tbuckley/cabot-search huggingface dataset:
Protein Synthesis Escapes mTORC1 Control and Constitutes a Promising Therapeutic Target in Acute Myeloid Leukemia.
Authors: Jerome Tamburini, Alexa Samantha Green, Valérie Bardet, Nicolas Chapuis, Lise Willems, Sophie Park, Madalina Uzunov, Norbert Ifrah, Francois Dreyfus, Patrick Mayeux, Catherine Lacombe, Didier Bouscary
Journal: Blood (2008)
Randomized phase II study of danusertib (D) in second-line metastatic castration-resistant prostate cancer (CRPC).
Authors: J. P. Bleuse, H. J. Meulenbeld, E. M. Vinci, E. Raymond, G. Vitali, A. Santoro, L. Dogliotti, R. Berardi, F. Cappuzzo, S. T. Tagawa, C. N. Sternberg, M. G. Jannuzzo, M. Mariani, A. Petroccione, R. De Wit
Journal: Journal of Clinical Oncology (2011)

4628 Background: D is a small molecule that inhibits Aurora kinases, proteins regulating mitosis, implicated in tumorigenesis and overexpressed in prostate cancer. After D administration, tumor regression in 3/16 mice and disease stabilization (SD) in 10/16 mice were seen in the transgenic prostate TRAMP model. Methods: Eligible patients (pts) were CRPC progressing after first-line docetaxel (DTX) based therapy. Two dose schedules were tested: 330 mg/m2 over 6h IV on Days 1, 8, 15 (A) and 500 mg/m2 over 24h IV on Days 1, 15 (B), every 4 wks. Before randomization (1:1 ratio), pts were stratified according to PSA response to prior DTX. Primary endpoint (EP): PSA response rate (i.e. proportion of pts with at least 50% PSA decline from baseline confirmed ≥4 wks apart) at 3 months (mos). Simon two-stage design tested Ha≥0.2 vs H0≤0.1 in each schedule; to proceed to the 2nd stage ≥3/29 PSA responses in either arm were required. Secondary EP: objective response (RECIST), progression free survival (PFS). Results: 43 pts (median age 69 years, Gleason score ≥7 in 88 % pts, visceral disease in 27.9%) and 37 pts (median age 67 years, Gleason score ≥7 in 95 % pts, visceral disease in 13.5%) were treated and 30/43 (A) and 28/37 (B) were evaluable for the primary EP. Major reasons for non evaluability were absence of PSA progression at baseline or ≤1 PSA assessment on treatment. PSA response was reported in 1/30 (A) and 1/28 (B) evaluable pts. Best Overall response was SD in 26% (A) and 43% (B) of pts. Long lasting SD (≥6 mos) was reported in 5/43 (A) and 7/38 (B) pts including 2 SD >20 mos and 1 pt still on treatment after 29+ mos, all in B. Median PFS (95% CI) was 12.14 (10.86-15.14) wks in A and 12.29 (10.71-17.29) wks in B. Uncomplicated neutropenia was the most frequent hematologic toxicity in both schedules: 93% (39% G3/4) in A and 89% (36% G3/4) in B. Febrile neutropenia occurred in 1 pt (A) and 2 pts (B). Non-hematologic drug-related events (≥10% of pts) were mostly of G1/2 fatigue, nausea, diarrhea, anorexia, pyrexia, vomiting, constipation, hypertension, phlebitis. Conclusions: Both schedules showed acceptable toxicity. The number of pts achieving PSA response was insufficient to activate the 2nd stage. Twelve pts achieved SD lasting ≥6 mos (range 6 – 29+).
