tbuckley/cabot-search huggingface dataset:
Local production of IgE and other immune mediators in the nasal lavage fluid of allergic rhinitis patients before and after specific immunotherapy with Dermatophagoides pteronyssinus
Authors: Adriana Rodrigues Teixeira, Beatriz M. Saraiva, Jorge Kalil, Fabio M. Castro, Clovis Eduardo S. Galvao
Journal: Journal of Allergy and Clinical Immunology (2017)
STMC-32. THE MESENCHYMAL SUBTYPE OF GLIOMA STEM-LIKE CELLS EXHIBITS REDUCED ENDOPLASMIC RETICULUM STRESS
Authors: Xing Guo, Alessandra Audia, Farah Mukheef, Hetshree Patel, Gang Li, Krishna Bhat
Journal: Neuro-Oncology (2016)

GBM is a lethal brain tumor that contains two major cancer stem cell subtypes (Proneural, PN and Mesenchymal, MES) bestowed with tumor initiating properties. Of these two subtypes, the MES glioma stem-like cells (GSCs) are associated with increased radioresistance, and thus it is important to identify essential molecules that regulate their survival and proliferation. Here, we performed 2D gel proteomic comparison of PN versus MES tumors and discovered higher expression of the endoplasmic chaperone protein GRP78 in the MES subtype of GBMs. In addition, TCGA analyses showed significantly higher expression of GRP78 and SOD2 in the MES GBM subtype compared to all other subtypes of GBM (Proneural, Classical, Neural). MES GSCs contained lower baseline levels of the unfolded protein response (UPR) and reactive oxygen species (ROS), verifying our hypotheses that MES GSCs exhibit reduced ER stress. Consistently, MES GSCs showed more resistance to low-glucose and tunicamycin-stimulation both of which induce the ER stress and oxidative stress. Intriguingly, lesser ER stress translates to increased protein synthesis and as consequence we found MES GSCs show increase protein synthesis and larger cell size. Currently we are exploring strategies to knockout GRP78 and study its impact on MES GSC self-renewal, proliferation and tumorigenesis.
Posaconazole Prophylaxis in Patients Undergoing Chemotherapy for Acute Myeloid Leukemia: A Single Center Experience of Therapeutic Drug Monitoring.
Authors: Laura Pavan, Arianna Loregian, Angela Maria Quinto, Speranza Antonia Di Maggio, Silvana Pagni, Marco Gazzola, Elena De March, Giorgio Palù, Gianpietro Semenzato, Livio Trentin, Fabrizio Vianello, Renato Zambello
Journal: Blood (2012)
FLT Imaging Reveals Kinetics and Biology of Engraftment after Myeloablative HSCT
Authors: Kirsten M Williams, Jennifer L. Holter Chakrabarty, Liza Lindenberg, Steve Adler, Juan Gea-Banacloche, Bazetta Blacklock-Schuver, Frances T. Hakim, Dennis D. Hickstein, James N Kochenderfer, Jennifer Wilder, Tracey Chinn, Karen Kurdziel, Seth M. Steinberg, Hanh Khuu, Frank I Lin, Daniel H. Fowler, David Halverson, Daniele N. Avila, George Selby, Tiffani N. Taylor, Jennifer Mann, Jennifer Hsu, Robert B. Epstein, Stacy L Anderson, Nguyen Chuong, Joseph Havlicek, Shibo Li, Tom Pham, Teresa Kraus, Sara K. Vesely, Steven Z. Pavletic, Catherine M. Bollard, Peter Choyke, Ronald E Gress
Journal: Blood (2014)
Phase I, open-label study of olaparib plus cisplatin in patients with advanced solid tumors.
Authors: Judith Balmaña, Nadine M. Tung, Steven J. Isakoff, Begoña Graña, Paula D. Ryan, Rezvan Rafi, Michael Tracy, Eric Winer, José Baselga, Judy Ellen Garber
Journal: Journal of Clinical Oncology (2012)

