tbuckley/cabot-search huggingface dataset:
Abstract LB-163: Pan-cancer analysis of the causes and consequences of Intra-tumor heterogeneity
Authors: Noemi Andor, Trevor A. Graham, Athena C. Aktipis, Claudia Petritsch, Hanlee P. Ji, Carlo C. Maley
Journal: Cancer Research (2015)

Abstract Tumors are typically mosaics of mutant clones that have evolved from a common ancestral cell. This intra-tumor heterogeneity (ITH) is thought to drive both neoplastic progression and acquired therapeutic resistance. Availability of just one sample per tumor and moderate sequencing depth have limited systematic analysis of ITH during previous TCGA pan-cancer analyses, confining the study of ITH to a small numbers of tumor samples and cancer types. The molecular and histopathological causes of ITH and its prognostic significance have thus far remained uncertain. To overcome these limitations, we used an analysis method called EXPANDS that estimates the proportion of cells harboring specific mutations from exome sequencing data, as well as other methods that quantify ITH. We extrapolate the number of genetically diverse clonal subpopulations in 1,165 primary tumors among 12 different cancer types from TCGA and investigate mechanisms underpinning ITH as well as the correlation of ITH and genomic instability with prognosis. Lastly we validate the prognostic significance of genomic instability in an independent, high-density SNP-array dataset consisting of 2010 tumor samples, across seven additional cancer types. We found evidence of ITH in the vast majority of tumors. Mutations in driver genes tended to have a characteristic clone size, suggesting differential fitness effects of those mutations. The detection of a mutation in a driver gene that typically appears in a small clone was a predictor of poor survival. Driver gene mutations, tumor microenvironment composition and prevalence of copy number gains were significantly associated with increased ITH. In general, the prevalence of copy number alterations was a universal biomarker of prognosis: tumors with intermediate copy number burden (50 to 75% of the genome affected by copy number alterations) progressed faster than tumors with higher copy number burden, independent of cancer type. Chemo-radiation therapy administration was more efficient in decelerating tumor progression among patients with intermediate copy number burden than among patients with low or high copy number burden. These results were validated and confirmed in the independent SNP-array dataset. This study suggests a tradeoff exists between the costs and benefits of genomic instability that impacts both the evolvability and fitness of the tumor cell population. In the future, this tradeoff might be exploited to improve survival. Citation Format: Noemi Andor, Trevor A. Graham, Athena C. Aktipis, Claudia Petritsch, Hanlee P. Ji, Carlo C. Maley. Pan-cancer analysis of the causes and consequences of Intra-tumor heterogeneity. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr LB-163. doi:10.1158/1538-7445.AM2015-LB-163
Allogeneic Stem Cell Transplantation as Treatment for Relapsed and High-Risk Peripheral T-Cell Lymphoma.
Authors: Hilary M. O’Leary, Kerry J. Savage, Cynthia L. Toze, Joseph M. Connors, Randy D. Gascoyne, Yasser Abou Mourad, Michael J. Barnett, Donna L. Forrest, Donna E. Hogge, Julye Lavoie, Stephen H. Nantel, Thomas J. Nevill, John D. Shepherd, Clayton Smith, Heather J. Sutherland, Nicholas Voss, Ryan Brinkmann, Kevin Song
Journal: Blood (2007)
Measurement of Spleen Stiffness With Acoustic Radiation Force Impulse Imaging Predicts Mortality and Hepatic Decompensation in Patients With Liver Cirrhosis
Authors: Yoshitaka Takuma, Youichi Morimoto, Hiroyuki Takabatake, Nobuyuki Toshikuni, Junko Tomokuni, Akiko Sahara, Kazuhiro Matsueda, Hiroshi Yamamoto
Journal: Clinical Gastroenterology and Hepatology (2016)
36. Genome-Wide Insight Into the Transcriptional Modulations Triggered By Lentiviral Transduction in Human Hematopoietic Stem Cells
Authors: Francesco Piras, Michela Riba, Dejan Lazarevic, Sara Bartolaccini, Elia Stupka, Davide Cittaro, Luigi Naldini, Anna Kajaste-Rudnitski
Journal: Molecular Therapy (2015)