Abstract 396: Ibrutinib exerts potent antifibrotic activity in a mouse model of pancreatic adenocarcinoma
Authors: Daniel Massó-Vallés, Toni Jauset, Erika Serrano, Nicole M. Sodir, Kim Pedersen, Nesrine I. Affara, Jonathan R. Whitfield, Marie-Eve Beaulieu, Gerard I. Evan, Laurence Elias, Joaquín Arribas, Laura Soucek
Journal: Cancer Research (2015)

Abstract Pancreatic ductal adenocarcinoma (PDAC) is a disease with a poor prognosis characterized by a dense stromal fibroinflammatory reaction that is a significant obstacle to effective therapy. The desmoplastic stroma comprises many inflammatory cells, in particular mast cells that are a key component of the PDAC microenvironment and whose infiltration often correlates with poor patient outcome. Reducing the stroma is of key importance for improving the standard of care. We have previously successfully utilized ibrutinib, a clinically-approved Bruton's Tyrosine Kinase inhibitor, as a mast cell blocker in a mouse model of β cell tumorigenesis. Here, we made use of a transgenic mouse model of PDAC and patient derived xenografts (PDXs) to assess ibrutinib's impact on the tumor microenvironment and animal survival. Across these various experimental pre-clinical models, we show that ibrutinib significantly diminishes tissue fibrosis, increases survival and improves the outcome of standard care. Our results suggest that ibrutinib could be deployed to one more type of cancer and open the way to new clinical trials assessing its therapeutic impact in PDAC patients. Citation Format: Daniel Massó-Vallés, Toni Jauset, Erika Serrano, Nicole M. Sodir, Kim Pedersen, Nesrine I. Affara, Jonathan R. Whitfield, Marie-Eve Beaulieu, Gerard I. Evan, Laurence Elias, Joaquín Arribas, Laura Soucek. Ibrutinib exerts potent antifibrotic activity in a mouse model of pancreatic adenocarcinoma. [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 396. doi:10.1158/1538-7445.AM2015-396
The use of intrathecal ziconotide to manage refractory malignant pain: Five case studies
Authors: G. C. McDowell, J. W. Mitchell, T. D. Moore
Journal: Journal of Clinical Oncology (2009)

e20737 Background: Chronic malignant pain is often difficult to manage. Intrathecal (IT) ziconotide monotherapy has been shown to be effective in treating patients with chronic pain associated with malignancy. Intrathecal admixtures containing ziconotide may also be viable treatment options for refractory malignant pain. Methods: The medical records of 5 patients with malignant pain managed with IT ziconotide as monotherapy or as a component of combination therapy were reviewed. Patient characteristics, medical history, IT drug doses, Numeric Pain Intensity (NPI: 0–10 scale, with higher scores indicating greater pain intensity) scores, and clinical observations (including adverse events [AEs]) were identified. Results: Four women (aged 27, 31, 46, and 68 years) with metastatic breast cancer and a 61-year-old man with metastatic prostate cancer were intolerant of or experienced inadequate analgesia with systemic analgesics and/or IT opioids with or without clonidine or bupivacaine. Ziconotide was either started as monotherapy or used in combination with an IT opioid with or without bupivacaine. Initial ziconotide doses of 0.46 to 1.50 mcg/d were titrated upward to 1.16 to 7.26 mcg/d at the last assessments. Although the 46-year-old woman experienced substantial pain relief (55.6% reduction in NPI score) and quality of life improvement during ∼3 months of ziconotide therapy, she died of cancer complications that were unrelated to ziconotide. From baseline to last assessment, the remaining 4 patients experienced 25% to 83% reductions in NPI scores with ziconotide therapy. Meaningful improvements in patient mobility and functionality were evident. The 68-year-old patient experienced transient dizziness after a 3-mcg bolus trial of ziconotide but did not experience any AEs during continuous infusion of ziconotide. No other ziconotide-related AEs were reported. Conclusions: These cases suggest that ziconotide, alone or in combination with other IT agents, can be a viable treatment option for patients with refractory malignant pain. [Table: see text]
Cediranib (C) in patients (pts) with malignant mesothelioma (MM): A phase II trial of The University of Chicago Phase II Consortium.
