not activated by somatic mutations in the same patients. Several genes have been validated in vivo and then characterized in vitro on primary cultures derived from the patients' cells. We analysed underlying molecular mechanisms of one of the identified drivers, the Histone-lysine N-methyltransferase KMT2D, and showed that it promotes tumorigenesis by dysregulating a subset of transcriptional enhancers and genes involved in cell migration. Citation Format: Daniela Bossi, Angelo Cicalese, Ivan Gaetano Dellino, Lucilla Luzi, Simona Punzi, Carolina D'Alesio, Elena Cavallaro, Saverio Minucci, PierGiuseppe Pelicci, Luisa Lanfrancone. Challenging new epigenetic vulnerabilities in human metastatic melanoma PDXs. [abstract]. In: Proceedings of the AACR Special Conference: Patient-Derived Cancer Models: Present and Future Applications from Basic Science to the Clinic; Feb 11-14, 2016; New Orleans, LA. Philadelphia (PA): AACR; Clin Cancer Res 2016;22(16_Suppl):Abstract nr A28.
NF-Kb Localization in Multiple Myeloma Plasmacells and Mesenchimal Cells
Authors: Concetta Conticello, Raffaella Giuffrida, Luana Adamo, Gabriele Anastasi, Gioacchin Iannolo, Edvige Salomone, Lorenzo Memeo, Gabriella Amato, Ausilia Gorgone, Alessandra Romano, Ruggero de Maria, Massimo Gulisano, Rosario Giustolisi, Francesco Di Raimondo
Journal: Blood (2008)
Single-cell RNA-seq and computational analysis using temporal mixture modeling resolves T <sub>H</sub> 1/T <sub>FH</sub> fate bifurcation in malaria
Authors: Tapio Lönnberg, Valentine Svensson, Kylie R. James, Daniel Fernandez-Ruiz, Ismail Sebina, Ruddy Montandon, Megan S. F. Soon, Lily G. Fogg, Arya Sheela Nair, Urijah N. Liligeto, Michael J. T. Stubbington, Lam-Ha Ly, Frederik Otzen Bagger, Max Zwiessele, Neil D. Lawrence, Fernando Souza-Fonseca-Guimaraes, Patrick T. Bunn, Christian R. Engwerda, William R. Heath, Oliver Billker, Oliver Stegle, Ashraful Haque, Sarah A. Teichmann
Journal: Science Immunology (2017)

Computational modeling defines T helper cell differentiation toward multiple fates during experimental malaria.
Disease Stage Strongly Modulates Responsiveness to Targeted Agents in Nf1 Mutant Mice with Myeloprolfierative Disease (MPD) and Acute Myeloid Leukemia (AML).
Authors: Jennifer O. Lauchle, Doan Le, Doris Kim, Mary Tran, Abigail Peterson, Sally Przybranowski, Luis Parada, Linda Wolff, Judith Leopold, Kevin M. Shannon
Journal: Blood (2005)
High Anti-Lymphoma Activity of Bendamustine/Mitoxantrone/Rituximab (BMR) in Rituximab Pretreated Relapsed or Refractory Indolent Lymphomas. A Multicentre Phase II Study of the German Low Grade Lymphoma Study Group (GLSG).
Authors: Rudolf Weide, Georg Hess, Hubert Koeppler, Jochen Heymanns, Joerg Thomalla, Ali Aldaoud, Christoph Losem, Stefan Schmitz, Ursula Haak, Christoph Huber, Michael Unterhalt, Wolfgang Hiddemann, Martin Dreyling
Journal: Blood (2006)
Endothelin Promotes Colorectal Tumorigenesis by Activating YAP/TAZ
Authors: Zhen Wang, Peng Liu, Xin Zhou, Tianxiang Wang, Xu Feng, Yi-Ping Sun, Yue Xiong, Hai-Xin Yuan, Kun-Liang Guan
Journal: Cancer Research (2017)