1009 Background: Olaparib (AZD2281) is an oral PARP inhibitor active in advanced ovarian and breast cancers. We conducted a multicenter, dose-finding study assessing safety/ tolerability of olaparib capsules plus cisplatin in patients (pts) with advanced solid tumors (NCT00782574), for potential use in the neoadjuvant setting. Methods: Pts received 21-day(d) cycles of olaparib, continuously (Cont) or intermittently (Int), plus cisplatin on d1 of each cycle.Each cohort recruited ≥3 evaluable pts with expansion to ≥6 pts if ≥1 had a dose-limiting toxicity. The last cohort was expanded to ensure ≥6 pts completed 4 treatment cycles. Pts who completed 6 combined therapy cycles or who stopped cisplatin due to cisplatin-related toxicity could enter the monotherapy phase (up to 400 mg BID olaparib). Primary objective: safety/ tolerability of ≥4 combined cycles; secondary objectives: pharmacokinetics, antitumor activity. Results: 54 pts received treatment; pts had breast (n=42), ovarian (n=10), pancreatic (n=1) or peritoneal (n=1) cancer. Median number of prior regimens = 4 (1–13). C2, C4 and C6 enrolled &gt;6 pts. Most common grade (G) 3/4 AEs: neutropenia (n=9; 16.7%), leukopenia (n=4; 7.4%), anemia (n=3; 5.6%), vomiting (n=3; 5.6%). In C1–C5, 3 pts had AEs leading to discontinuation: 1 in C2 (thrombocytopenia); 2 in C3 (fatigue; complex migraine, dyspnea). In C6, all pts have ended combination phase and no G3/4 hematologic AEs were seen. Overall, 46% of pts had a dose reduction; 32% due to hematologic AEs. There were no drug-related deaths. 35 pts (65%) completed ≥4 combined cycles (C6, n=8). 18/54 evaluable pts (33%) had an objective response (complete, n=1; partial, n=17); 23 (43%) achieved stable disease. 7 pts (13%) had durable responses on monotherapy for ≥1 year. PK and BRCA1/2 data will be presented. Conclusions: Hematologic AEs led to dose reductions + schedule changes of olaparib with cisplatin 75 mg/m 2 . Tolerability improved with cisplatin 60 mg/m 2 . Antitumor activity was seen during combination and olaparib monotherapy phases, with some long responders. [Table: see text]
Exploratory analyses EGFR, kRAS mutations and other molecular markers in tumors of NSCLC patients (pts) treated with chemotherapy +/- erlotinib (TALENT)
Authors: U. Gatzemeier, A. Heller, D. Foernzler, J. Moecks, C. Ward, F. de Rosa, G. Sauter, U. Brennscheidt
Journal: Journal of Clinical Oncology (2005)

7028 Background: Erlotinib is a potent HER1/EGFR TKI that provides survival benefit as a single agent in 2nd and /3rd line NSCLC. The combination trial TALENT failed to show survival benefit for erlotinib and chemotherapy in 1st line NSCLC and has been described previously. The current objective was to analyze the relationship between biomarkers and treatment-related benefit. Tumor tissue was collected on 500 pts. Biomarker analyses by IHC, FISH, and sequencing were performed. Pts were assessed for survival, response, and TTP. Outcomes were correlated with biomarker data in retrospective subset analyses. Methods: EGFR and kRAS mutation analysis was performed on a set of 293 formalin-fixed tissue samples. Tumor cells were microdissected to extract tumor DNA, which was PCR amplified and sequenced for EGFR exons 18–21, 23 and kRAS exon 2 and 3. IHC analysis of biomarkers, such as EGFR, EGF, EGFRvIII, HER2, TGFα, and pAKT, as well as FISH assays for EGFR, HER2 and AKT were performed on tissue sections and/or tissue microarrays. Results: To date complete sequencing data is available for 191 (EGFR) and 163 (kRAS) samples, with the majority of EGFR mutations found in adenocarcinomas. EGFR mutations have been confirmed in 15 samples by independent PCR and sequencing reactions. For kRAS 24 mutations were confirmed. Correlations of response rates to mutation status were not statistically significant at the p = 0.05 level. Analyses of survival, TTP against mutation status will be presented. Gene amplification of EGFR, HER2 or AKT assessed by FISH was only seen in single samples. IHC showed mainly low expression rates for all assessed biomarkers except EGFR and pAKT: 57% showed pAKT 3+ staining. Statistical analysis on other biomarkers and combinations will be presented. Conclusions: Predictive biomarkers and their patterns may offer tailored therapy in NSCLC. Identification is still in an early phase. For this study no single marker was identified that consistently predicts tumor sensitivity or resistance to erlotinib. Tissue collection and analysis is recommended for future trials with erlotinib. Author Disclosure Employment or Leadership Consultant or Advisory Role Stock Ownership Honoraria Research Funding Expert Testimony Other Remuneration Hoffmann-La Roche, Hoffmann-La Roche AG, Roche Diagnostics GmbH AstraZeneca, Lilly Oncology, Roche Hofffmann-La Roche, Roche Abbott, AstraZeneca, Pierre Fabre, Roche AstraZeneca, Ligand, Lilly Oncology, Roche
MNGO-13. GERMLINE MUTATIONS IN INDIVIDUALS WITH MENINGIOMA AND BREAST CANCER
Authors: Michelle Jackson, Amanda Bergner
Journal: Neuro-Oncology (2016)

