tbuckley/cabot-search huggingface dataset:
Brain metastases (BM) in breast (BC) and lung cancer (LC) patients
Authors: A. S. Braverman, K. Hengel, J. Choi, E. Nwokedi, G. Sidhu, J. Weedon, C. Axiotis, X. Song
Journal: Journal of Clinical Oncology (2009)

e12029 Background: Most BM arise from BC or LC. Few studies compare their attributes and distribution, though BC BM have been reported to more often involve the cerebellum. Methods: Brain scanning was for clinical evidence of BM. Contrast-enhanced computer-automated tomograms (CT) or magnetic resonance images (MRI) of brains of all BC and LC patients irradiated for BM between 1996 and 2008 were reviewed. BC epidermoid growth factor receptor2 (HER-2) expression was determined. Results: Data was from 63 BC and 59 LC patients; 58% of the BC and 55% of the LC patients had MRIs. MRIs showed more cerebellar BM (p = 0.047). Primary to BM diagnosis intervals were shorter for LC than for BC patients (p = 0.001), but LC BM were more edematous (0.019). BC patients had more cerebellar BM (p = 0.004) than LC patients, and more BM in the cerebellum only (p = 0.017). LC patient gender and small cell histology did not correlate with cerebellar BM. Both cerebrums and cerebellums of BC patients had more BM than those with LC (p = 0.020; 0.013). Cerebellar BMs were more frequent in brains with more cerebral BM (p = 0.0020). Amongst BC over-expressing HER-2 was a trend to more cerebellar BM (p = 0.072). Conclusions: LC BM, which elicit more edema, produce symptoms earlier than BC BM. There are larger numbers of BC BM, perhaps due to BC's longer disease course and responsiveness to therapy. BC causes more cerebellar mets than LC, often without cerebral BM. This may be due both to the larger number of BC BM, and a predilection for the cerebellum. Periodic brain MRI, more sensitive than CT to posterior fossa lesions, may be indicated in some BC patients, and early radiation may control multiple small BM. No significant financial relationships to disclose.
Implementation of clinical sequencing using a comprehensive gene panel (OncoPrimeTM)
Authors: Masashi Kanai, Tadayuki Kou, Tomohiro Sakuma, Hiroaki Mochizuki, Mayumi Kamada, Masashiko Nakatsui, Shigemi Matsumoto, Hidehiko Miyake, Yasushi Okuno, Manabu Muto
Journal: Annals of Oncology (2016)
Chemosensitivity of IDH1-Mutated Gliomas Due to an Impairment in PARP1-Mediated DNA Repair
Authors: Yanxin Lu, Jakub Kwintkiewicz, Yang Liu, Katherine Tech, Lauren N. Frady, Yu-Ting Su, Wendy Bautista, Seog In Moon, Jeffrey MacDonald, Matthew G. Ewend, Mark R. Gilbert, Chunzhang Yang, Jing Wu
Journal: Cancer Research (2017)

Abstract Mutations in isocitrate dehydrogenase (IDH) are the most prevalent genetic abnormalities in lower grade gliomas. The presence of these mutations in glioma is prognostic for better clinical outcomes with longer patient survival. In the present study, we found that defects in oxidative metabolism and 2-HG production confer chemosensitization in IDH1-mutated glioma cells. In addition, temozolomide (TMZ) treatment induced greater DNA damage and apoptotic changes in mutant glioma cells. The PARP1-associated DNA repair pathway was extensively compromised in mutant cells due to decreased NAD+ availability. Targeting the PARP DNA repair pathway extensively sensitized IDH1-mutated glioma cells to TMZ. Our findings demonstrate a novel molecular mechanism that defines chemosensitivity in IDH-mutated gliomas. Targeting PARP-associated DNA repair may represent a novel therapeutic strategy for gliomas. Cancer Res; 77(7); 1709–18. ©2017 AACR.
RTHP-37. RATES AND IMPACT OF COMPLIANCE WITH TUMOR TREATING FIELDS THERAPY IN A GLIOMA COHORT
Authors: Yazmin Odia, Jessica Schulte, Fabio Iwamoto
Journal: Neuro-Oncology (2016)

