tbuckley/cabot-search huggingface dataset:
Clinical characteristics and treatment outcomes of patients with metastatic, <i>MET-</i>amplified esophagogastric cancers.
Authors: Eunice Lee Kwak, Jochen K Lennerz, Jackie Szymonifka, Ryan Bruce Corcoran, Jeffrey W. Clark, Andrea Lyn Russo, Darrell R. Borger, Lawrence Scott Blaszkowsky, Lauren Elizabeth Dias, Jason Edward Faris, Janet E. Murphy, Panos Fidias, Inga Tolin Lennes, Christopher G. Azzoli, Justin F. Gainor, John Thomas Mullen, Gregory Y Lauwers, David P. Ryan, A. John Iafrate, Theodore S. Hong
Journal: Journal of Clinical Oncology (2015)

4043 Background: The Cancer Genome Atlas (TCGA) reported MET gene alterations in 6% of gastric cancers (Nature 2014; 513: 202–209). Though rare, MET amplification is a biomarker for dramatic responses to single-agent MET inhibitors in esophagogastric cancer (J Clin Oncol 33, 2015, suppl 3; abstr 1). Clinical characteristics and outcomes were evaluated in patients (pts) with MET-amplified esophagogastric cancers (EGC) to facilitate identification of pts and establishment of treatment paradigms. Methods: Pts with metastatic MET-amplified EGC were identified between 2007 and 2014. MET amplification was determined in paraffin-embedded tissue using fluorescence in-situ hybridization (FISH), with a gene to control ratio of > 2.2 defined as positive. Clinical characteristics, treatment factors, and survival were recorded. A cohort of pts diagnosed between 8/2002 and 10/2012 with metastatic non-MET-amplified EGCs was evaluated as a comparison group. Results: We identified 23 pts with MET-amplified EGCs, 15 of whom were identified between 2012-2014. Compared to 37 non-MET-amplified tumors, MET-amplified EGCs were more typically poorly differentiated and located in the distal esophagus or gastroesophageal junction rather than distal stomach. Patterns of metastases did not differ between MET-amplified and non-MET-amplified pts. In the 17 pts for whom HER2 status was obtained, 4/17 EGCs showed co-amplification of MET and HER2. One EGC had concurrent MET and EGFR amplification. Additionally, 1/17 genotyped tumors harbored a PIK3CA mutation. Progression-free survival (PFS) from the time of metastatic diagnosis was 5 months for pts with MET-amplified EGCs. Including 7/23 pts who had received MET-directed therapy, overall survival (OS) was 13.2 months (3.4-7.8 and 6.0-21.1, 95% CI estimate of PFS and OS, respectively). Updated OS and comparison to the non-MET-amplified cohort will be presented. Conclusions: This series represents the largest cohort of clinically annotated MET-amplified EGCs and highlights this subgroup as a distinct clinical entity characterized by rapid progression. Patients should be identified early and directed to appropriate MET-targeted clinical trials.
A phase II study of dose-dense neoadjuvant chemotherapy with weekly paclitaxel and carboplatin followed by chemoradiation in locally advanced cervical carcinoma.