An association between meningioma and breast cancer in women has been described, indicating a moderately increased risk to develop one if already diagnosed with the other. However, the mechanism of this association is not fully elucidated. Given the potential impact of heritability within a family and the need for appropriate risk assessment and medical management, exploring the contribution of germline genetic mutations in these cases is important. All sequential cases submitted to our laboratory for hereditary cancer panels between March 2012 and December 2015 were retrospectively reviewed. Test request forms indicating meningioma were selected, and cases that did not undergo testing for BRCA1 and BRCA2 were excluded. Analysis of personal history of breast cancer and test results was conducted. Testing did not include NF2, PTCH1, SMARCB1, or SMARCE1, all established germline causes of meningioma. Of 115 cases with meningioma, 61 (53%) also had breast cancer; 33% had meningioma first, 23% had breast cancer first, 12% were concurrent, and the remainder were unable to be determined. In 10% (n=6), cases were found to harbor a germline genetic mutation in one of four genes: BRCA2 (2), CHEK2 (2), BRCA1 (1), and CDKN2A (1). In the 54 cases of meningioma without breast cancer, germline mutations were identified in 15% (n=8): 2 in BRCA2 and 1 each in ATM, BAP1, CHEK2, PTEN, SDHB, and SDHD. Our findings are consistent with previously reported associations between breast cancer and meningioma, however, germline mutations in known hereditary cancer genes such as BRCA1/2 and CHEK2 have not been described before. Additionally, the spectrum of genetic alternations seen in the larger meningioma cohort provides new information about the role that germline mutations may play in hereditary meningioma, which could have important implications for the provision of genetic counseling and test selection. Further studies are needed to clarify this association.
Amrubicin, a Novel Investigational Anthracycline, in Combination with Lenalidomide and Dexamethasone in Patients with Relapsed/Refractory Multiple Myeloma: Results of a Phase 1 Dose-Escalation Study
Authors: Shira N. Dinner, Tamara J. Dunn, Bruno C. Medeiros, Steven E. Coutre, Caroline Berube, Jason Gotlib, Michaela Liedtke
Journal: Blood (2012)
Notes from the field: emergence of Shigella flexneri 2a resistant to ceftriaxone and ciprofloxacin - South Carolina, October 2010.
Authors: S. Jue, R. Hardee, M. Overman, E. Mays, A. Bowen, J. Whichard, K. Greene, G. Pecic, E. Taylor
Journal: MMWR Morbidity and Mortality Weekly Report (2010)
Evaluation of Different Co-Stimulatory Signals in the Priming and Expansion of HLA-B*0702/CMV_pp65 Restricted CTLs after Stimulation with aAPC
Authors: Markus Kapp, Kerstin Fick, Stefanie Jackob, Rainer Thiele, Mathias Oelke, Harald Wajant, Jonathan P. Schneck, Andreas Opitz, Hermann Einsele, G.ötz Ulrich Grigoleit
Journal: Blood (2008)
Interleukin-1 receptor antagonist, a biomarker of response to anti-TB treatment in HIV/TB co-infected patients
Authors: Janin Nouhin, Polidy Pean, Yoann Madec, Mathieu F. Chevalier, Celine Didier, Laurence Borand, François-Xavier Blanc, Daniel Scott-Algara, Didier Laureillard, Laurence Weiss
Journal: Journal of Infection (2017)
Three lymphocyte subsets (CD45+ CD4- CD8-IFN gamma+ (CD16/56+), CD3+ CD4+ IL-4+ IFN gamma-, CD3+ CD8+ CD60+ IL-4+ IFN gamma-) are required for human specific memory IgE responses.
Authors: Tsz Wah Ho, Charles Kim, Bryan McCarthy, Seto M. Chice, Ayla Safran, Yitzchok Norowitz, Maja Nowakowski, Stephan Kohlhoff, Rauno Joks, Tamar A. Smith-Norowitz, Helen G. Durkin
Journal: Journal of Allergy and Clinical Immunology (2017)
The Impact of Maintenance Lenalidomide on the Mutational Status of the Myeloma Clone at Relapse in the NCRI Myeloma XI Trial for Newly Diagnosed Multiple Myeloma Patients (NDMM)
Authors: John R Jones, Niels Weinhold, Shweta S. Chavan, Charlotte Pawlyn, Lorenzo Melchor, David A Cairns, Dil B Begum, Charlotte Smith, Sidra Ellis, Amy Price, Amy L Sherborne, Brian A Walker, Christopher P Wardell, Gordon Cook, Matthew W Jenner, Nigel H Russell, Mark T Drayson, Roger G Owen, Faith E Davies, Martin F Kaiser, Graham H Jackson, Walter M Gregory, Mel Greaves, Gareth J Morgan
Journal: Blood (2016)
C/EBPβ-Mediated Expansion of Hematopoietic Stem/Progenitors Precedes ‘Emergency’ Granulopoiesis Induced by Candidemia.
Authors: Akihiro Tamura, Hideyo Hirai, Yoshihiro Hayashi, Hisayuki Yao, Satoshi Yoshioka, Yasuo Miura, Eishi Ashihara, Taira Maekawa
Journal: Blood (2012)
Once-daily Tiotropium Respimat® Add-on Therapy Improves Lung Function and Control in Adolescents and Children with Moderate Symptomatic Asthma
Authors: Christian Vogelberg, Eckard Hamelmann, Stanley J. Szefler, Georges El Azzi, Petra Moroni-Zentgraf, Michael Engel, Ralf Sigmund, Mark L. Vandewalker
Journal: Journal of Allergy and Clinical Immunology (2017)
Vatican faces outcry for inviting Chinese official to organ summit
Authors: Josephine McKenna
Journal: BMJ (2017)