Recent studies suggest that hematopoietic stem cells (HSC) can sense foreign nucleic acids and pathogen-associated molecular patterns (PAMPs). Exposure to lentiviral vectors (LV) upon gene transfer may thus trigger acute host responses in HSC that could potentially impact on their biological properties, although no comprehensive studies are available to date. We have performed a high throughput RNA-Seq analysis on human cord-blood (CB)-derived CD34+ hematopoietic stem and progenitor cells (HSPC) exposed to research- or clinical-grade VSV-g pseudotyped (SIN) LV at a high multiplicity of infection, matching current clinical vector dose requirements. As controls, cells were exposed to non-transducing Env-less, genome-less or heat inactivated control vectors or kept in culture untreated. RNA was extracted at different times early after transduction, processed and ran in Illumina HiSeq2000. Analysis of Differential Expression in Time Course was performed using LIMMA R/BioConductor library. Key pathways were assessed by Term Enrichment Analysis considering KEGG pathways and Gene Ontology Biological processes. Transduction with both research-and clinical-grade LV significantly triggered DNA damage and apoptosis-related responses. In particular, p53 signaling was among the most significantly altered pathways (p<3.47×10−14) and induction of several key players, including a 8-fold increase in p21 mRNA, was further confirmed by Taqman. This signaling occurred also in bone-marrow-derived CD34+ cells and was integration-independent as Integrase-Defective LV (IDLV) induced p21 to a similar extent as LV. Furthermore, equal induction was observed in all CD34+ subpopulations, including in the most primitive CD38-CD133+ fraction. Finally, LV/IDLV exposure lead to a slight but significant increase in the percentage of apoptotic HSPC in culture (p<0.001) as compared to control vector exposed cells and untreated controls. Experiments are ongoing to further investigate the potential short and long-term consequences of this signaling on the biological properties of HSPC in vitro and in vivo. Overall, our results suggest for the first time that LV transduction triggers transcriptional changes in HSPC involving pathways pivotal for their biology. Better understanding of the potential functional consequences this may have will be important for the development of improved gene therapy protocols.
Characterization of colon cancer–associated antigens that would be key therapeutic targets in the prevention of disease relapse or progression.
Authors: Elizabeth Kyungsun Broussard, Andrew L. Coveler, Samuel H. Whiting, Rachel Kim, Lauren Rastetter, Ekram Gad, Doreen Higgins, Meredith Slota, Grace Gyurkey, Jennifer Childs, Mary Lenora Disis
Journal: Journal of Clinical Oncology (2012)

594 Background: Colon cancer (CRC) is an immunogenic tumor and adaptive immunity may play a role in inhibiting disease relapse. A vaccine to boost cellular immunity in CRC patients could prevent disease recurrence, but there have been few defined immunogenic proteins identified as vaccine candidates. TVG has shown that overexpressed tumor associated proteins, abundant in the cancer state but expressed at basal levels in normal cells, can be immunogenic. We hypothesized that ideal candidate antigens would be ones already validated as prognostic markers in multivariate analysis. Methods: From a directed literature review we selected antigens based on (1) incidence of expression, (2) independent predictor of poor prognosis or early disease recurrence, and (3) known biologic function in CRC pathogenesis. We identified peptides that were predicted to be high affinity binders across multiple HLA DR alleles. We evaluated immunogenicity of peptides with IFN-g ELISPOT assays in CRC and control patients. We then evaluated the efficacy of vaccination in reducing tumors in the AOM mouse model. We evaluated immunogenicity of peptides with IFN-g ELISPOT assays using vaccinated mice splenocytes. We quantified antigen protein expression in AOM tumors. Results: The eight proteins are: CDC25B, COX-2, EBAG9, EGFR, Fascin-1, IGF-1R, PRL-3 and VCP. For all candidate antigens there was a greater IFN-g response in CRC patients than in controls. Four antigens (COX-2 p&lt;.0001, CDC25B p&lt;.0002, and EGFR p=.01, Fascin-1 p=.05) demonstrated a statistically significant reduction in the development of colon tumors compared to vaccination with adjuvant alone. Conclusions: We conclude that: 1. biologically relevant CRC associated proteins can be identified that are associated with prognosis, 2. epitopes predicted to bind multiple DR alleles, derived from candidate antigens, elicit T cell responses greater in CRC patients than in normal controls, 3. vaccination with peptides derived from four antigens resulted in a statistically significant reduction in the development of colon tumors in a mouse model, and 4. these antigens may represent novel immunologic targets for CRC.