Authors: N. P. Campbell, R. Kunnavakkam, N. B. Leighl, M. D. Vincent, D. R. Gandara, M. Koczywas, B. J. Gitlitz, E. S. Agamah, S. P. Thomas, W. M. Stadler, E. E. Vokes, H. L. Kindler
Journal: Journal of Clinical Oncology (2011)

7027 Background: Vascular endothelial growth factor (VEGF) signaling plays a key role in MM biology. In preclinical models, agents that target VEGF inhibit MM growth. In phase II trials, several VEGF inhibitors have demonstrated modest activity in MM pts. We performed a multi-center phase II trial of C, an oral tyrosine kinase inhibitor of VEGFR 1, 2, 3 and PDGFR-α, in MM pts. Methods: Eligible pts had unresectable, histologically-confirmed MM, measurable disease, and PS 0-1. No more than 1 prior regimen of chemotherapy was permitted. C was initially dosed at 45 mg orally daily. Due to toxicity, an amendment in 6/07 decreased the dose to 30 mg daily. CT scans were obtained Q2 28-day cycles. Primary endpoint: objective response rate. A Simon, optimal, 2-stage design required 3 responses in 21 pts to proceed to a 2nd stage, and 8 responses in 50 MM pts for further investigation. Results: 50 pts enrolled 3/06-9/10 at 9 centers. Pt characteristics: male 84%; median age 64 (range 44-81); PS 0/1: 30%/70%; disease site pleural/peritoneal: 94%/6%; epithelial/sarcomatoid/biphasic/unknown: 72%/4%/12%/12%; prior chemotherapy: 88%; thrombocytosis: 26%. Median cycles delivered: 2 (range 1-14); 48% pts required dose reduction. Discontinued C for toxicity: 26% of all pts, 47% of pts at 45 mg dose. Partial responses (PR): 10% (3/15 pts at 45 mg, 2/35 pts at 30 mg), stable disease (SD): 34% (7/15 pts at 45 mg, 10/35 pts at 30 mg). Disease control rate (PR + SD): 44%. Median response duration: 8.3 mo (range 7.3-12.9). Survival: median progression-free: 1.9 mo (95% CI: 0.1, 14.2); median overall: 4.4 mo (95% CI: 0.9, 41.7); 1-year: 15%. Grade 3/4 toxicity: fatigue 24%, hypertension 22%, diarrhea 8%, hyponatremia 6%, thrombosis 6%, acute renal failure 4%, mucositis 4%, angioedema 2%, arrhythmia 2%, headache 2%, obstruction 2%, posterior leukoencephalopathy 2%, seizure 2%. Conclusions: This trial did not meet its prespecified response endpoint. The 45 mg dose of C was poorly tolerated. Supported by NCI grant N01-CM-62201.
Four Genetic Lymphoma-Specific Events (MYC, BCL2, BCL6 and CCND1) in High Grade B-Cell Lymphoma: Aggressive Mantle Cell Lymphoma or Cyclin D1-Positive DLBCL?
Authors: Antoine Ittel, Catherine Helias, Laurie Monier, Marie-Pierrette Chenard, Marie-Pierre Wissler, Elise Toussaint, Carine Gervais, Laurent Mauvieux
Journal: Blood (2014)
Age Distribution and Pattern of Myeloid Marrow Mutations in Patients (pts) with Higher-Risk Myelodysplastic Syndromes (HR-MDS) after Failure of Hypomethylating Agents (HMAs)
Authors: Ghulam J Mufti, Lewis R. Silverman, Steven Best, Steve Fructman, Nozar Azarnia, Michael E. Petrone, Guillermo Garcia-Manero
Journal: Blood (2015)
Chemical Genomic Screening Reveals That PI3K/mTOR Inhibition Enhances Activity of the Anti-Leukemia Stem Cell Compound Parthenolide.