Abstract Endothelin receptor A (ETAR) promotes tumorigenesis by stimulating cell proliferation, migration, and survival. However, the mechanism of ETAR in promoting tumor growth is largely unknown. In this study, we demonstrate that ETAR stimulates colon cell proliferation, migration, and tumorigenesis through the activation of YAP/TAZ, two transcription coactivators of the Hippo tumor suppressor pathway. Endothelin-1 treatment induced YAP/TAZ dephosphorylation, nuclear accumulation, and transcriptional activation in multiple colon cancer cells. ETAR stimulation acted via downstream G-protein Gαq/11 and Rho GTPase to suppress the Hippo pathway, thus leading to YAP/TAZ activation, which was required for ETAR-induced tumorigenesis. Overall, these results indicate a critical role of the YAP/TAZ axis in ETAR signaling. Cancer Res; 77(9); 2413–23. ©2017 AACR.
Alpha-1-antitrypsin deficiency associated panniculitis caused by PiMZ genotype in a thirteen-year-old boy
Authors: Elizabeta Ozimec, Nives Pustišek, Jasna Čepin Bogović, Alma Rožman, Agneza Marija Kapović, Alenka Gagro
Journal: JAMA Dermatology (2014)

Importance: Panniculitis is an uncommon initial manifestation of alpha-1-antytripsin deficiency (AAD), with fewer than 100 cases reported in the English literature. It is commonly associated with ZZ phenotype. In the English literature available, there are only few reported cases of AAD panniculitis with MZ phenotype in adults and none in children with this phenotype. We present a case of a 13-year-old boy with panniculitis as the first manifestation of AAD secondary to PiMZ phenotype. Observation: A 13-year-old boy presented with recurrent panniculitis on his chest and proximal parts of extremities for 2 years following a trauma. A biopsy of the lesion showed septal panniculitis with no evidence of vasculitis. Enzyme genotyping demonstrated a MZ pattern, so the diagnosis of AAD was established. Conclusions and relevance: The AAD is in rare cases associated with the development of panniculitis, especially in children. This case is unique because of the age of appearance, the genotype and the fact that panniculitis was the first manifestation of this disorder. Our case highlights AAD as an important differential diagnosis in children with recurrent panniculitis.
PP22. PROGRESSING RADIOTHERAPY-DRUG COMBINATIONS TOWARDS EARLY PHASE CLINICAL TRIALS
Authors: Dr Hazel Jones, Dr Julie Stock, Prof Anthony Chalmers
Journal: Neuro-Oncology (2017)

The Radiotherapy-Drug Combinations consortium (RaDCom) works with UK-based investigators to design and deliver high quality preclinical projects evaluating specific radiotherapy-drug combinations. We have several collaborations with industry, from in vitro projects to understand the novel agent in the context of radiobiology, through to preclinical studies that will generate data to support the development of radiotherapy combination trials. RaDCom facilitates the coordination of industry interactions, triage new proposals, monitor active projects, and engages with the radiotherapy community to promote collaboration and networking (via a capability map). The CRUK New Agents Committee Preclinical Combination Grant scheme provides one of the funding options for these studies, with the potential to feed into early phase clinical trials via the ECMC Combinations Alliance. RaDCom also supports broader radiotherapy research initiatives, by working to improve preclinical quality assurance and identifying a route to registration for radiotherapy-drug treatments. These activities will place the UK at the forefront of radiotherapy-drug preclinical research and provide a significant incentive for pharmaceutical companies to invest in this area and utilise the RaDCom network. Further information can be found on our webpage: http://ctrad.ncri.org.uk/research-support/radiation-drug-combinations-radcom Successful projects from RaDCom can then move into early phase combinations trials within the Combinations Alliance. The Combinations Alliance supports early phase combination studies in the UK via the ECMC (Experimental Cancer Medicine Centres) network. It focuses on translational research, and enables clinical project teams to work with disease experts to set up investigator led trials. The CRUK Centre of Drug Development (CDD) supports these studies with further management and coordination ensuring more robust timelines and delivery. The Combinations Alliance framework and funding structure allows more combination studies to be established in UK broadening academic access to innovative drugs. It also increases the commercial value for each drug and decreases the risks for later development. Further information can be found on our webpage: http://www.ecmcnetwork.org.uk/ca