Abstract 3369: Nuclear hormone receptor profiling of skin cancer-associated fibroblasts for targeted pharmacological modulation of skin squamous cell carcinoma
Authors: Jeremy Soon Kiat Chan, Ming Keat Sng, Zi Qiang Teo, Nguan Soon Tan
Journal: Cancer Research (2015)

Abstract Background: Cutaneous squamous cell carcinoma (SCC) is the second-most frequently diagnosed non-melanoma skin cancer that commonly manifests in sun-exposed areas of the skin, resulting in permanent disfigurement and potentially death when untreated. The development and malignant progression of skin SCC is dependent not only on the properties of the tumor epithelia but also the effects of the tumor stroma. Cancer associated fibroblasts (CAFs) are enriched in the stroma of skin SCC tumors and supply paracrine factors that encourage tumor growth. However, the transcription regulatory networks enabling this pro-tumor secretory phenotype of CAFs remain largely unknown. Nuclear receptors, being ligand-inducible transcription factors, are relevant therapeutic candidates for modulation of CAF-dependent SCC tumor advancement. Materials and methods: Laser capture microdissected CAFs from archived patient SCC biopsies were profiled for their expression of 48 known nuclear receptors. siRNA knockdown and overexpression of specific nuclear receptors in CAFs was performed, and their impact on the SCC transcriptome and phenotype was evaluated in a co-culture system. Co-administration of nuclear receptor ligands and conventional anticancer chemotherapeutics was also carried out in a 3D-organotypic skin tumor model to investigate synergistic and sensitizing effects on SCC. Findings and conclusions: Our study is the first to define a nuclear receptor profile for SCC CAFs, wherein the expression of 5 nuclear receptors was unchanged, 18 nuclear receptors were highly expressed and 3 nuclear receptors were lowly expressed in CAFs relative to normal fibroblasts. We showed that SCC tumor epithelia are transcriptionally and functionally sensitive to this nuclear receptor profile of CAFs. Simultaneous and differential attenuation of multiple aggressive SCC phenotypes was possible through the manipulation of specific nuclear receptor expression and activity in CAFs. Our results highlight the utility of CAF nuclear receptor profiling and a role for nuclear receptor-directed drugs in the multimodal treatment of skin SCC. Citation Format: Jeremy Soon Kiat Chan, Ming Keat Sng, Zi Qiang Teo, Nguan Soon Tan. Nuclear hormone receptor profiling of skin cancer-associated fibroblasts for targeted pharmacological modulation of skin squamous cell carcinoma. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 3369. doi:10.1158/1538-7445.AM2015-3369
Abstract 2730: Additional mutations in genes relevant to the Ras signaling pathway promote the malignant characteristics of NF1-associated malignant peripheral nerve sheath tumor (NF1-MPNST) cells
Authors: Yoshimi Arima, Kenjiro Kosaki, Chikako Hirose, Hideyuki Saya
Journal: Cancer Research (2015)

Abstract Malignant peripheral nerve sheath tumors (MPNST) are soft tissue sarcomas surrounding the peripheral nerve and occur sporadically or more often in association with neurofibromatosis type 1 (NF1, von Recklinghausen disease), which is an inherited disease caused by NF1 gene germline mutations. The NF1 tumor suppressor gene encodes neurofibromin and is a functional Ras GTPase-activating protein (RasGAP) that regulates the Ras signal negatively by accelerating the conversion of activated Ras-GTP to inactive Ras-GDP. We hypothesized that additional genetic alterations promote malignancy of NF1-associated tumors. Hence, we inoculated a GFP-labeled human NF1-MPNST cell line, sNF96.2-GFP, which has a frame-shift mutation (c.3683delC, p.Asn1229MetfsTer11) in the NF1 gene, into the renal sub-capsules of immunodeficient mice. A subclonal cell line, the A-1 cell, was established from the developed tumor. We found that A-1 cells show much higher tumorigenic activity and Akt activation than parental sNF96.2-GFP cells. We analyzed the genomic DNA of both the sNF96.2 and the A-1 cells by using the next-generation sequencing and