Authors: Duane Hassane, Siddhartha Sen, Cheryl A Corbett, Marlene Balys, Randall M Rossi, Peter A Crooks, Monica L. Guzman, Craig T. Jordan
Journal: Blood (2009)
Abstract 4581: Genetic variations in CDKN1A and RHPN2 associated with prognosis for patients with colorectal cancer
Authors: Byung Woog Kang, Jong Gwang Kim, Yee Soo Chae, Shin Yup Lee, Soo Jung Lee, Shinkyo Yoon
Journal: Cancer Research (2015)

Abstract Genome-wide association studies (GWASs) have already identified at least 22 common susceptibility loci associated with an increased risk of colorectal cancer (CRC). This study examined the relationship between these single nucleotide polymorphisms (SNPs) and the clinical outcomes of patients with colorectal cancer. Seven hundred seventy-six patients with surgically resected colorectal adenocarcinoma were enrolled in the present study. Twenty-two of the GWAS-identified SNPs were genotyped using a Sequenom MassARRAY. Among the 22 SNPs, two (rs1321311G&amp;gt;T in CDKN1A and rs10411210C&amp;gt;T in RHPN2) were significantly associated with the survival outcomes of CRC in a multivariate survival analysis. In a recessive model, the rs1321311 TT genotype (vs. GG + GT) and rs10411210 TT genotype (vs. CC + CT) were associated with a worse prognosis for disease-free survival (adjusted HR = 1.90; 95% confidence interval = 1.00-3.60; P = 0.050, adjusted HR = 1.94; 95% confidence interval = 1.05-3.57; P = 0.034, respectively) and overall survival (adjusted HR = 2.05; 95% confidence interval = 1.00-4.20; P = 0.049, adjusted HR = 2.06; 95% confidence interval = 1.05-4.05; P = 0.036, respectively). None of the other SNPs was significantly associated with any clinicopathologic features or survival. The present results suggest that the genetic variants of the CDKN1A (rs1321311) and RHPN2 (rs10411210) genes can be used as prognostic biomarkers for patients with surgically resected colorectal cancer. Citation Format: Byung Woog Kang, Jong Gwang Kim, Yee Soo Chae, Shin Yup Lee, Soo Jung Lee, Shinkyo Yoon. Genetic variations in CDKN1A and RHPN2 associated with prognosis for patients with colorectal cancer. [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 4581. doi:10.1158/1538-7445.AM2015-4581
Limited Value of the Multi‐Biomarker Disease Activity Assay Compared to the Routine Assessment of Patient Index Data 3 (RAPID3) Score in the Prognosis of Important Clinical Outcomes in Rheumatoid Arthritis: Comment on the Article by Fleischmann et al and Accompanying Editorial by Davis
Authors: Theodore Pincus, Joel A. Block, Yusuf Yazici, Martin J. Bergman, Tuulikki Sokka
Journal: Arthritis & Rheumatology (2016)
269. Ultrasound-Targeted Delivery of Chemotherapeutic Drug and Nucleic Acids By Gas-Filled Cationic Liposomes
Authors: Anthony Delalande, Simona Manta, Luka Horvat, Safia Ezzine, Michel Bessodes, Patrick Midoux, Paul-Alain Jaffres, Nathalie Mignet, Chantal Pichon
Journal: Molecular Therapy (2015)

Ultrasound is widely used in the medical imaging field for diagnostic purposes. Twenty years ago, their use has turned to therapeutic applications for musculoskeletal disorders mainly The invention of gas microbubble ultrasound contrast agent was the trigger of a large number of studies on extra-molecules delivery into cells by coupling ultrasound and gas microbubbles. This technique called sonoporation has the advantage to deliver locally drugs near or loaded inside microbubbles. Gas microbubble is therefore serves as a drug reservoir that could be triggered by ultrasound.
Recombinant Circularly Permuted TRAIL (CPT) for the Treatment of Relapsed or Refractory Multiple Myeloma: An Open-Label, Multicenter Phase II Clinical Trial
Authors: Wenming Chen, Lugui Qiu, Jian Hou, Yaozhong Zhao, Ling Pan, Shifang Yang, Yun Leng, Hao Xi, Xuejun Zhang, Junsheng Cui, Na Wei
Journal: Blood (2012)
407. Sensitivity and Reproducibility of a Metabolic Assay for Quality Control of Cell Therapy Lots
Authors: Kavita Gupta, Gala Dulatova, Terry Tandeski, Kevin Foley, Lara I. Silverman
Journal: Molecular Therapy (2015)

Determining cell viability via dye exclusion assays (ie; Trypan Blue, TB) is routinely used in lot release testing of cell therapy products. However, such assays provide a limited snapshot of viability and may not be adequate for monitoring the overall quality of cells intended for clinical use, where injection of nonviable cells could lead to safety issues. TB assay may show high viability at thaw, but could fail to capture cryopreservation-driven apoptosis seen after 24 hours. We developed a custom assay based upon resazurin dye conversion to assess changes in cell metabolic activity after cryopreservation.