Authors: Rajkumar Bikramjit Singh, Lalit Kumar, Subhash Chandra, B. K Mohanti, Sushmita Pathy, K. Sunesh Kumar, Neerja Bhatla, Sanjay Thulkar, Sreenivas Vishnubhatla
Journal: Journal of Clinical Oncology (2012)

5104 Background: We prospectively studied dose dense neoadjuvant chemotherapy (NACT) designed for an enhanced cell kill, better local control and eradication of micrometastases prior to standard concurrent chemoradiation (CRT) in locally advanced cervical cancer. Methods: Between June 2010 and December 2011, 21 patients (median age - 51 years, range 35 - 67) of cervical cancer with locally advanced disease received NACT using paclitaxel (60mg/m 2 ) and carboplatin (AUC-2) weekly for 6 doses. Patients (pts) then received concurrent CRT (external and brachytherapy) with weekly cisplatin (40mg/m 2 for 6 doses) at a mean interval of 15 days (range 7–20 days). The primary end-point was response rate i.e. complete response (CR) and partial response (PR) 12 weeks post CRT. Results: Baseline stages were: stage 2A - 19%, 3B - 71.4%, 4A - 9.5%. Squamous cell carcinoma and adenocarcinoma constituted 95.2% and 4.7% pts respectively. Following NACT, 66.6% pts responded (CR -9.5% %; PR – 57.1 %), 23.8% had stable disease (SD) and 4.7% had progressive disease (PD). A total of 18 pts completed NACT and CRT of which 17 were in CR and 1 in PR. One patient with stage 4A disease developed vesicovaginal fistula at end of NACT for which she underwent pelvic exenteration and was in pathological CR. After NACT, one patient developed choroid metastases and was taken off study protocol while another patient was lost to follow up. At a mean follow up 5.8 months (range 1 - 14), 90% pts were in CR, 5% in PR and 5% had PD. During NACT, Grade 3/4 neutropenia, thrombocytopenia and anemia were seen in 33.3%, 4.7% &amp; 9.5% of pts, respectively and grade 3/4 non-hematological toxicities in 9.5% pts. Following CRT, Grade 3/4 neutropenia, thrombocytopenia and anemia were seen in 25%, 5% and 10% of pts, respectively while 20% pts had grade 3/4 non-hematological toxicities. G-CSF was used in 30% pts during NACT and 25% pts during CRT, respectively. Conclusions: NACT with weekly paclitaxel and carboplatin followed by radical CRT is feasible and is associated with a high response rate in locally advanced cervical cancer. This approach needs to be studied in a phase III trial.
A Lysa Phase II Study of Oral JAK1/2 Inhibitor Ruxolitinib in Advanced Relapsed/Refractory (R/R) Hodgkin Lymphoma (HL)
Authors: Eric W Van Den Neste, Marc Andre, Thomas Gastinne, Aspasia Stamatoullas, Corinne Haioun, Amine Belhabri, Oumedaly Reman, Olivier Casasnovas, Herve Ghesquieres, Gregor Verhoef, Marie-José Claessen, Hélène A Poirel, Marie-Christine Copin, Romain Dubois, Peter Vandenberghe, Ioanna-Andrea Stoian, Anne Ségolène Cottereau, Laurent Knoops, Franck Morschhauser
Journal: Blood (2016)
Therapeutic Immune Monitoring of Chronic Myeloid Leukemia Patients Treated with Tyrosine Kinase Inhibitors: Focus on CD4+ CD25+ t Cells
Authors: Ziyuan Lu, Na Xu, Xuan Zhou, Guanlun Gao, Lin Li, Jixian Huang, Yuling Li, Qisi Lu, Bolin He, Chengyun Pan, Liu Xiaoli
Journal: Blood (2015)
Multicenter Phase I Dose-Escalation Study of Lenalidomide in Patients with Relapsed Adult T-Cell Leukemia-Lymphoma (ATL) or Peripheral T-Cell Lymphoma (PTCL).
Authors: Naokuni Uike, Michinora Ogura, Yoshitaka Imaizumi, Norio Asou, Atae Utsunomiya, Toshiki Uchida, Tomohiro Aoki, Kunihiro Tsukasaki, Jun Taguchi, Ilseung Choi, Dai Maruyama, Kisato Nosaka, Nianhang Chen, Tetsuhiro Shiota, Kensei Tobinai
Journal: Blood (2012)
Gene Expression of Gamma Secretase (GS) Complex-Related Proteins, the Enzyme That Sheds B-Cell Maturation Antigen (BCMA), Among Patients with Multiple Myeloma (MM) and Effects of the GS Inhibitor LSN424354 on Solubilized Bcma in MM and Chronic Lymphocytic Leukemia
Authors: Haiming Chen, Mingjie Li, Eric Sanchez, Cathy S Wang, Kyle A Udd, Camilia M Soof, Christian E Casas, Jessica Wang, Jasmin Cao, Kevin DeCorso, Tara Hekmati, George Tang, James R. Berenson
Journal: Blood (2016)
Laboratory and Clinical Investigations to Identify the Optimal Dosing Strategy for Quizartinib (AC220) Monotherapy in FLT3-Itd-Positive (+) Relapsed/Refractory (R/R) Acute Myeloid Leukemia (AML)
Authors: Mark J. Levis, Jorge E. Cortes, Guy M. Gammon, Denise Trone, Dongwoo Kang, Jianke Li
Journal: Blood (2016)
Recurrent Chromosomal Rearrangements and a Homozygous Deletion Spanning 1-Mb Region at 10p11.2 in Adult T-Cell Leukemia/Lymphoma.
