tbuckley/cabot-search huggingface dataset:
Early Switching From Imatinib to Nilotinib In CML Patients Failing to Achieve Early Molecular Targets May Not Be An Effective Approach In Patients with Very Low OCT-1 Activity: A TIDEL II Sub-Study
Authors: Deborah L. White, Verity Saunders, Amity Frede, Kelvin GrootObbink, Cassandra Slader, David T. Yeung, Michael Osborn, Anthony K. Mills, Andrew Grigg, Timothy Hughes
Journal: Blood (2010)
Hypermethylation of <i>BMPR2</i> Promoter Occurs in Patients with Heritable Pulmonary Arterial Hypertension and Inhibits <i>BMPR2</i> Expression
Authors: Dong Liu, Yi Yan, Ji-Wang Chen, Ping Yuan, Xiao-Jian Wang, Rong Jiang, Lan Wang, Qin-Hua Zhao, Wen-Hui Wu, Gerald Simonneau, Jie-Ming Qu, Zhi-Cheng Jing
Journal: American Journal of Respiratory and Critical Care Medicine (2017)
Clinical Relevance of HLA Supertype Matching after Myeloablative Conditioning 7/8 Unrelated Donor Hematopoietic Cell Transplantation: A CIBMTR Study
Authors: Aleksandr Lazaryan, Tao Wang, Stephen R. Spellman, Hai-Lin Wang, Carlheinz R. Müller, Marcelo A. Fernandez-Viña, Michael R. Verneris, Mukta Arora, Daniel J. Weisdorf, Mary M. Horowitz, Stephanie J. Lee
Journal: Blood (2014)
Feasibility, Reproducibility and Reliability for the T2* Iron Evaluation At 3T in Comparison with 1.5T
Authors: Antonella Meloni, Vincenzo Positano, Petra Keilberg, Daniele De Marchi, Pasquale Pepe, Angelo Zuccarelli, Saveria Campisi, Maria Antonietta Romeo, Tommaso Casini, Pier Paolo Bitti, Calogera Gerardi, Maria Eliana Lai, Basilia Piraino, Gaetano Giuffrida, Giuseppina Secchi, Lucia De Franceschi, Massimo Midiri, Massimo Lombardi, Alessia Pepe
Journal: Blood (2011)
Early Progression of Disease (&lt; 2 Years) Is a Negative Predictor of Survival in Patients (Pts) with Chronic Lymphocytic Leukemia (CLL): An Analysis from the Connect® CLL Registry
Authors: Inhye E Ahn, Charles Michael Farber, Matthew Davids, David L. Grinblatt, Nicole Lamanna, Anthony R. Mato, Chadi Nabhan, Pavel Kiselev, Arlene S. Swern, E. Dawn Flick, Shriya Bhushan, Kristen Sullivan, Jeff Sharman, Christopher R. Flowers
Journal: Blood (2016)
BMI1, a new target of CK2α
Authors: Soumyajit Banerjee Mustafi, Prabir Kumar Chakraborty, Shailendra Kumar Dhar Dwivedi, Kai Ding, Katherine M. Moxley, Priyabrata Mukherjee, Resham Bhattacharya
Journal: Molecular Cancer (2017)

The polycomb group protein, BMI1 plays important roles in chromatin modification, stem cell function, DNA damage repair and mitochondrial bioenergetics. Such diverse cellular functions of BMI1 could be, in part, due to post-translational modifications, especially phosphorylation. To date, AKT has been reported as a kinase that by site specific phosphorylation of BMI1 modulates its oncogenic functions.Immunoprecipitation in conjunction with kinase assay and mass spectrometry was used to determine association with and site specific phosphorylation of BMI1 by CK2α. Functional implications of the BMI1/CK2α axis was examined in cancer cells utilizing siRNA and exogenous gene expression followed by biochemical and phenotypic studies. Correlations between expression of CK2α and BMI1 were determined from cell lines and formalin fixed paraffin embedded tissues representing the normal fallopian tube epithelium and high grade serous ovarian cancer samples.Here we report that CK2α, a nuclear serine threonine kinase, phosphorylates BMI1 at Serine 110 as determined by in-vitro/ex-vivo kinase assay and mass spectrometry. In ovarian cancer cell lines, expression of CK2α correlated with the phospho-species, as well as basal BMI1 levels. Preventing phosphorylation of BMI1 at Serine 110 significantly decreased half-life and stability of the protein. Additionally, re-expression of the phosphorylatable but not non-phosphorylatable BMI1 rescued clonal growth in endogenous BMI1 silenced cancer cells leading us to speculate that CK2α-mediated phosphorylation stabilizes BMI1 and promotes its oncogenic function. Clinically, compared to normal fallopian tube epithelial tissues, the expression of both BMI1 and CK2α were significantly higher in tumor tissues obtained from high-grade serous ovarian cancer patients. Among tumor samples, the expression of BMI1 and CK2α positively correlated (Spearman coefficient = 0.62, P = 0.0021) with each other.Taken together, our findings establish an important regulatory role of CK2α on BMI1 phosphorylation and stability and implicate the CK2α/BMI1 axis in ovarian cancer.