Tumor-treating fields (TTF) was approved in 2011 for recurrent glioblastomas then for adjuvant therapy in 2016 given the significant survival benefit shown in recent trials. Since 12/2012, 46 patients were treated with TTF for recurrent or newly diagnosed gliomas at Columbia University. We detail demographics, compliance rates and outcomes in this retrospective cohort. Of 42 treated patients with available compliance data, 16 (38%) were women and 2 (4.8%), 4 (9.5%) and 36 (85.7%) had WHO grade II, III and IV gliomas, respectively. Median age at diagnosis was 56 (23-84) years. TTF was used at recurrence in 33 (79%), with a median of 2 (0-4) prior recurrences, while 9 (21%) were treated at diagnosis. Prior therapies included bevacizumab (18, 43%), surgery [25 (60%) gross total], radiation and temozolomide. Median time to TTF initiation was 15 months, ranging 2.8 months to 17 years, from diagnosis. Median weighted compliance rate was 63% (6-89.4%). Patients were treated a median of 1.8 months, ranging 0.1 to 20.3 months. Concurrent systemic therapy was used in 34 (81%), including temozolomide (12, 29%), nitrosourea (2, 5%), bevacizumab (16, 38%), immunotherapy (23, 55%) or other (6, 14%). Objective response based on RANO was noted in 25 (60%) with combination TTF and systemic therapy. Only 2 (5%) experienced skin toxicity requiring interruptions. Progression free survival was 4.1 months, not significantly different among compliant (11, 26%) versus noncompliant users (median 4.4 vs. 4.1 months, p=0.3005), defined as the use of TTF for >75% of the time. The impact of compliance will be better assessed in multivariable analyses adjusted for potential confounders, especially for the glioblastoma subgroup. In randomized controlled trials, TTF therapy significantly increased survival for patients with glioblastomas. Highly variable and lower than advised compliance rates, however, may limit its benefit, despite the limited toxicities and safety of combination therapy.
Long-Term Follow-up of Patients With Multiple Myeloma Who Received Allogeneic Hematopoietic Stem Cell Transplantation
Authors: Michele L. Donato, David S Siegel, David H. Vesole, Phyllis McKiernan, Themba Nyirenda, Melissa Baker, Anthony Mato, Joshua R. Richter, Andrew L Pecora, Scott D Rowley
Journal: Blood (2013)
NIMG-60. DIFFUSION IMAGING INTERPRETATION FOR GRADE 2 AND 3 GLIOMAS DEPENDS UPON NEW VS RECURRENT STATUS AND ENHANCING VS NON-ENHANCING STATUS
Authors: Tracy Luks, Tracy McKnight, Evan Neill, Manisha Dayal, Llewellyn Jalbert, Aurelia Williams, Khadjia Lobo, Anders Persson, Arie Perry, Soonmee Cha, Joanna Phillips, Annette Molinaro, Susan Chang, Sarah Nelson, Mitchel S. Berger
Journal: Neuro-Oncology (2016)

The Apparent Diffusion Coefficient (ADC) and Fractional Anisotropy (FA) are diffusion imaging parameters that are associated with degree of abnormal tissue microstructure in grade 2 and 3 gliomas. In the current study, we investigated whether the relationship between diffusion imaging and tumor histopathology score, tumor grade, and molecular characteristics is dependent on non-enhancing (NE) vs contrast-enhancing (CE) and newly-diagnosed (ND) vs recurrent (REC) disease status. We examined the median nADC and nFA values for the T2-FLAIR hyperintensity region and at the location of tissue samples in 110 ND-NE, 24 ND-CE, 60 REC-NE, and 40 REC-CE grade 2 and 3 glioma patients. We determined whether the effects of grade, histological diagnosis, and IDH and 1p19q status varied according to enhancement and recurrence status. Patients underwent a pre-surgical 3T MRI (T1-weighted IRSPGR, T2-weighted 3D FSE and/or XETA T2 FLAIR, and 6 directional axial Diffusion Weighted Imaging with b=1000s/mm2). In ND-NE patients, higher nADC and lower nFA were significantly associated with worse tumor score, higher grade, astrocytoma-like diagnosis, intact 1p19, and IDH mutation. However, in REC-NE patients, lower nADC was significantly associated with worse tumor score, intact 1p19q, and IDH wild-type. In CE patients, lower nADC and higher nFA were significantly associated with worse tumor score, and higher grade, and did not differ by recurrence status, diagnostic group or molecular characteristics. In ND-NE patients, higher nADC and lower nFA in may be driven by increased disruption of normal tissue architecture, whereas in CE patients and REC-NE patients, increased tumor cell density may drive lower nADC. These results suggest that when considering nADC and nFA values in tissue sample targeting and in evaluations of tumor severity and treatment response in grade 2 and 3 gliomas, the interpretation of these values depends upon the patient’s enhancement and newly-diagnosed vs. recurrent status.
CSIG-07. SIMULTANEOUS EXPLORATION OF A SET OF PRECLINICAL GBM-MODELS PROVIDES PREDICTIVE DATA ON CLINICALLY RELEVANT DRUGS
Authors: Rainer Glass, Christel Herold-Mende, Angelo Vescovi, Joerg-Christian Tonn, Roland Kälin
Journal: Neuro-Oncology (2016)