Doctors and medical ethicists have strongly criticised the Vatican for inviting a Chinese health official to a summit on organ trafficking, despite claims that China still sanctions the removal of organs from executed prisoners and ethnic minorities.

Huang Jiefu, a former health minister and chairman of China’s national organ donation and transplant body, dismissed suggestions that the practice of organ removal was ongoing.

“That is a rumour,” Huang told The BMJ outside the summit hosted by the Pontifical Academy of Sciences. “I am the person who arranged to stop using prisoners’ organs from January 2015,” he said. “I had strong support from the highest leaders.”

The Vatican invited Huang to the two day summit which included 80 transplant doctors, health officials, and legal experts from around the world. Archbishop Marcelo …
t(4;14) Positive Multiple Myeloma Is Chemosensitive to Dexamethasone and/or Thalidomide but Not Alkylating Agents: Rapid Relapse and Not Primary Drug Resistance Explains Poor Outcomes.
Authors: Wilfrid J. Jaksic, Suzanne Trudel, Hong Chang, Xi Qi, Joseph R. Mikhael, Donna E. Reece, Christine Chen, A. Keith Stewart
Journal: Blood (2004)
Hypercoagulability Study in Patients with Angioedema.
Authors: Gemma Vilà-Nadal, Daiana Guillén, Mariana Díaz-Almirón, María Soledad García-Muñoz, María Jesús Blanco Bañares, Carmen Gómez-Traseira, María Concepción López-Serrano, Teresa Caballero
Journal: Journal of Allergy and Clinical Immunology (2017)
Eradication of experimental brain metastases of human non-small cell lung cancer by macitentan, a dual antagonist of the endothelin A and B receptor, combined with paclitaxel.
Authors: Masaki Hanibuchi, Sun-Jin Kim, Kenji Otsuka, Sho Tabata, Takuya Kuramoto, Hisatsugu Goto, Yasuhiko Nishioka, Isaiah Josh Fidler
Journal: Journal of Clinical Oncology (2012)