Abstract P5-06-09: Cyclin d1 binding to chromatin and the induction of chromosomal instability requires the fuzzy domain
Authors: RG Pestell, G Di Sante, A Di Rocco, C Pupo, M Crosariol, P Tompa, A Tantos, C Wang, Z Yu, R Vadlamudi, M Mann, MC Casimiro
Journal: Cancer Research (2017)

Abstract The cyclin D1 gene encodes the regulatory subunit of a holoenzyme that phosphorylates and inactivates the retinoblastoma (Rb) and the nuclear respiratory factor 1 (NRF1) proteins to regulate nuclear DNA synthesis and mitochondrial biogenesis. Cyclin D1 is required for oncogene-dependent growth and genetic ablation of the murine cyclin D1 gene resulted in resistance to Ras or ErbB2-induced mammary tumorigenesis and APC-induced gastrointestinal tumorigenesis. Cyclin D1 overexpression occurs in human breast, prostate, lung, and gastrointestinal malignancies and its abundance is induced at the level of transcription, translation and through post-translational modifications. Cyclin D1 plays a key role in transcriptional regulation inducing gene expression governing chromosomal instability (CIN) and cell-cycle progression. Cyclin D1 is also known to bind TF regulatory regions in chromatin immuno-precipitation (ChIP) assays. Genome wide analysis of cyclin D1 occupancy using ChIP-Seq identified binding sites including both the coding and non-coding genome with enrichment for genes regulating CIN and the G2/M phase (Top2A, AurkB, Cenpp, Mlf1ip, Zw10, Ckap2) consistent with enrichment of cyclin D1 at G2/M and the finding that cyclin D1 induces CIN. We sought to identify the molecular mechanisms governing the recruitment of cyclin D1 in the context of local chromatin to promote CIN. In order to define the domain of cyclin D1 involved in aneuploidy and tumorigenesis, we transduced and assessed the induction of aneuploidy in MEF cells using cyclin D1 wt (wt), cyclin D1 C-terminus domain (C4), cyclin D1 mutant lacking of the E-box motif (ΔE) or ctrl. We also searched for potential histone protein interaction motifs in cyclin D1 and determined the epigenetic motif recognized by cyclin D1 using a histone peptide array. The recognition of an epigenetic code by cyclin D1 may facilitate genome wide expression changes during cell-cycle progression and tumorigenesis. We finally identified a “fuzzy” domain of cyclin D1 which is required to local chromatin access for regulatory promoter regions governing and promoting CIN. Citation Format: Pestell RG, Di Sante G, Di Rocco A, Pupo C, Crosariol M, Tompa P, Tantos A, Wang C, Yu Z, Vadlamudi R, Mann M, Casimiro MC. Cyclin d1 binding to chromatin and the induction of chromosomal instability requires the fuzzy domain [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 P5-06-09.
Sigma 2-Agonist CB-64D Induces Apoptosis in Non Hodgkin’s Lymphoma Cells: Association with Decreased Akt Expression.