Authors: Tomonori Hidaka, Kazuhiro Nishida, Daisuke Shimizu, Hidenori Sasaki, Kiyoshi Yamashita, Yoko Kubuki, Kenichi Nomura, Tomohiko Taki, Hirohito Tsubouchi, Kazuhiro Morishita, Masafumi Taniwaki
Journal: Blood (2004)
Abstract P4-07-06: MicroRNAs associated with acquired taxane resistance in a breast cancer cell line model
Authors: KJ Taylor, T Chong, A D'Costa, C Yao, C Gourley, DA Cameron, JMS Bartlett, M Spears
Journal: Cancer Research (2017)

Abstract Background: Acquired chemoresistance remains the major cause of therapeutic failure in the treatment of breast cancer. Improved knowledge of the transition from drug sensitive to resistant breast cancer will pave the way for novel preventative and therapeutic strategies. MicroRNAs (miRNA) are endogenous, small non-coding RNAs that regulate gene expression by targeting the 3'UTR region of messenger RNAs. There is a growing body of evidence to suggest miRNAs may be involved in the development of chemoresistance and may play a role in the regulation of drug resistance pathways. Methods: An in vitro model of paclitaxel resistance was developed through the generation of resistant MDA-MB-231 cell lines by serial culture in escalating doses of taxane until resistance was achieved. The chemoresistant model was used to compare differential miRNA expression with the sensitive, parental line using the Nanostring® platform, analysing 800 human miRNAs. Confirmation of differential expression was performed by QRT-PCR. Results: This analysis resulted in 30 significantly altered miRNA (1.5 fold, p value &amp;lt; 0.05) at 25nM paclitaxel and 48 significantly altered miRNA at 50nM paclitaxel. The top up-regulated miRNA cluster in MDA-MB-231 25PACR is hsa-miR-548l (fold change: 2.89, p value: 0.016) and top down-regulated was hsa-miR-449a (fold change: -4.1. p value: 0.001). In MDA-MB-231 50PACR the top up-regulated miRNA cluster is hsa-miR-193a-5p (fold change: 3.746, p value: 0.008) and the top down-regulated miRNA cluster is hsa-miR-135a (fold change: -4.085, p value: 0.001). To explore the molecular mechanisms of the differentially expressed miRNAs in paclitaxel resistance, targets were predicted by in silico analysis. Pathways and networks designated by miRNA targets included the cell cycle, PI3K/Akt pathways and focal adhesion. Conclusion: In this study we identified candidate resistance-associated miRNAs which were differentially expressed between in vitro derived paclitaxel resistant MDA-MB-231 and the sensitive parental line. Further validation to ascertain their role in the transition to a chemoresistant phenotype is currently ongoing. Citation Format: Taylor KJ, Chong T, D'Costa A, Yao C, Gourley C, Cameron DA, Bartlett JMS, Spears M. MicroRNAs associated with acquired taxane resistance in a breast cancer cell line model [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 P4-07-06.
Multicenter, Phase III, Randomized, Double-Blind, Placebo-Controlled Trial of Pravastatin Added to First-Line Standard Chemotherapy in Small-Cell Lung Cancer (LUNGSTAR)
Authors: Michael J. Seckl, Christian H. Ottensmeier, Michael Cullen, Peter Schmid, Yenting Ngai, Dakshinamoorthy Muthukumar, Joyce Thompson, Susan Harden, Gary Middleton, Kate M. Fife, Barbara Crosse, Paul Taylor, Stephen Nash, Allan Hackshaw
Journal: Journal of Clinical Oncology (2017)

Purpose Treating small-cell lung cancer (SCLC) remains a therapeutic challenge. Experimental studies show that statins exert additive effects with agents, such as cisplatin, to impair tumor growth, and observational studies suggest that statins combined with anticancer therapies delay relapse and prolong life in several cancer types. To our knowledge, we report the first large, randomized, placebo-controlled, double-blind trial of a statin with standard-of-care for patients with cancer, specifically SCLC. Patients and Methods Patients with confirmed SCLC (limited or extensive disease) and performance status 0 to 3 were randomly assigned to receive daily pravastatin 40 mg or placebo, combined with up to six cycles of etoposide plus cisplatin or carboplatin every 3 weeks, until disease progression or intolerable toxicity. Primary end point was overall survival (OS), and secondary end points were progression-free survival (PFS), response rate, and toxicity. Results Eight hundred forty-six patients from 91 United Kingdom hospitals were recruited. The median age of recruited patients was 64 years of age, 43% had limited disease, and 57% had extensive disease. There were 758 deaths and 787 PFS events. No benefit was found for pravastatin, either in all patients or in several subgroups. For pravastatin versus placebo, the 2-year OS rate was 13.2% (95% CI, 10.0 to 16.7) versus 14.1% (95% CI, 10.9 to 17.7), respectively, with a hazard ratio of 1.01 (95% CI, 0.88 to 1.16; P = .90. The median OS was 10.7 months v 10.6 months, respectively. The median PFS was 7.7 months v 7.3 months, respectively. The median OS (pravastatin v placebo) was 14.6 months in both groups for limited disease and 9.1 months versus 8.8 months, respectively, for extensive disease. Adverse events were similar between groups. Conclusion Pravastatin 40 mg combined with standard SCLC therapy, although safe, does not benefit patients. Our conclusions are the same as those found in all four much smaller, randomized, placebo-controlled trials specifically designed to evaluate statin therapy in patients with cancer.