92 Background: Treatment of patients with lung cancer brain metastases remains a major challenge because of the limited availability of standard therapy. Thus, the development of successful treatment options for these patients is mandatory. Recently, the endothelin axis was reported to be involved in cancer progression through its pleiotropic biological effects on cell survival, proliferation, invasion, and metastasis. Methods: In this study, we evaluated both the in vitro and in vivoeffects of macitentan, an orally bioavailable, dual endothelin A receptor and endothelin B receptor antagonist, as monotherapy, and in combination with paclitaxel. Results: In human non-small cell lung cancer PC-14 cells, macitentan treatment inhibited cell proliferation, corresponding with inhibition of Akt and p42/44 mitogen-activated protein kinase phosphorylation, and increased apoptosis. The combination of macitentan and paclitaxel resulted in the potentiation of all of these effects, suggesting that macitentan could enhance sensitivity to paclitaxel. Moreover, macitentan completely abrogated astrocyte-mediated protection of tumor cells against paclitaxel. In an experimental brain metastasis model of human lung cancer, the combination of macitentan and paclitaxel significantly inhibited the growth of brain metastasis and produced a striking survival prolongation of tumor-bearing mice. Conclusions: The endothelin A and B receptor blockade by macitentan could be a promising therapeutic strategy for brain metastases of non-small cell lung cancer.
Comparison of Outcomes after Reduced-Intensity Versus Myeloablative Stem Cell Transplantation in 128 Patients with Acute Myeloid Leukemia: A Single-Center Analysis.
Authors: Fusako Ohara, Takahiro Fukuda, Ruri Kato, Satoshi Yamasaki, Sung-Won Kim, Shin-ichiro Mori, Ryuji Tanosaki, Yuji Heike, Atsushi Makimoto, Kensei Tobinai, Yoichi Takaue
Journal: Blood (2006)
Serum IgG4 to food proteins, but not to the barrier function proteins desmoglein 1 or 3, are increased in eosinophilic esophagitis
Authors: Jeffrey Wilson, Alexander J. Schuyler, Anubha Tripathi, Scott P. Commins, Elizabeth A. Erwin, Thomas A.E. Platts-Mills
Journal: Journal of Allergy and Clinical Immunology (2017)
Pharmacokinetics (PK) and pharmacogenetics (PG) of the MEK1/2 inhibitor, selumetinib, in Asian and Western healthy subjects: a pooled analysis
Authors: A. Dymond, C. Elks, P. Martin, D. Carlile, G. Mariani, S. Lovick, Y. Huang, U. Lorch, H. Brown, K. So
Journal: Annals of Oncology (2016)
Downregulation of miR-130b~301b cluster is mediated by aberrant promoter methylation and impairs cellular senescence in prostate cancer
Authors: João Ramalho-Carvalho, Inês Graça, Antonio Gomez, Jorge Oliveira, Rui Henrique, Manel Esteller, Carmen Jerónimo
Journal: Journal of Hematology & Oncology (2017)

Numerous DNA-damaging cellular stresses, including oncogene activation and DNA-damage response (DDR), may lead to cellular senescence. Previous observations linked microRNA deregulation with altered senescent patterns, prompting us to investigate whether epigenetic repression of microRNAs expression might disrupt senescence in prostate cancer (PCa) cells.Differential methylation mapping in prostate tissues was carried using Infinium HumanMethylation450 BeadChip. After validation of methylation and expression analyses in a larger series of prostate tissues, the functional role of the cluster miR-130b~301b was explored using in vitro studies testing cell viability, apoptosis, invasion and DNA damage in prostate cancer cell lines. Western blot and RT-qPCR were performed to support those observations.We found that the miR-130b~301b cluster directs epigenetic activation of cell cycle inhibitors required for DDR activation, thus stimulating the senescence-associated secretory phenotype (SASP). Furthermore, overexpression of miR-130b~301b cluster markedly reduced the malignant phenotype of PCa cells.Altogether, these data demonstrate that miR-130b~301b cluster overexpression might effectively induce PCa cell growth arrest through epigenetic regulation of proliferation-blocking genes and activation of cellular senescence.
High Risk Myeloma Is Characterized By the Bi-Allelic Inactivation of CDKN2C and RB1
Authors: Shweta S. Chavan, Christoph Heuck, Jie He, Rusiana Tytarenko, Shayu Deshpande, Purvi Patel, Mark Bailey, Caleb K. Stein, Owen W Stephens, Niels Weinhold, Nathan Petty, Doug Steward, Leo Rasche, Michael A Bauer, Cody Ashby, Erich Allen Peterson, Shan Zhong, Michelle Nahas, Siraj M Ali, Jo-Anne Vergillo, Jeff Ross, Vincent A. Miller, Phillip J Stephens, Carolina Schinke, Maurizio Zangari, Frits van Rhee, Bart Barlogie, Tariq I Mughal, Faith E Davies, Gareth J Morgan, Brian A Walker
Journal: Blood (2016)
Clinical Efficacy and Tolerability of Granulocyte Transfusions for the Treatment of Febrile Neutropenia in the Patients with Hematologic Malignancies.
Authors: Ki Hwan Kim, Hyo-Jeong Lim, Byung-Su Kim, Sang-Min Lee, Soo-Mee Bang, Inho Kim, Sung-Soo Yoon, Kyou-Sup Han, Seonyang Park, Byoung-Kook Kim
Journal: Blood (2009)
ACTR-10. PHASE 0 TRIAL OF AZD1775 IN FIRST-RECURRENCE GLIOBLASTOMA PATIENTS
Authors: Nader Sanai, Jing Li, Julie Boerner, Harshil Dhruv, Michael Berens, Patricia LoRusso
Journal: Neuro-Oncology (2016)