Authors: Chiara Dell’Agnola, Wojciech Wojciechowski, Shannon Marshall, Natalia E. Lopez, Huifen Li, Wayne D. Bowen, Igor J. Espinoza-Delgado
Journal: Blood (2004)
Abstract P4-12-11: Up-regulation of SPARC is associated with breast tumor progression and epithelial SPARC expression is correlated with poor survival and MMP-2 expression in patients with breast carcinoma
Authors: JS Lee, G-E Kim, MH Park, JH Yoon
Journal: Cancer Research (2017)

Abstract Background: Secreted protein acidic and rich in cysteine (SPARC) plays a crucial role in the process of tumor invasion and metastasis in many cancers. Matrix metalloproteinases (MMPs) degrade the extracellular matrix and participate in several key processes of invasion and metastasis. The aims of this study were to evaluate the potential involvement of SPARC in the progression of breast tumor and to determine its association with outcome variables and MMPs expression in patients with breast carcinoma (BC). Materials and Methods: SPARC expression was examined in 8 pairs of BC tissues and surrounding normal tissues at mRNA and protein levels by quantitative real-time PCR (qRT-PCR), RNAscope in situ hybridization (ISH), Western blotting, and immunohistochemistry techniques. Immunohistochemical staining of SPARC on tissue microarray was done in 26 normal breasts, 76 ductal carcinoma in situ (DCIS), and 198 BC samples. In addition, we performed immunohistochemical staining for MMP-2 and MMP-9 in BC. Results: SPARC expression at mRNA and protein levels by qRT-PCR and Western blotting was significantly increased in BC tissues compared to the surrounding normal tissues (p &amp;lt; 0.05 and p &amp;lt; 0.01, respectively). RNAscope ISH and immunohistochemistry of SPARC confirmed that SPARC expression was increased in BC tissues compared with their normal tissues and its expression was more pronounced in the stromal compartment than in epithelial compartment. SPARC expression was different among the normal, DCIS and BC groups and epithelial SPARC expression increased progressively from normal breast through DCIS to BC (p &amp;lt; 0.001). In patients with BC, high epithelial SPARC expression was associated with worse disease-free and overall survival (p = 0.002 and p = 0.048, respectively) and independently predicted worse disease-free survival (p = 0.002). Epithelial SPARC expression was significantly correlated with MMP-2 expression (p &amp;lt; 0.05). Conclusion: Our results suggest that up-regulation of SPARC contributes to breast tumor progression. SPARC expression may be a useful biomarker for the prognostic prediction in patients with BC. SPARC can control extracellular matrix degradation through up-regulation of MMP-2. Citation Format: Lee JS, Kim G-E, Park MH, Yoon JH. Up-regulation of SPARC is associated with breast tumor progression and epithelial SPARC expression is correlated with poor survival and MMP-2 expression in patients with breast carcinoma [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 P4-12-11.
Abstract P5-03-06: Clinical value of 89Zr-trastuzumab PET in HER2-positive breast cancer patients with a clinical dilemma
Authors: CP Schröder, F Bensch, AH Brouwers, MN Lub-de Hooge, JR de Jong, B van der Vegt, S Sleijfer, EG de Vries
Journal: Cancer Research (2017)

Abstract Background: Information on human epidermal growth factor receptor 2 (HER2) is essential for management of metastatic breast cancer (mBC). In patients suspected of HER2-positive mBC, standard work up may fail to clarify whole body HER2 status. We aimed to assess whether 89Zr-trastuzumab PET can support treatment decisions in patients posing this clinical dilemma. Methods: 89Zr-trastuzumab PET was performed as described earlier (Gaykema et al, Clin Cancer Res 2014) in patients in whom standard work up with bone scan, FDG PET, CT and if feasible a biopsy, failed to evaluate HER2 status of their disease. 89Zr-trastuzumab PET was defined positive, when at least a dominant part of the tumor load showed substantial tracer uptake (Gebhart et al, Ann Oncol 2015), when tumor tracer uptake in single lesions (except brain) was ≥ normal liver uptake or when brain metastases had a tracer uptake &amp;gt; background. Circulating tumor cell (CTC) analysis prior to tracer injectionwas performed using the CellSearch System (Janssen Diagnostics LLC) and CTC HER2 status was assessed immunofluorescently. Questionnaires about treatment decisions were completed before, directly after and ≥3 months after 89Zr-trastuzumab PET. Results: Twenty patients were enrolled: 8 with two primary cancers (HER2-positive and HER2-negative BC or BC and non-BC), 7 with metastases inaccessible for biopsy, 4 with prior HER2-positive and HER2-negative metastases, 1 with primary BC with equivocal HER2 status (average 4.23 HER2 gene copies/nucleus). 89Zr-trastuzumab PET was positive in 12 patients, negative in 7 and equivocal in one patient. In 15/20 patients 89Zr-trastuzumab PET supported treatment decision. The scan altered treatment of 8 patients, increased physicians' confidence without affecting treatment in 10, and improved physicians' understanding of disease in 18 patients. Ten patients had 1-99 CTCs, 6 with HER2 expression. There was no correlation between HER2 expression by CTCs and 89Zr-trastuzumab PET results or subsequent treatment decision. Conclusion: 89Zr-trastuzumab PET, but not CTC analysis, supports clinical decision making in BC patients in whom standard work up fails to evaluate HER2 status. (Funded by the Dutch A Sister's Hope). Citation Format: Schröder CP, Bensch F, Brouwers AH, Lub-de Hooge MN, de Jong JR, van der Vegt B, Sleijfer S, de Vries EG. Clinical value of 89Zr-trastuzumab PET in HER2-positive breast cancer patients with a clinical dilemma [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 P5-03-06.