A retrospective study of early toxicity of weekly paclitaxel as second line chemotherapy for advanced gastric cancer
Authors: Hiroyuki Arai, Shuichi Hironaka, Takuto Suzuki, Kentaro Sudo, Kazuyoshi Nakamura, Keiko Minashi, Taro Hara, Tadamichi Denda, Taketo Yamaguchi
Journal: Annals of Oncology (2015)
PI3K Inhibition Reduces Mammary Tumor Growth and Facilitates Antitumor Immunity and Anti-PD1 Responses
Authors: Jiqing Sai, Philip Owens, Sergey V. Novitskiy, Oriana E. Hawkins, Anna E. Vilgelm, Jinming Yang, Tammy Sobolik, Nicole Lavender, Andrew C. Johnson, Colt McClain, Gregory D. Ayers, Mark C. Kelley, Melinda Sanders, Ingrid A. Mayer, Harold L. Moses, Mark Boothby, Ann Richmond
Journal: Clinical Cancer Research (2016)

Abstract Purpose: Metastatic breast cancers continue to elude current therapeutic strategies, including those utilizing PI3K inhibitors. Given the prominent role of PI3Kα,β in tumor growth and PI3Kγ,δ in immune cell function, we sought to determine whether PI3K inhibition altered antitumor immunity. Experimental Design: The effect of PI3K inhibition on tumor growth, metastasis, and antitumor immune response was characterized in mouse models utilizing orthotopic implants of 4T1 or PyMT mammary tumors into syngeneic or PI3Kγ-null mice, and patient-derived breast cancer xenografts in humanized mice. Tumor-infiltrating leukocytes were characterized by IHC and FACS analysis in BKM120 (30 mg/kg, every day) or vehicle-treated mice and PI3Kγnull versus PI3KγWT mice. On the basis of the finding that PI3K inhibition resulted in a more inflammatory tumor leukocyte infiltrate, the therapeutic efficacy of BKM120 (30 mg/kg, every day) and anti-PD1 (100 μg, twice weekly) was evaluated in PyMT tumor–bearing mice. Results: Our findings show that PI3K activity facilitates tumor growth and surprisingly restrains tumor immune surveillance. These activities could be partially suppressed by BKM120 or by genetic deletion of PI3Kγ in the host. The antitumor effect of PI3Kγ loss in host, but not tumor, was partially reversed by CD8+ T-cell depletion. Treatment with therapeutic doses of both BKM120 and antibody to PD-1 resulted in consistent inhibition of tumor growth compared with either agent alone. Conclusions: PI3K inhibition slows tumor growth, enhances antitumor immunity, and heightens susceptibility to immune checkpoint inhibitors. We propose that combining PI3K inhibition with anti-PD1 may be a viable therapeutic approach for triple-negative breast cancer. Clin Cancer Res; 23(13); 3371–84. ©2016 AACR.
Abstract POSTER-BIOL-1308: Macrophage infiltration in high-grade serous carcinomas of humans and mice
Authors: Tanja Pejovic, Yukie Bean, Jaeyeon Kim, Martin M. Matzuk, Seth B. Coffelt
Journal: Clinical Cancer Research (2015)

Abstract Over the past 10-15 years, focus on the immune system has reinvigorated cancer research and oncology. Both clinical and experimental evidence generated during this time has shown that immune cells and their molecular mediators represent viable targets for therapeutic manipulation. The immune cell composition of high-grade serous carcinoma (HGSC) consists primarily of macrophages and various T cell subsets. However, the functional contribution of each of these cell types is largely unknown. In order to gain insight into whether these cells are pro- or anti-tumorigenic, we generated tissue microarrays containing tumors from 169 patients with pretreated ovarian cancer and quantified the number of CD68+ macrophages in each biopsy. Tumors were divided into high- or low-infiltrated groups based on the median number of macrophages amongst all HGSCs. Interestingly, patients whose tumors were highly infiltrated with macrophages exhibited worsened overall survival, suggesting that macrophages function as pro-tumorigenic cells in these tumors. To investigate the role of macrophages in HGSC progression, we have begun to characterize their abundance and phenotype in tumors of Dicerflox/flox;Ptenflox/flox;Amhr2cre/+ mice, a genetically engineered mouse model of HGSC. Macrophages constituted the predominant stromal and immune cell population in both primary tumors and secondary metastatic lesions. By contrast, macrophages were only found at low frequency in normal oviduct and ovaries. Gene expression analysis of these Dicer/Pten-deficient mouse tumors also revealed the increase in many macrophage-associated genes, as compared with normal oviduct tissue. Taken together, our data from mice and humans strongly indicate a crucial role for macrophages in facilitating ovarian cancer progression. Current efforts are underway to understand how macrophages promote ovarian tumor progression. Citation Format: Tanja Pejovic, Yukie Bean, Jaeyeon Kim, Martin M. Matzuk, Seth B. Coffelt. Macrophage infiltration in high-grade serous carcinomas of humans and mice [abstract]. In: Proceedings of the 10th Biennial Ovarian Cancer Research Symposium; Sep 8-9, 2014; Seattle, WA. Philadelphia (PA): AACR; Clin Cancer Res 2015;21(16 Suppl):Abstract nr POSTER-BIOL-1308.