AZD1775 is a first-in-class Wee1 inhibitor with dual-function as a DNA damage sensitizer and cytotoxic agent. A Phase I trial for solid tumors suggested CNS activity, but a preclinical study indicated limited blood-brain-barrier penetration in mice. To resolve this controversy, we examined the pharmacokinetic (PK) and pharmacodynamics (PD) of AZD1775 in first-recurrence glioblastoma (GBM) patients. 20 adult patients received a single dose of AZD1775 (100/200/400mg), and tumor was resected at 4h, 8h, or 24h post-dosing. Sparse blood sampling was performed and tumor samples were collected intraoperatively. AZD1775 concentrations in plasma and tumor were determined by validated LC-MS/MS methods. PD endpoints were compared to matched archival tissue. AZD1775 plasma exposure increased with increasing dose and exhibited an absorption rate constant (Ka) of 0.84 h-1, an elimination rate constant (K) of 0.11 h-1, and an apparent oral clearance (CL/F) of 187 L/h, with interindividual variability (IIV) of 98%, 28% and 52%, respectively. Glomerular filtration rate was a significant covariate on CL/F, explaining 25% of the IIV of CL/F. Total and unbound brain tumor-to-plasma ratios appeared dose- and time-independent, with mean values of 9.1 (3.8–40.4) and 3.2 (1.3–24.4), respectively. 1 to 24h after a 400mg dose, unbound concentrations in tumor ranged from 18–315 ng/g, with the mean (85 ng/g) above the in vitro IC50 (42 ng/mL) for Wee1 inhibition. Following drug exposure, Wee1 suppression was inferred by double-strand DNA breakage (phosphorylated H2AX, p=0.005), cell-cycle re-entry (phosphohistone-3, p=0.037), and apoptosis (caspase-3, p=0.028). Within 6 months of study activation, we obtained data to justify Phase II study of AZD1775 in GBM. Unlike preclinical models, our findings show adequate tumor penetration in patients, provide the first evidence of biological activity in human GBM, and confirm the utility of Phase 0 trials as part of an accelerated paradigm for drug development in glioma patients.
Global gene expression profile reveals a distinct transcriptomic profile predictive of clinical outcome in stage III colorectal cancer patients treated with adjuvant chemotherapy
Authors: R. Tassi, E. Mini, R. D'Aurizio, G. Perrone, A. Magi, A. Lapucci, C. Napoli, L. Picariello, M. Brugia, I. Landini, T. Mazzei, F. Tonelli, S. Nobili
Journal: Annals of Oncology (2016)
CD34+/CD90+/GST-PI- And CD34+/CD90-/GST-PI+ CELLS during two years hematopoiesis in a cytokines-free, serum-free liquid culture system: application in transplants
Authors: Alejandro Marche-Cova, Pedro Sobrevilla-Calvo, Ana A. Fernandez-Ortiz, Rocio Mendez-Martinez, Maria T. Salles-Manuel
Journal: Blood (2000)
An Insertional Mutagenesis Screen for Genes That Cooperate with Mll-AF9 in Leukemogenesis.
Authors: Rachel Joy Bergerson, Lara S Collier, Sanne Lugthart, Raha Allaei, Molly J Nixon, Kevin A.T. Silverstein, Aaron Sarver, Danhua Flora Fan, Anne-Francoise J Lamblin, Linda Wolff, John H. Kersey, M. Gerard O'Sullivan, Ruud Delwel, Scott C. Kogan, David J Adams, David Largaespada
Journal: Blood (2009)