Glioblastoma (GBM) is characterized by genetic loss of tumor suppressors like e.g. p53, cdkn2a, PTEN, NF1 and overexpression of proto-oncogenes like e.g. PDGFRB, EGFR or EGFRvIII. Significant efforts are being made in the discovery of potential therapeutics, but without tailor-made stratification schemes and predictive markers many drug candidates fail in clinical trials. While the phytovanilloid cannabidiol (CBD) is advanced to phase II clinical trials, little is known on how it induces GBM cell-death, the exact molecular pathways it triggers, and potential biomarkers that could be used to predict therapy outcome. We engineered more than 30 different transgenic mouse glioma lines to mimic the genetic diversity of the four human GBM subtypes. Then, we investigated CBD cytotoxicity comparing our repertoire of 24 patient-derived GBMs to the transgenic mouse tumors. In both settings we show that CBD induced cytotoxicity in GBM cells with distinct genetic signatures and categorize GBMs according to genetic profiles into prospective CBD-responsive and unresponsive subsets. Furthermore, we identify the mode of CBD induced GBM death and pinpoint differentially regulated targets. With our preclinical work we contribute valuable information to stratify patients for ongoing clinical trials using CBD as a therapeutic. Overall, we show a preclinical strategy to uncover biomarkers that can gain predictive power in clinical trials.
Association of iron overload (IO) with time to progression (TTP) in patients with multiple myeloma (MM) undergoing autologous hematopoietic stem cell transplant (HSCT).
Authors: M. Lee, L. M. Thomas, N. Newman, H. Khadim, T. Gentile
Journal: Journal of Clinical Oncology (2010)

e17003 Background: IO resulting principally from red blood cell (RBC) transfusions is not an uncommon complication in HSCT recipients. Organ dysfunction and increased risk of infection associated with IO in early post-transplant period is increasingly being reported. Long-term effects of IO including risk of relapse/progression are less well described. Methods: A retrospective chart review identified 26 patients diagnosed with MM and treated with high-dose melphalan (200 mg/m2) followed by autologous HSCT at our institution from 1999 to 2007. Patients with serum ferritin level (F) < and > 1,000 ng/dl, measured at steady state (3–24 mos post transplant), were compared regarding demographics, disease stage, disease type, end organ complications, β-2 microglobulin, presence of adverse chromosomal abnormalities, RBC transfusion history and TTP as measured by the international myeloma working group criteria. Results: Results are shown in the Table. Five patients had F>1000 ng/dL and 21 <1,000 ng/dL with median TTP 12.9 versus 30.1 months (p 0.01). All five patients with F>1,000 ng/dl had relapsed at time of analysis. There was no significant difference between the 2 groups when comparing disease stage, heavy/light chain type, chromosomal abnormalities, end organ involvement or pre-transplant therapy. Conclusions: Serum ferritin level > than 1,000 ng/dL was associated with a decreased TTP in patients with MM undergoing autologous HSCT. These results support the need for prospective studies evaluating IO in HSCT patients and consideration of treatment strategies. Iron overload n=5 No iron overload n=21 p* O.R. C.I. n % n % Alive 1 20.0 15 71.4 0.06 0.10 0.01-1.09 Relapse 5 100.0 14 66.7 0.18 Type IgA 0 0 5 23.8 IgG 3 60.0 12 57.1 Light chain 2 40.0 4 19.0 Stage 1A 0 0 2 9.5 2A 2 40.0 5 23.8 2B 0 0 2 9.5 3A 2 40.0 12 57.1 3B 1 20.0 0 0 Chromosomal abnormality 2 40.0 3 15.8 0.27 3.56 0.41-31.23 Thrombocytopenia 1 20.0 2 9.5 0.49 2.38 0.17-33.00 Bony disease Bone only 3 60.0 10 47.6 Other disease 2 40.0 5 23.8 No bone disease 0 0 6 28.6 PS 0 0 0 5 23.8 1 5 100.0 15 71.4 3 0 0 1 4.8 Treatment (pre-HSCT) VAD 5 100.0 8 38.1 TD 0 0 7 33.3 Other 0 0 6 28.6 Median time to progression in months/std error 12.7 3.5 30.1 4.9 0.01 No significant financial relationships to disclose.
TMIC-08. GLIOBLASTOMA-INDUCED ASTROCYTE REPROGRAMMING GENERATES A POSITIVE FEEDBACK LOOP TO GLIOBLASTOMA CELLS
Authors: Mette Hartmark Nilsen, Lina Wik Leiss
Journal: Neuro-Oncology (2016)