Heterozygosity for Loss-of-Function Mutation in SERPINE1 (PAI-1 Gene) Linked with Longer Absolute Telomere Length
Authors: Sweta Gupta, Sadiya Khan, Sanjiv Shah, Ekaterina Klyachko, Abigail S Baldridge, Mesut Eren, Aaron T Place, Meadow Heiman, Abraham Aviv, Amy D. Shapiro, Douglas E Vaughan
Journal: Blood (2016)
Changes In Apoptotic Gene Expression Profile In CLL Patients Treated with Cladribine, Cyclophosphamide and Rituximab (CCR)
Authors: Ida Franiak-Pietryga, Aleksandra Salagacka, Henryk Maciejewski, Jerzy Z. Blonski, Aleksandra Kotkowska, Marek Mirowski, Tadeusz Robak, Anna Korycka-Wolowiec
Journal: Blood (2010)
Laminar flow downregulates Notch activity to promote lymphatic sprouting
Authors: Dongwon Choi, Eunkyung Park, Eunson Jung, Young Jin Seong, Jaehyuk Yoo, Esak Lee, Mingu Hong, Sunju Lee, Hiroaki Ishida, James Burford, Janos Peti-Peterdi, Ralf H. Adams, Sonal Srikanth, Yousang Gwack, Christopher S. Chen, Hans J. Vogel, Chester J. Koh, Alex K. Wong, Young-Kwon Hong
Journal: Journal of Clinical Investigation (2017)

The major function of the lymphatic system is to drain interstitial fluid from tissue. Functional drainage causes increased fluid flow that triggers lymphatic expansion, which is conceptually similar to hypoxia-triggered angiogenesis. Here, we have identified a mechanotransduction pathway that translates laminar flow-induced shear stress to activation of lymphatic sprouting. While low-rate laminar flow commonly induces the classic shear stress responses in blood endothelial cells and lymphatic endothelial cells (LECs), only LECs display reduced Notch activity and increased sprouting capacity. In response to flow, the plasma membrane calcium channel ORAI1 mediates calcium influx in LECs and activates calmodulin to facilitate a physical interaction between Krüppel-like factor 2 (KLF2), the major regulator of shear responses, and PROX1, the master regulator of lymphatic development. The PROX1/KLF2 complex upregulates the expression of DTX1 and DTX3L. DTX1 and DTX3L, functioning as a heterodimeric Notch E3 ligase, concertedly downregulate NOTCH1 activity and enhance lymphatic sprouting. Notably, overexpression of the calcium reporter GCaMP3 unexpectedly inhibited lymphatic sprouting, presumably by disturbing calcium signaling. Endothelial-specific knockouts of Orai1 and Klf2 also markedly impaired lymphatic sprouting. Moreover, Dtx3l loss of function led to defective lymphatic sprouting, while Dtx3l gain of function rescued impaired sprouting in Orai1 KO embryos. Together, the data reveal a molecular mechanism underlying laminar flow-induced lymphatic sprouting.
Inhibition of T315I Bcr-Abl and Other Imatinib-Resistant Bcr-Abl Mutants by the Selective Abl Kinase Inhibitor SGX70393.