the medical exome panel including 4813 genes, which are known to be responsible for most human genetic disorders. We identified 18 heterozygous variants in 17 genes that were present in the A-1 cells, but not in the original sNF96.2 cells. Two of these genes are associated with the regulation of the Ras signaling pathway. Our data suggests that the additional gene mutations that regulate Ras pathways do in fact promote the malignant characteristics of NF1-associated tumors through the Akt activation. Citation Format: Yoshimi Arima, Kenjiro Kosaki, Chikako Hirose, Hideyuki Saya. Additional mutations in genes relevant to the Ras signaling pathway promote the malignant characteristics of NF1-associated malignant peripheral nerve sheath tumor (NF1-MPNST) cells. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 2730. doi:10.1158/1538-7445.AM2015-2730
Multisystem, Induced Pluripotent Stem Cell (iPSC) Modeling Reveals a Role for Growth Differentiation Factors (GDFs) in the Etiology of β Thalassemia and Ineffective Erythropoiesis
Authors: Liz B. Wang, Andreia Gianotti Sommer, Amy Leung, Seonmi Park, David H.K. Chui, Martin H. Steinberg, Gustavo Mostoslavsky, George J. Murphy
Journal: Blood (2014)
Unremitting Presence of Marrow Immunoglobulin Heavy Chain Gene Rearrangement (IGH-GR) 3 Months Following Autotransplant Is Associated with Poor Outcome in Disease Control in Patients with Multiple Myeloma (MM).
Authors: Choon Kee Lee, Qi Wei, Mark Lovell, Karen Swisshelm, John Ryder, Han Myint, J. Fred Kolhouse, William Robinson
Journal: Blood (2009)
The Joint Role of Comorbidity and Performance Status (PS) in Predicting Morbidity after Allogeneic Nonmyeloablative Hematopoietic Cell Transplantation (HCT).
Authors: Mohamed Sorror, Barry Storer, Brenda M. Sandmaier, David G. Maloney, Michael Pulsipher, Amelia Langston, Michael B. Maris, Dietger Niederwieser, Rainer Storb
Journal: Blood (2006)
Telomere Length In Ph - Negative Chronic Myeloproliferative Neoplasms: It Is Reduced According to JAK2 V617F Mutation Allele Burden and It Is Not Affected by Cytoreductive Treatment with Hydroxyurea
Authors: Marco Ruella, Silvia Salmoiraghi, Alessandra Risso, Alessandra Carobbio, Piera Sivera, Irene Ricca, Tiziano Barbui, Corrado Tarella, Alessandro Rambaldi
Journal: Blood (2010)
A possible mechanism of antibody-dependent cellular cytotoxicity (ADCC) of lymphokine-activated killer cells (LAK) with cetuximab for the treatment of mutated KRAS or BRAF metastatic colorectal cancer (mCRC).
Authors: Y. Inoue, S. Hazama, M. Irie, Y. Shindo, Y. Maeda, N. Suzuki, K. Yoshimura, S. Yoshino, M. Oka
Journal: Journal of Clinical Oncology (2011)

e14084 Background: Cetuximab, a chimeric IgG1 antibody, recognizing the extracellular domain of epidermal growth factor (EGFR) to inhibit the activation signaling of proliferation, angiogenesis and anti-apoptosis is used in first line mCRC treatment. In addition to this mechanism, ADCC activity has been suggested. In this study, we investigated the antitumor activity of cetuximab in combination with activated immune cells against CRC cell lines. Methods: Peripheral blood mononuclear cells (PBMCs) were activated to LAK and CD3-LAK by incubation for 4 days with IL-2 (500 U/mL) or both IL-2 and immobilized anti-CD3 antibody, respectively. LAK and CD3-LAK were co-cultured with CRC cell lines, OMUS-23 (wild-type: wt), OUMSmt (BRAFmutant: mt) and HCC-56 (KRASmt), with or without cetuximab. The antitumor activity was evaluated by adherent target detachment (ATD) assay. Results: The inductions of Fcg IIIa (CD16)+ NK cells were significantly higher in LAK than CD3-LAK (P<0.05). The ATD activity of LAK was significantly higher (P<0.05) than that of CD3-LAK. Moreover, the ATD activities of LAK in combination with cetuximab were strongly enhanced especially against mutated KRAS or BRAF tumor cells. Conclusions: Our results suggest that cetuximab in combination with Fcg IIIa+ NK lich effecter cells induced by the addition of IL-2 exerts effective anti-tumor activity. Cetuximab may therapeutic not only mCRC patients with wild-type KRAS and BRAF but also patients with mutant KRAS or BRAF by its ADCC activity.