Gliomas are lethal primary brain tumors inherently resistant to therapy. Several reports suggest a role for a stromal involvement in the progression of these tumors. We have previously isolated tumor associated astrocytes (TAGs) from mouse models of primary glioblastoma. We show for the first time that TAGs have a different gene expression profile from primary glial cells from mice without tumors. TAGs upregulate angiogenic factors and reprogramming factors like SOX2 and POU3F2 as well as Nestin and PDGFRa, normally expressed in neuronal precursors and oligodendrocyte precursors, respectively. Moreover, when isolated by FACS and reimplanted with tumor cells in mice, TAGs promoted tumor growth compared to control tumors co-injected primary glia from mice without tumors. In vitro experiments confirmed that tumor-secreted factors induce these transcriptional changes in human astrocytes, as conditioned media from primary glioblastoma biopsies lead to an upregulation of POU3F2, SOX2 and Nestin in a human astrocyte (HA) cell line. In addition, conditioned media from HA promoted growth and induced migration of glioblastoma cell lines. These data suggest an interplay between human astrocytes and glioblastoma cells, that could potentially work as a new therapeutic target. Current work aims at further investigating the expression profile and secretome of glioma cells and HAs grown in conditioned media from the other cell type, as well as elucidating mechanisms behind their tumor promoting role in further in vitro and in vivo experiments.
NHS cuts have played part in rise in excess deaths, study claims
Authors: Adrian O’Dowd
Journal: BMJ (2017)

A controversial study has claimed that failures in the health and social care system in England and Wales have played a part in a rise in the number of excess deaths in 2015.

The government, however, has reacted strongly to the study’s conclusions, saying that they are highly speculative and biased.

The study,1 with an accompanying commentary,2 published on 17 February in the Journal of the Royal Society of Medicine , was an analysis carried out by the London School of Hygiene and Tropical Medicine, the University of Oxford, and Blackburn with Darwen Borough Council.

The researchers had sought to analyse why there were 30 515 excess deaths in 2015 in England …
NIMG-19. DIFFUSION KURTOSIS IMAGING OF THE SUBVENTRICULAR ZONE IN GLIOBLASTOMA
Authors: Arindam Rano Chatterjee, David Cachia, Bruce M Frankel, Pierre Giglio, Arabinda Das, Sunil J. Patel
Journal: Neuro-Oncology (2016)

