tbuckley/cabot-search huggingface dataset:
IRS2 Associates With JAK2 and May Be Involved In Cell Proliferation Pathways In Chronic Myeloproliferative Neoplasms
Authors: Paula de Melo Campos, Joao Machado-Neto, Adriana Silva Santos Duarte, Rafaela Mendonça, Irene Lorand-Metze, Fernando F. Costa, Sara T O Saad, Fabiola Traina
Journal: Blood (2013)
Cathepsin B modulates lysosomal biogenesis and host defense against <i>Francisella novicida</i> infection
Authors: Xiaopeng Qi, Si Ming Man, R.K. Subbarao Malireddi, Rajendra Karki, Christopher Lupfer, Prajwal Gurung, Geoffrey Neale, Clifford S. Guy, Mohamed Lamkanfi, Thirumala-Devi Kanneganti
Journal: The Journal of Experimental Medicine (2016)

Lysosomal cathepsins regulate an exquisite range of biological functions, and their deregulation is associated with inflammatory, metabolic, and degenerative diseases in humans. In this study, we identified a key cell-intrinsic role for cathepsin B as a negative feedback regulator of lysosomal biogenesis and autophagy. Mice and macrophages lacking cathepsin B activity had increased resistance to the cytosolic bacterial pathogen Francisella novicida. Genetic deletion or pharmacological inhibition of cathepsin B down-regulated mechanistic target of rapamycin activity and prevented cleavage of the lysosomal calcium channel TRPML1. These events drove transcription of lysosomal and autophagy genes via transcription factor EB, which increased lysosomal biogenesis and activation of autophagy initiation kinase ULK1 for clearance of the bacteria. Our results identified a fundamental biological function of cathepsin B in providing a checkpoint for homeostatic maintenance of lysosome populations and basic recycling functions in the cell.
Lupus high-density lipoprotein induces proinflammatory responses in macrophages by binding lectin-like oxidised low-density lipoprotein receptor 1 and failing to promote activating transcription factor 3 activity
Authors: Carolyne K Smith, Nickie L Seto, Anuradha Vivekanandan-Giri, Wenmin Yuan, Martin P Playford, Zerai Manna, Sarfaraz A Hasni, Rui Kuai, Nehal N Mehta, Anna Schwendeman, Subramaniam Pennathur, Mariana J Kaplan
Journal: Annals of the Rheumatic Diseases (2016)

Recent evidence indicates that high-density lipoprotein (HDL) exerts vasculoprotective activities by promoting activating transcription factor 3 (ATF3), leading to downregulation of toll-like receptor (TLR)-induced inflammatory responses. Systemic lupus erythematosus (SLE) is associated with increased cardiovascular disease risk not explained by the Framingham risk score. Recent studies have indicated oxidised HDL as a possible contributor. We investigated the potential mechanisms by which lupus HDL may lose its anti-inflammatory effects and promote immune dysregulation.
Open-label, randomized study of individualized, pharmacokinetically (PK)-guided dosing of paclitaxel combined with carboplatin or cisplatin in patients with advanced non-small-cell lung cancer (NSCLC)
Authors: M. Joerger, J. von Pawel, S. Kraff, J.R. Fischer, W. Eberhardt, T.C. Gauler, L. Mueller, N. Reinmuth, M. Reck, M. Kimmich, F. Mayer, H.-G. Kopp, D.M. Behringer, Y.-D. Ko, R.A. Hilger, M. Roessler, C. Kloft, A. Henrich, B. Moritz, M.C. Miller, S.J. Salamone, U. Jaehde
Journal: Annals of Oncology (2016)
Abnormal Mirna Expression Profile and Cytokine Production in Myelodysplastic Vascular Niche
Authors: Maurizio Martini, Luciana Teofili, Sara Capodimonti, Eugenia Rosa Nuzzolo, Maria Grazia Iachininoto, Alessandra Cocomazzi, Maria Teresa Voso, Luigi Maria Larocca
Journal: Blood (2014)
Особливості моторно-евакуаторної функції кишечника в пацієнтів із різними формами синдрому подразненого кишечника
Authors: S.A. Nagieva, A.S. Svintsytskyi, N.Ye. Dolgaya, I.V. Korendovych
Journal: GASTROENTEROLOGY (2016)