Authors: Thomas O’Hare, Christopher A. Eide, Jeffrey W. Tyner, Matthew J. Wong, Caitlyn A. Smith, Amie S. Corbin, Sean Buchanan, Katayoun A. Jessen, Crystal Tang, Kevin Holme, Stephen K. Burley, Michael W.N. Deininger
Journal: Blood (2006)
MyD88-dependent interplay between myeloid and endothelial cells in the initiation and progression of obesity-associated inflammatory diseases
Authors: Minjia Yu, Hao Zhou, Junjie Zhao, Nengming Xiao, Sanjoy Roychowdhury, David Schmitt, Bingqing Hu, Richard M. Ransohoff, Clifford V. Harding, Amy G. Hise, Stanley L. Hazen, Anthony L. DeFranco, Paul L. Fox, Richard E. Morton, Paul E. Dicorleto, Maria Febbraio, Laura E. Nagy, Jonathan D. Smith, Jian-an Wang, Xiaoxia Li
Journal: The Journal of Experimental Medicine (2014)
An Expanding Role for Immunotherapy in Colorectal Cancer
Authors: Katherine M. Bever, Dung T. Le
Journal: Journal of the National Comprehensive Cancer Network (2017)

Colorectal cancer (CRC) is a leading cause of cancer-related mortality in the United States. Response rates to second- and third-line therapy for metastatic CRC (mCRC) remain low, and immunotherapy is an attractive strategy for treatment in these patients given generally better tolerability than conventional chemotherapy and the potential for long-lasting durable responses. In particular, the novel checkpoint inhibitors (CPIs) have demonstrated unprecedented clinical activity in a wide range of cancers. The observation of clinical activity in microsatellite instability-high (MSI-H) mCRC was the first indication of a potential for CRC to respond to these agents, and has led to a breakthrough designation by the FDA for CPI use in this subset. Despite this, a proportion of MSI-H and nearly all microsatellite stable disease will not respond to single-agent checkpoint inhibition, and clinical trials are ongoing to increase responses to immunotherapy in mCRC through both better patient selection and novel combinations of immunotherapeutic agents. This review will provide a focused update on the most compelling clinical results of immunotherapy in CRC to date, as well as a summary of current strategies being tested in clinical trials in increase responses to immunotherapy in CRC.
Liver transplantation in the morbidly obese: Do the outcomes justify the use of scarce organs?
Authors: George Therapondos, David S. Bruce, Humberto E. Bohorquez, Natalie H. Bzowej, Ian C. Carmody, Ari J. Cohen, Nigel Girgrah, Shobha Joshi, Trevor W. Reichman, George E. Loss
Journal: Hepatology (2013)
Monitoring in vivo T cell traficking to tumors by positron emission tomography and magnetic resonance imaging
Authors: M. Hokland, M. S. Petersen, C. C. Fleischer, S. B. Hansen, H. Stüdkilde-Jürgensen, U. Skands, J. Marqversen, T. Blankenstein, H. J. Gundersen, R. Agger
Journal: Journal of Clinical Oncology (2004)

2571 Background: Tracking adoptively transfered cells is an essential prerequisite for devising better protocols for cellular therapy. Thus, a highly sensitive method for non-invasive visualization of labeled lymphocytes in vivo by combined PET and magnetic resonance imaging (MRI) has been developed and applied for tracking adoptively transfered tumor-specific T cells in a mouse model system. Methods: C57BL/6J mice carrying subcutaneous tumors of the ovalbumin (OVA)-expressing malignant melanoma cell line B16-OVA were adoptively transfered with OVA-specific CD8+ T cells labeled with 124-iodine-conjugated deoxyuridine (124-IdU). Five days after transfer of T cells, mice were killed and subjected to PET and MR imaging. Using a newly developed method for co-registration of the two image modalities, the anatomical localization of the transfered cells was visualized and the amount of radioactivity in various anatomical locations were very accurately determined. Results: Results showed a clear homing of the transfered cells to the tumors. In two independent experiments comprising 12 and 13 evaluable mice, respectively, we found a mean value of 0.909Â±0.468 Bq and 0.926Â±0.553 Bq in the tumors, and only 0.182Â±0.479 Bq and 0.026Â±0.480 Bq in the corresponding contralateral control volumes. The difference in activity between the tumor regions and the control regions was statistically highly significant with 2p-values of 0.002 and 0.006 for the two experiments. Conclusions: This method may represent a significant advancement for studies of adoptively transfered specific T cells, and could potentially be developed for diagnostic purposes. Moreover, since these studies show that tumor-specific T cells home to subcutaneous tumors in substantial numbers, we suggest that these migrating cells could be employed in a new form of therapy as carriers of toxic substances to tumors. Author Disclosure Employment or Leadership Consultant or Advisory Stock Ownership Honoraria Research Funding Expert Testimony Other Remuneration t-cellic t-cellic t-cellic
Characterization of CEBPA Mutations in Acute Myeloid Leukemia in Taiwan - Most Patients with CEBPA Mutations Have Biallelic Mutations and Show a Distinct Immunophenotype of the Leukemic Cells.