There is increasing evidence that glial cells lining the lateral ventricles in the subventricular zone (SVZ) play a role in gliomagenesis, as gliomas often occur in close proximity to the ventricular system and the SVZ. Diffusion kurtosis imaging (DKI) is an MRI technique that provides a clinically feasible extension of diffusion tensor imaging (DTI) that recapitulates DTI metrics including axial diffusivity, radial diffusivity, and fractional anisotropy (FA) with greater accuracy. DKI also allows for calculation of the dimensionless metric quantifying non-Gaussian diffusion, termed diffusional kurtosis (K). MR imaging was acquired with clinical DKI sequences on twenty control subjects and ten glioblastoma (GB) patients. Using established tools developed in MatLab (Mathworks, Natick, Massachusetts), regions of interest (ROIs) including the cerebral hemispheres, genu of the corpus callosum, splenium of the corpus callosum, and SVZ were verified by a neuroradiologist. DTI and DKI metrics including FA and K were calculated using Mat Lab tools for each ROI. Kurtosis metrics in controls showed no statistically significant difference between hemispheres (p=0.464). GB patients demonstrated a statistically significant lower mean K on the affected-side SVZ that the unaffected size (p=0.0312). While the small size of the SVZ and relatively low resolution of DKI limits robust interpretation of the results, these findings suggest that early changes of gliomagenesis may be detected as early changes in K in the SVZ. Further prospective studies could help determine if SVZ K value changes precede clinical or current imaging detection of gliomagenesis to allow for earlier detection.
AHA/ACCF 2009 Performance Measures for Primary Prevention of Cardiovascular Disease in Adults
Authors: Rita F. Redberg, Emelia J. Benjamin, Vera Bittner, Lynne T. Braun, David C. Goff, Stephen Havas, Darwin R. Labarthe, Marian C. Limacher, Donald M. Lloyd-Jones, Samia Mora, Thomas A. Pearson, Martha J. Radford, Gerald W. Smetana, John A. Spertus, Erica W. Swegler
Journal: Circulation (2009)
FC-Gamma Receptor (FCGR) 2A and 3A Polymorphisms Do Not Influence the Outcome of Relapsed or Refractory CLL Patients Treated with Rituximab, Fludarabine, and Cyclophosphamide (R-FC) or Fludarabine, and Cyclophosphamide (FC) Alone.
Authors: David Dornan, Olivia Spleiss, Ru-Fang T Yeh, Guillemette Duchateau-Nguyen, Tadeusz Robak, Sergey I Moiseev, Anna Dmoszynska, Philippe Solal-Celigny, Krzysztof Warzocha, Javier Loscertales, John Catalano, Boris V Afanasiev, Loree Larratt, Viktor A Rossiev, Isabelle Bence-Bruckler, Christian H. Geisler, Marco Montillo, Michael K. Wenger, Martin Weisser
Journal: Blood (2009)
Early Mortality of Newly Diagnosed Adult Acute Promyelocytic Leukemia Treated with the AIDA Protocol.
Authors: George Gortzolidis, Athanasios Zomas, Theodore Marinakis, Evridiki Michalis, Athanasios Galanopoulos, Vasiliki Grigoraki, John Tsourveloudis, Anastasia Tsakiridou, Freda Passam, Nikolaos I. Anagnostopoulos
Journal: Blood (2005)
Clinical activity, safety and predictive biomarkers results from a phase Ia atezolizumab (atezo) trial in extensive-stage small cell lung cancer (ES-SCLC)
Authors: L.V. Sequist, A. Chiang, J. Gilbert, M. Gordon, P.R. Conkling, D. Thompson, J.P. Marcoux, S.J. Antonia, B. Liu, D.S. Shames, A. Lopez-Chavez, C. O'Hear, M. Fasso, S. Gettinger
Journal: Annals of Oncology (2016)
Pleural Effusion in Dasatinib-Treated Chronic Myeloid Leukemia Patients after Imatinib Failure
Authors: Dongho Kim, Il-Young Kweon, Sa-Hee Park, Ji-Sun Lim, Hey-Sun Chung, Ha-Na Kim, Harriet Goh, Soo-Hyun Kim, Jung Lee, Won- Seok Kim, Dong-Wook Kim
Journal: Blood (2008)
Ibrutinib Combined with Rituximab in Treatment-Naive Patients with Follicular Lymphoma: Arm 1 + Arm 2 Results from a Multicenter, Open-Label Phase 2 Study
Authors: Nathan Fowler, Loretta Nastoupil, Sven de Vos, Mark Knapp, Ian W. Flinn, Robert W Chen, Ranjana H Advani, Sumeet Bhatia, Peter Martin, Raul Mena, Samuel Suzuki, Darrin M. Beaupre, Jutta K. Neuenburg, M. Lia Palomba
Journal: Blood (2016)
MicroRNA-31 overexpression is able to predict pathological response and outcome in locally advanced rectal cancer
Authors: C. Carames, I. Cristobal, P. Minguez, V. Moreno, A. Leon, H. Callata-Carhuapoma, J.I. Martin, M. Domine, R. Hernandez, M. Pedregal, I. Martinez, I. Moreno, A. Correa, F. Rojo, J.M. García-Foncillas López
Journal: Annals of Oncology (2016)
Tumor heterogeneity affects the activity of epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) in EGFR mutant non-small cell lung cancer (NSCLC) patients (pts)
Authors: N. Normanno, A.M. Rachiglio, M. Lambiase, F. Fenizia, A. Iannaccone, N. Chicchinelli, A. Morabito, G. Rocco, D. Galetta, E.S. Montagna, L. Crinò, V. Ludovini, B. Vincenzi, E. Barletta, C. Pinto, F. Ferraù, G. Botti, M.C. Piccirillo, F. Perrone
Journal: Annals of Oncology (2016)
Prevalence of Light-Chain Monoclonal Gammopathy of Undetermined Significance (LC-MGUS) among Olmsted County, Minnesota Residents Aged 50 Years or Greater.
Authors: S. Vincent Rajkumar, Robert Kyle, Matthew Plevak, Raynell Clark, Dirk Larson, Terry Therneau, Arthur Bradwell, Angela Dispenzieri, L. Joseph Melton, Jerry Katzmann
Journal: Blood (2006)
Oncology Network ASL1 Abruzzo: first year activity bridging the gap between Hospital and Territorial Care
Authors: G. Bruera, A. Cortellini, L. Napoleoni, D. Di Giacomo, S. Candria, F. Pignatelli, A. Giusti, D. Tacconella, R. De Santis, S. La Civita, L. Giacco, F. Marinangeli, E. Ricevuto
Journal: Annals of Oncology (2016)
Phase 2, multicenter, randomized, open-label trial assessing efficacy and safety of talimogene laherparepvec (T-VEC) neoadjuvant treatment (tx) plus surgery vs surgery for resectable stage IIIB/C and IVM1a melanoma (MEL).
Authors: Robert Hans Ingemar Andtbacka, Michael Chastain, Ai Li, Mark Shilkrut, Merrick I. Ross
Journal: Journal of Clinical Oncology (2015)