AHSP Knockdown in Human Erythroleukemia Cell Line and Human Hematopoietic Stem Cells Results in Alpha Hemoglobin Chain Precipitation, Decreased Hemoglobin Levels and Increased Cell Death.
Authors: Flavia O. Pinho, Dulcineia M. Albuquerque, Sara T.O Saad, Fernando F. Costa
Journal: Blood (2007)
The Safety and Tolerability of Azacitidine (AZA) Are Comparable in Patients with Acute Myeloid Leukemia (AML) or Higher-Risk Myelodysplastic Syndromes (MDS)
Authors: John F. Seymour, Lewis R. Silverman, Hartmut Döhner, Pierre Fenaux, Ghulam J. Mufti, Valeria Santini, Mark D. Minden, Richard M. Stone, Lela M. Lucy, Stephen Songer, Donna Dougherty, Randy Hinkle, Dominique Gambini, C.L. Beach, Hervé Dombret
Journal: Blood (2015)
Tyrosine Phosphorylation of WASP Promotes Calpain-Mediated Podosome Disassembly In Myeloid Cells.
Authors: Lee Macpherson, James Monypenny, Michael P Blundell, Giles O Cory, Jessica Tomé-García, Adrian Thrasher, Gareth E Jones, Yolanda Calle
Journal: Blood (2010)
A phase I/II study of TRC105 in combination with sorafenib in hepatocellular carcinoma (HCC).
Authors: Austin G. Duffy, Chi Ma, Susanna Varkey Ulahannan, Oxana V. Makarova-Rusher, Suzanne Fioravanti, Melissa Walker, Aradhana Venkatesan, Ismail B. Turkbey, Peter L. Choyke, Jane B. Trepel, Liang Cao, Kathryn Compton, William Douglas Figg, Tim F. Greten
Journal: Journal of Clinical Oncology (2015)

291 Background: Endoglin (CD105) is an endothelial cell membrane receptor highly expressed on proliferating tumor vasculature, including HCC. CD105 is essential for angiogenesis and its expression is upregulated by hypoxia and VEGF inhibition. TRC105 is a chimeric IgG1 anti-CD105 monoclonal antibody that inhibits angiogenesis and causes ADCC and apoptosis of proliferating endothelium. Sorafenib is the only FDA-approved drug in HCC. Methods: Preclinical: Murine BNL HCC cells were grown subcutaneously in wildtype Balb/c mice and treated with antibody to murine CD105, (clone MJ7/18; 10-200ug) + sorafenib (10 mg/kg daily p.o.) or sorafenib alone with assessment for CD105 expression, tumor size. Clinical: Patients with HCC (Childs Pugh A/B7), ECOG 0/1, were enrolled in a phase I study of TRC105 at 3, 6, 10, 15mg/kg q 2wks plus sorafenib 400mg bid. Correlative biomarkers included DCE-MRI, color Doppler ultrasonography, circulating endothelial and endothelial progenitor cells, plasma levels of angiogenic factors, soluble CD105 and tumor IHC for CD105. Samples were also collected for immunogenicity and pharmacokinetics. Results: Preclinical studies: CD105 expression was increased in BNL HCC tumors by sorafenib. Anti-CD105 antibody + sorafenib reduced tumor volume compared to sorafenib alone. Clinical trial: 19 pts were enrolled; Hep B/C/NA: 2/10/7; M:F 13:6; Mean age of 60 (range 18-76); 1 DLT (increased AST) occurred at 10mg/kg. Three of 14 (21%) evaluable pts achieved PR by RECIST. Four patients had confirmed stable disease, one of whom was treated for 22 months. Median time on study was 4 months (range 2 to 22 months). Conclusions: TRC105 combined with sorafenib was well tolerated at the recommended single agent doses of both drugs. Encouraging evidence of activity was observed and the study is proceeding to the phase 2 stage. Full correlative and clinical data will be presented. Clinical trial information: NCT01306058.