Для оцінки моторно-евакуаторної функції шлунково-кишкового тракту при синдромі подразненого кишечника (СПК) можливе використання ряду методів. Мета даного дослідження полягала в тому, щоб вивчити моторику товстого кишечника у хворих на різні клінічні варіанти СПК, використовуючи метод динамічної сцинтиграфії. Матеріали та методи. У дослідження було включено 107 пацієнтів із СПК (згідно з Римськими критеріями III (2006)). Усі пацієнти були розподілені на 4 групи: I група — хворі на СПК із запором (36 осіб — 33,6 %), II група — на СПК із діареєю (35 — 32,7 %), III група — на неспецифічний варіант СПК (22 — 20,7 %), IV група — на змішаний варіант СПК (14 — 13,0 %). Динамічна сцинтиграфія була виконана з використанням сцинтиляційної гамма-камери OFECT‑1 і електронно-розрахункової машини. Середня активність радіофармпрепаратів (РФП) була взята в розмірі 10 МБк/кг маси тіла пацієнта. Результати. Результати показали, що при СПК із запором проходження РФП зменшується (збільшується радіоактивність у ділянці живота (&gt; 60 %), асиметрія правої та лівої частини кишечника — &lt; 31 %, р &lt; 0,05 у всіх випадках). При СПК із діареєю швидкість проходження РФП збільшилася (радіоактивність у ділянці живота &lt; 60 %, асиметрія правої та лівої частини кишечника &gt; 25 %, р &lt; 0,05 у всіх випадках). Статистично значимих змін у моториці при неспецифічному та змішаному варіанті СПК не виявлено (р &gt; 0,05). Висновок. Використовуючи метод динамічної сцинтиграфії, ми виявили помітне уповільнення проходження РФП у хворих на СПК із запором (р &lt; 0,05), тоді як при СПК із діареєю швидкість проходження РФП була збільшена (р &lt; 0,05). При інших варіантах СПК не було виявлено статистично значимих змін.
Dual CD19 and CD123 targeting prevents antigen-loss relapses after CD19-directed immunotherapies
Authors: Marco Ruella, David M. Barrett, Saad S. Kenderian, Olga Shestova, Ted J. Hofmann, Jessica Perazzelli, Michael Klichinsky, Vania Aikawa, Farzana Nazimuddin, Miroslaw Kozlowski, John Scholler, Simon F. Lacey, Jan J. Melenhorst, Jennifer J.D. Morrissette, David A. Christian, Christopher A. Hunter, Michael Kalos, David L. Porter, Carl H. June, Stephan A. Grupp, Saar Gill
Journal: Journal of Clinical Investigation (2016)

Potent CD19-directed immunotherapies, such as chimeric antigen receptor T cells (CART) and blinatumomab, have drastically changed the outcome of patients with relapsed/refractory B cell acute lymphoblastic leukemia (B-ALL). However, CD19-negative relapses have emerged as a major problem that is observed in approximately 30% of treated patients. Developing approaches to preventing and treating antigen-loss escapes would therefore represent a vertical advance in the field. Here, we found that in primary patient samples, the IL-3 receptor α chain CD123 was highly expressed on leukemia-initiating cells and CD19-negative blasts in bulk B-ALL at baseline and at relapse after CART19 administration. Using intravital imaging in an antigen-loss CD19-negative relapse xenograft model, we determined that CART123, but not CART19, recognized leukemic blasts, established protracted synapses, and eradicated CD19-negative leukemia, leading to prolonged survival. Furthermore, combining CART19 and CART123 prevented antigen-loss relapses in xenograft models. Finally, we devised a dual CAR-expressing construct that combined CD19- and CD123-mediated T cell activation and demonstrated that it provides superior in vivo activity against B-ALL compared with single-expressing CART or pooled combination CART. In conclusion, these findings indicate that targeting CD19 and CD123 on leukemic blasts represents an effective strategy for treating and preventing antigen-loss relapses occurring after CD19-directed therapies.
Fat pads adjacent to tendinopathy: more than a coincidence?
Authors: Ella Rose Ward, Gustav Andersson, Ludvig J Backman, Jamie E Gaida
Journal: British Journal of Sports Medicine (2016)