TPS9094 Background: Risk of recurrence and death after resection of stage IIIB/C and IVM1a MEL is high. T-VEC is an HSV-1-derived oncolytic immunotherapy designed to selectively replicate in tumors, produce GM-CSF, and enhance systemic antitumor immune responses. In OPTiM, a randomized phase 3 trial of T-VEC vs GM-CSF in patients (pts) with unresected stage IIIB/C and IVM1a MEL, T-VEC improved the primary endpoint (EP) of durable response rate (continuous PR/CR for ≥ 6 mos) from 2% to 16%, P < 0.0001. Median overall survival (OS, secondary EP) was 23.3 mos with T-VEC vs 18.9 mos with GM-CSF; HR = 0.79, 95% CI: 0.62-1.00; P = 0.051. We hypothesize that neoadjuvant T-VEC will improve local control rates and decrease distant metastases (DM) in pts with resectable stage IIIB/C and IVM1a MEL. Methods: 150 pts with resectable stage IIIB/C and IVM1a cutaneous MEL with ≥ 1 injectable cutaneous, subcutaneous, or nodal lesion will be randomized 1:1 to immediate surgical resection vs 6 doses of neoadjuvant T-VEC for up to 12 wks, followed by surgical resection. T-VEC is administered as ≤ 4 mL x 106 pfu/mL, then after 3 wks ≤ 4 mL x 108 pfu/mL q2w until all injectable tumors have disappeared, intolerance to tx, or alternative tx initiated. Eligible pts are ≥ 18 y old, ECOG PS 0-1, with adequate hematologic, hepatic, and renal function; prior systemic, regional, radiation therapies for MEL were completed ≥ 3 mos before randomization; history or evidence of symptomatic autoimmune disease, immunodeficiency, active herpes, prior HSV-1 complications, systemic tx with antiherpetic drugs, and prior tumor vaccines are not allowed. Primary EP is recurrence-free survival (RFS); key secondary EPs are 2 y, 3 y, and 5 y RFS, OS, overall tumor response, R0 resection, pathological CR, local RFS, DM-free survival, and safety. Blood and tumor biomarkers for response to T-VEC will be explored. Primary analysis of RFS will be at the later of 2 y after the end of randomization (EOR) or 64 events. Additional analyses will occur 3 and 5 y after EOR. The trial is planned at ~50 sites in Australia, Brazil, Europe, and USA. Accrual began in February 2015. Clinical trial information: NCT02211131.
Pertuzumab and trastuzumab-emtansine in HER2 positive metastatic colorectal cancer: the HERACLES B TRIAL
Authors: A. Sartore-Bianchi, S. Marsoni, L. Trusolino, C. Martino, S. Lonardi, F. Leone, F. Cottino, V. Vurchio, E. Valtorta, C. Lauricella, V. Zagonel, P. Racca, F. Ciardiello, A. Ardizzoni, G. Tonini, M. Aglietta, S. Siena
Journal: Annals of Oncology (2016)
Comparative Analysis of Downstream Genetic Targets of the Variant Acute Promyelocytic Leukemia Fusion Proteins NPM-RARA and NuMA-RARA.
Authors: Mariam Thomas, Mahadeo A. Sukhai, Yali Xuan, Soheila A. Hamadanizadeh, Rashmi S. Goswami, Rikki R. Bharadwaj, Patricia P. Reis, Suzanne Kamel-Reid
Journal: Blood (2007)