Authors: Liang In Lin, Chien Yuan Chen, Dong Tsamn Lin, You Chia Yeh, Hwei Fang Tien
Journal: Blood (2004)
Dasatinib in advanced HER2/neu amplified and ER/PR-positive breast cancer: Phase II study CA180088
Authors: E. Mayer, J. Baurain, J. Sparano, L. Strauss, M. Campone, P. Fumoleau, H. Rugo, A. Awada, O. Sy, A. Llombart
Journal: Journal of Clinical Oncology (2009)

1011 Background: SRC family kinases (SFKs) are involved in numerous signaling pathways including from ER and HER-2 receptors, as well as osteoclast function. Dasatinib is a potent oral inhibitor of SFKs. A phase II trial was performed in patients (pts) with ER+ and/or PR+ and/or HER-2-amplified progressive advanced breast cancer. Subsequent to study initiation, dasatinib demonstrated similar efficacy with a lower incidence of key side-effects at 100 mg once daily in CML and prostate cancer. Methods: Pts with measurable disease and progression after chemotherapy and other targeted agents were treated with dasatinib on a continuous twice-daily (BID) schedule; RECIST-defined response rate was primary endpoint. Results: Sixty-eight pts, 24 with HER-2-amplified and 44 with HER-2-normal, ER+ and/or PR+ disease, were treated. Original starting dose of 100 mg BID (23 pts) was reduced to 70 mg BID (45 pts) due to fluid retention, fatigue, or GI toxicity. Median age was 55 years; nearly all pts (93%) had prior therapy in advanced setting. 59 were radiographically-evaluable (8 discontinued for toxicity and 1 inevaluable). We observed 3 partial responses lasting 9, 9 and 8+ mos plus 6 stable disease ≥16 weeks (range 24–33 wks). All 9 controlled tumors were ER/PR+, 2 were also HER-2-amplified; thus, disease control rate was 19% in the 47 radiographically-evaluable pts with ER/PR+ disease. Median dose intensity was 136 mg/day at 70 mg BID and 175 mg/day at 100 mg BID; median duration of therapy was 1.8 mos in both dose groups. Most pts (75%) discontinued for disease progression. The most common drug-related AEs were diarrhea (49%), headache (34%), nausea (34%), asthenia (32%), pleural effusion (31%), musculoskeletal pain (25%), and vomiting (24%). Drug-related grade 3–4 AEs were reported in 37% of pts and comparable between doses, but related serious AEs were less frequent at 70 mg BID than 100 mg BID (16% vs 26%). Grade 3–4 laboratory abnormalities were uncommon. PK and biomarker analyses will be presented. Conclusions: Encouraging single-agent activity was observed with dasatinib in pts with advanced ER+ breast cancers. Future studies will address the combination of dasatinib with hormonal therapies using a better-tolerated once daily schedule. [Table: see text]
Quadruplet Vs Sequential Triplet Induction Therapy Approaches to Maximise Response for Newly Diagnosed, Transplant Eligible, Myeloma Patients
Authors: Charlotte Pawlyn, Faith E Davies, David A Cairns, Corinne Collett, Anna Chalmers, Alina Striha, John R Jones, Mamta Garg, David Allotey, Kamaraj Karunanithi, Donald Milligan, Martin F Kaiser, Matthew W Jenner, Gordon Cook, Nigel H. Russell, Mark T Drayson, Roger G Owen, Walter M Gregory, Graham H Jackson, Gareth J Morgan
Journal: Blood (2015)