Consolidation with Alemtuzumab Improves Progression-Free Survival in Patients with Chronic Lymphocytic Leukemia (CLL) in First Remission - Long-Term Follow-Up of a Randomized Phase III Trial of the German CLL Study Group (GCLLSG).
Authors: C. Schweighofer, M. Ritgen, B. Eichhorst, R. Busch, M. Kneba, M. Hallek, Clemens Wendtner
Journal: Blood (2006)
641. Cancer Detection Via Expression-Targeted Gene Delivery in Transitional Cell Carcinoma
Authors: Yunlan Fang, W. Godbey
Journal: Molecular Therapy (2015)

Expression-targeted gene delivery was used to detect cancer cells by delivering exogenous secretory reporter genes into them under the control of cancer-specific promoters. Almost all cancer biomarkers currently in use are secreted proteins or cell surface proteins. Our strategy takes advantage of cancer-specific promoters, even those associated with exons encoding proteins that are not secreted. Plasmids that coupled such promoters with exons encoding secretable (and excretable) reporters were constructed. This strategy has yielded relatively high reporter expression in cancer cells as compared to normal cells and tissues, both in vitro in cell supernatants and in vivo, as detected in mouse urine. This technology could be used eventually for early cancer detection or the detection of cancer cells remaining following tumorectomy. Gaussia luciferase (LUC) is a secreted protein that has been used for monitoring bioprocesses. Plasmids carrying luc, driven by the promoters for cyclooxygenase type 2 (Pcox2), osteopontin (Popn), or the universally strong cytomegalovirus promoter (Pcmv) (used as a positive control) were constructed and delivered to cells using the branched polycation poly(ethyleneimine). The empty pUC19 vector was used as a negative control. The reporter levels detected in cell supernatants via a Gaussia luciferase assay showed that Pcox2- or Popn-driven luc expression was significantly higher in the bladder cancer cell line MB49 versus normal murine fibroblasts. In vivo experiments in an orthotopic model of transitional cell carcinoma showed that delivery of Pcox2-luc into tumor-bearing mice yielded detectable LUC excretion that was significantly higher versus negative controls. Interestingly, tumor-bearing mice excreting LUC did so with a 24-hour periodicity. This seemingly circadian phenomenon was counterintuitive. The implanted cells did not have synchronous cell cycles upon instillation 8 days prior, and had not developed organized vascular networks (data not shown). Urine concentration also was not seen as a factor, since total LUC per sample was quantified, and such values are independent of concentration. Circadian products known to be excreted in the urine were administered to transfected cells in vitro with no effects upon LUC expression. It was ultimately determined that urine collected at the onset of mouse morning (6:00 pm, mice being nocturnal), contained an agent that masked the detection of LUC. It was also found that serum shock could also induce increased LUC detection in vitro. Additional human reporters, including secreted alkaline phosphatase, human chorionic gonadotropin, and prostate-specific antigen were examined in this study for the purpose of developing a non-invasive urinary lateral flow assay for cancer detection which would detect more than one reporter protein simultaneously by delivering multiple plasmids containing different cancer-specific promoters.
Clinical Significance of Molecular Monitoring in Chronic Myeloid Leukemia (CML) in Chronic Phase (CP) with Imatinib Therapy.
Authors: Jorge Cortes, Moshe Talpaz, Susan O’Brien, Dan Jones, Raja Luthra, Guillermo Garcia-Manero, Francis Giles, Jenny Shan, Srdan Verstovsek, Mary Beth Rios, Hagop Kantarjian
Journal: Blood (2004)