Gender differences in comprehensive geriatric assessment (CGA): Results from the IN-GHO registry.
Authors: Friedemann Honecker, Carsten Bokemeyer, Gerd Kallischnigg, Susanne Huschens, Ulrich Wedding
Journal: Journal of Clinical Oncology (2013)

9553 Background: Elderly cancer patients (pts) are a heterogeneous population. As chronological age does not provide sufficient information on individual limitations and resources, a CGA helps to describe the heterogeneity in a structured way. Assessment instruments might be sensitive to gender differences. We therefore analyzed the IN-GHO registry for gender associated differences in results of CGA. Methods: The internet based IN-GHO registry prospectively collects data of elderly cancer pts from &gt; 100 centres in Germany and Austria. Data from 1,580 pts aged 70+ years were analyzed comparing results between female (n=883) and male (n=697) pts by Chi-square or Mann-Whitney U test. Analyses included results from CGA, physicians´ rating (fit vs. compromised vs. frail) and pts´ self rating of fitness for treatment (Likert scale 1 = very fit to 6 = very unfit), type (combination vs. monotherapy vs. no), and dosage (full vs. adapted) of treatment. Results: Mean age was 76.7 years (range 70-97), 71.5% had a solid tumor, and 28.5% a hematological malignancy. Mean age was slightly but significantly higher in women than in men (76.9 vs. 76.4; p=0.02), reflected in a higher number of pts. aged 80+ (26.5% vs. 21.1%; p=0.013). No gender differences were observed in physicians´ rating and pts´ self rating of fitness for therapy, or in type or dosage of treatment. Furthermore, no gender associated differences were noted in Karnofsky-Performance-Scale, comorbidity (Charlson-Comorbidity-Score), polypharmacy, and cognition (Mini-Mental-Status-Examination). Gender associated differences, however, were noted in body mass index (more women in categories &lt;19 and &gt;35), mean ADL (91.7 vs. 93.4, p=0.03), mean IADL (6.9 vs. 6.7 (p=0.049), and timed-up-and-go test (&lt; 10 seconds 36.1% vs. 43.6%, p=0.005). The main differences between women and men in ADL and IADL scores were noted in the item bathing (ADL) and food preparation, housekeeping, and laundry (IADL). Conclusions: The internet based registry is a valuable tool to gain data on prognostic factors, treatment, and outcome in old cancer pts. In several items of CGA, significant differences exist between women and men.