Elevation of Hypercoagulability Markers in Hemoglobin SC Disease
Authors: Marina P Colella, Erich V De Paula, Nicola Conran, João Machado-Neto, Susan K.P. Quaino, Joyce M Annichino-Bizzacchi, Fernando Ferreira Costa, Sara T Olalla Saad, Fabiola Traina
Journal: Blood (2012)
The ubiquitin E3 ligase TRIM31 promotes aggregation and activation of the signaling adaptor MAVS through Lys63-linked polyubiquitination
Authors: Bingyu Liu, Meng Zhang, Honglei Chu, Honghai Zhang, Haifeng Wu, Guanhua Song, Peng Wang, Kai Zhao, Jinxiu Hou, Xueer Wang, Lei Zhang, Chengjiang Gao
Journal: Nature Immunology (2016)
Role of Enhanced Microenvironmental Interleukin-1 (IL-1) Expression and Increased IL-1 Responsiveness in Persistence of Leukemia Stem Cells in TKI Treated CML Patients
Authors: Bin Zhang, YinWei Ho, Tinisha McDonald, Allen Lin, David S Snyder, Vu N. Ngo, Tessa L. Holyoake, Ravi Bhatia
Journal: Blood (2014)
Relation Between Cereblon Expression and Survival in Patients with Newly Diagnosed Multiple Myeloma Treated with Thalidomide
Authors: Annemiek Broyl, Rowan Kuiper, Mark van Duin, Bronno van der Holt, Laila el Jarari, Uta Bertsch, Sonja Zweegman, Arjan Buijs, Dirk Hose, Henk Lokhorst, Hartmut Goldschmidt, Pieter Sonneveld
Journal: Blood (2012)
Five-Year Direct Cost of Pediatric Patients with Acute Lymphoblastic Leukemia (ALL) Undergoing Allogeneic Stem Cell Transplantation (HSCT): An Analysis from US Payers' Perspective
Authors: Richard T. Maziarz, Annie Guerin, Genevieve Gauthier, Julie Heroux, Maryia Zhdanava, Eric Q Wu, Simu K Thomas, Lei Chen
Journal: Blood (2015)
Kinetics of Early Donor Chimerism after Nonmyeloablative Haematopoietic Stem Cell Transplantation Monitored with High-Resolution Real Time Quantitative PCR.
Authors: Tania N. Masmas, Soren L. Petersen, Hans O. Madsen, Lars Ryder, Ebbe Dickmeiss, Arne Svejgaard, Lars Vindelov
Journal: Blood (2005)
Inhibition of c-Rel Signaling: A Novel Small Molecule-Based Therapy Diminishing T Cell Alloactivation While Preserving Anti-Tumor Activity
Authors: Yusuke Shono, Andrea Tuckett, Hsiou-Chi Liou, Gregoire Atlan-Bonnet, Jennifer J. Tsai, Odette M. Smith, Mallory L. West, Natalie V. Singer, Marcel R.M. van den Brink, Johannes Zakrzewski
Journal: Blood (2012)
Body Mass Index and Mortality Among Adults Undergoing Cardiac Surgery
Authors: Giovanni Mariscalco, Marcin J. Wozniak, Alan G. Dawson, Giuseppe F. Serraino, Richard Porter, Mintu Nath, Catherine Klersy, Tracy Kumar, Gavin J. Murphy
Journal: Circulation (2016)

In an apparent paradox, morbidity and mortality are lower in obese patients undergoing cardiac surgery, although the nature of this association is unclear. We sought to determine whether the obesity paradox observed in cardiac surgery is attributable to reverse epidemiology, bias, or confounding.
Assessment of HbF QTLs Affecting Disease Severity and Genetic Analysis in Patients Homozygous for Codon 8 (–AA) β0-Thalassemia Mutation
Authors: Zhihua Jiang, Shengwen Huang, Hong Yuan Luo, Nejat Akar, A.Nazli Basak, Nasir Al-Allawi, Sule Unal, Fatma Gumruk, Lance Davis, Tasha Morrison, Andrew Campbell, Patrick G. Gallagher, Bernard G Forget, Martin H. Steinberg, David H.K. Chui
Journal: Blood (2014)