Results of a Phase III Trial Including Arsenic Trioxide Consolidation for Pediatric Patients with Acute Promyelocytic Leukemia (APL): A Report from the Children's Oncology Group Study AAML0631
Authors: Matthew A. Kutny, Todd A. Alonzo, Robert B. Gerbing, Yi-Cheng Wang, Cecilia Fu, Soheil Meshinchi, Alan S. Gamis, James H. Feusner, John Gregory
Journal: Blood (2015)
Beyond the <i>BRAF</i> <sup> <i>V</i> </sup> <sup> <i>600E</i> </sup> hotspot: biology and clinical implications of rare <i>BRAF</i> gene mutations in melanoma patients
Authors: G. Richtig, C. Hoeller, K. Kashofer, A. Aigelsreiter, A. Heinemann, L.N. Kwong, M. Pichler, E. Richtig
Journal: British Journal of Dermatology (2017)

BRAF gene mutations can be found in approximately 50% of melanomas, but the most common BRAF mutation leads to substitution at residue 600 of the protein, from valine to glutamic acid. BRAFV600E occurs in up to 95% of all melanoma cases and can be successfully blocked by using a combination of BRAF‐ and MEK inhibitors. The wider availability of next‐generation sequencing is revealing more non‐V600 BRAF mutations, and the clinical implications of these mutations are widely unknown. In this review, we will discuss the biology of the MAPK pathway and the different types of BRAF mutations as well as their effect on MEK activation. Current literature will be reviewed including in vitro data, case reports and case series.
Value of Cardiovascular Magnetic Resonance Imaging in Noninvasive Risk Stratification in Tetralogy of Fallot
Authors: Jouke P. Bokma, Koen C. de Wilde, Hubert W. Vliegen, Arie P. van Dijk, Joost P. van Melle, Folkert J. Meijboom, Aeilko H. Zwinderman, Maarten Groenink, Barbara J. M. Mulder, Berto J. Bouma
Journal: JAMA Cardiology (2017)

Adults late after total correction of tetralogy of Fallot (TOF) are at risk for major complications. Cardiovascular magnetic resonance (CMR) imaging is recommended to quantify right ventricular (RV) and left ventricular (LV) function. However, a commonly used risk model by Khairy et al requires invasive investigations and lacks CMR imaging to identify high-risk patients.To implement CMR imaging in noninvasive risk stratification to predict major adverse clinical outcomes.This multicenter study included 575 adult patients with TOF (4.083 patient-years at risk) from a prospective nationwide registry in whom CMR was performed. This study involved 5 tertiary referral centers with a specialized adult congenital heart disease unit. Multivariable Cox hazards regression analysis was performed to determine factors associated with the primary end point. The CMR variables were combined with the noninvasive components of the Khairy et al risk model, and the C statistic of the final noninvasive risk model was determined using bootstrap sampling. The data analysis was conducted from January to December 2016.The composite primary outcome was defined as all-cause mortality or ventricular arrhythmia, defined as aborted cardiac arrest or documented ventricular fibrillation and ventricular tachycardia (lasting ≥30 seconds or recurrent symptomatic).Of the 575 patients with TOF, 57% were male, and the mean (SD) age was 31 (11) years. During a mean (SD) follow-up of 7.1 (3.5) years, the primary composite end point occurred in 35 patients, including all-cause mortality in 13 patients. Mean (SD) RV ejection fraction (EF) was 44% (10%), and mean (SD) LV EF was 53% (8%). There was a correlation between RV EF and LV EF (R, 0.36; 95% CI, 0.29-0.44; P < .001). Optimal thresholds for ventricular function (RV EF <30%: hazard ratio, 3.90; 95% CI, 1.84-8.26; P < .001 and LV EF <45%: hazard ratio, 3.23; 95% CI, 1.57-6.65; P = .001) were independently predictive in multivariable analysis. Both thresholds were included in a point-based noninvasive risk model (C statistic, 0.75; 95% CI, 0.63-0.85) and combined with the noninvasive components of the Khairy et al risk model.In patients with repaired TOF, biventricular dysfunction on CMR imaging was associated with major adverse clinical outcomes. The quantified thresholds (RV EF <30% and LV EF <45%) may be implemented in noninvasive risk stratification.
A Phase I Study of GSK2816126, an Enhancer of Zeste Homolog 2(EZH2) Inhibitor, in Patients (pts) with Relapsed/Refractory Diffuse Large B-Cell Lymphoma (DLBCL), Other Non-Hodgkin Lymphomas (NHL), Transformed Follicular Lymphoma (tFL), Solid Tumors and Multiple Myeloma (MM)
Authors: Timothy A. Yap, Jane N. Winter, John P. Leonard, Vincent Ribrag, Anastasia Constantinidou, Lisa Giulino-Roth, Jean-Marie Michot, Tariq A Khan, Thierry Horner, Jennifer Carver, Teodora Pene Dumetrescu, Zangdong He, Michael T. McCabe, Caretha L. Creasy, Arindam Dhar, Christopher Carpenter, Peter M Johnson
Journal: Blood (2016)
30-year trends in admission rates for encephalitis in children in England and effect of improved diagnostics and measles-mumps-rubella vaccination: a population-based observational study
Authors: Mildred A Iro, Manish Sadarangani, Raphael Goldacre, Alecia Nickless, Andrew J Pollard, Michael J Goldacre
Journal: The Lancet Infectious Diseases (2017)
The Role of Interim-PET and Final-PET in the Outcome of Peripheral T-Cell Lymphoma (PTCL) Treated At the Diagnosis with CHOP.
Authors: Cinzia Pellegrini, Beatrice Casadei, Enrico Derenzini, Alessandro Broccoli, Vittorio Stefoni, Letizia Gandolfi, Federica Quirini, Lisa Argnani, Pier Luigi Zinzani
Journal: Blood (2012)
Exome Sequencing of Oral Squamous Cell Carcinoma Reveals Molecular Subgroups and Novel Therapeutic Opportunities
Authors: Shih-Chi Su, Chiao-Wen Lin, Yu-Fan Liu, Wen-Lang Fan, Mu-Kuan Chen, Chun-Ping Yu, Wei-En Yang, Chun-Wen Su, Chun-Yi Chuang, Wen-Hsiung Li, Wen-Hung Chung, Shun-Fa Yang
Journal: Theranostics (2017)

Oral squamous cell carcinoma (OSCC), an epithelial malignancy affecting a variety of subsites in the oral cavity, is prevalent in Asia.The survival rate of OSCC patients has not improved over the past decades due to its heterogeneous etiology, genetic aberrations, and treatment outcomes.Improvement in therapeutic strategies and tailored treatment options is an unmet need.To unveil the mutational spectrum, whole-exome sequencing of 120 OSCC from male individuals in Taiwan was conducted.Analyzing the contributions of the five mutational signatures extracted from the dataset of somatic variations identified four groups of tumors that were significantly associated with demographic and clinical features.In addition, known (TP53, FAT1, EPHA2, CDKN2A, NOTCH1, CASP8, HRAS, RASA1, and PIK3CA) and novel (CHUK and ELAVL1) genes that were significantly and frequently mutated in OSCC were discovered.Further analyses of gene alteration status with clinical parameters revealed that the tumors of the tongue were enriched with copy-number alterations in several gene clusters containing CCND1 and MAP4K2.Through defining the catalog of targetable genomic alterations, 58% of the tumors were found to carry at least one aberrant event potentially targeted by US Food and Drug Administration (FDA)-approved agents.Strikingly, if targeting the p53-cell cycle pathway (TP53 and CCND1) by the drugs studied in phase I-III clinical trials, those possibly actionable tumors are predominantly located in the tongue, suggesting a better prediction of sensitivity to current targeted therapies.Our work revealed molecular OSCC subgroups that reflect etiological and prognostic correlation as well as defined the landscape of major altered events in the coding regions of OSCC genomes.These findings provide clues for the design of clinical trials for targeted therapies and stratification of OSCC patients with differential therapeutic efficacy.
Everolimus Plus RCHOP-21 Is Safe and Highly Effective for New Untreated Diffuse Large B-Cell Lymphoma (DLBCL): Results of the Phase I Trial NCCTG1085 (Alliance)
Authors: Patrick B. Johnston, Betsy R. Laplant, Ellen D. McPhail, Thomas M. Habermann, David J. Inwards, Ivana N. Micallef, Joseph P. Colgan, Grzegorz S. Nowakowski, Stephen Ansell, Thomas E. Witzig
Journal: Blood (2015)
Efficacy and Long Term Survival of Genetically Modified T Cells Targeting CD19 in a Syngeneic Immune Competent Transgenic Murine Tumor Model Is Dependent on Prior Lymphodepleting Chemotherapy.
Authors: James Lee, Yan Nikhamin, Gavin Imperato, Adam Cohen, Michel Sadelain, Renier Brentjens
Journal: Blood (2007)