Is it merely a curiosity that fat pads are found adjacent to the area of tendon affected by tendinopathy? We propose that fat pads share an anatomical and functional relationship with their adjacent tendons and may therefore contribute to the pathogenesis of tendinopathy. Fat pads and tendons have a shared blood supply,1 and cytokines produced in the fat pad have only a short distance to travel in order to affect the tendon.2

Fat pads lubricate, insulate, protect and provide structural support for tendons. However, the functional significance of the fat pad is often overlooked. In an early study of fat pad function, the distal tip of Kager's fat pad migrated into the retrocalcaneal bursa during ankle movement in healthy individuals, but not in an individual with a hindfoot disorder.3 This ‘variable plunger’ mechanism minimises pressure changes within the bursa during ankle movement. …
Oral inflammation and infection, and chronic medical diseases: implications for the elderly
Authors: Frank A. Scannapieco, Albert Cantos
Journal: Periodontology 2000 (2016)

Abstract Oral diseases, such as caries and periodontitis, not only have local effects on the dentition and on tooth‐supporting tissues but also may impact a number of systemic conditions. Emerging evidence suggests that poor oral health influences the initiation and/or progression of diseases such as atherosclerosis (with sequelae including myocardial infarction and stoke), diabetes mellitus and neurodegenerative diseases (such as Alzheimer's disease, rheumatoid arthritis and others). Aspiration of oropharyngeal (including periodontal) bacteria causes pneumonia, especially in hospitalized patients and the elderly, and may influence the course of chronic obstructive pulmonary disease. This article addresses several pertinent aspects related to the medical implications of periodontal disease in the elderly. There is moderate evidence that improved oral hygiene may help prevent aspiration pneumonia in high‐risk patients. For other medical conditions, because of the absence of well‐designed randomized clinical trials in elderly patients, no specific guidance can be provided regarding oral hygiene or periodontal interventions that enhance the medical management of older adults.
Happle-Tinschert syndrome can be caused by a mosaic<i>SMO</i>mutation and is suggested to be a variant of Curry-Jones syndrome: reply from the authors
Authors: Z. Khamaysi, E. Sprecher, R. Bergman
Journal: British Journal of Dermatology (2016)

We read with interest Happle and Tinschert's comment ‘Happle–Tinschert syndrome can be caused by a mosaic SMO mutation and is suggested to be a variant of Curry–Jones syndrome’.1

We believe that our case belongs to the spectrum of Gorlin syndrome (MIM #109400) because most of the biopsies in our patient demonstrated classical nodular, pigmented, adenoid and superficial basal cell carcinomas (BCCs) (Fig. 2a–c in our article).2 This is not congruent with the findings typical of Happle–Tinschert syndrome (HTS), in which the skin lesions are basaloid follicular hamartomas (BFHs) by definition.

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<i>DPYD c.1905+1G&gt;A and c.2846A&gt;T</i> and <i>UGT1A1*28</i> allelic variants as predictors of toxicity: Pharmacogenetic translational analysis from the phase III TRIBE study in metastatic colorectal cancer.
Authors: Marzia Del Re, Chiara Cremolini, Fotios Loupakis, Federica Marmorino, Valentina Citi, Marta Palombi, Francesca Bergamo, Marta Schirripa, Daniele Rossini, Enrico Cortesi, Gianluca Tomasello, Rosella Spadi, Angela Buonadonna, Domenico Amoroso, Stefano Vitello, Samantha Di Donato, Cristina Granetto, Mauro D'Amico, Romano Danesi, Alfredo Falcone
Journal: Journal of Clinical Oncology (2015)

3532 Background: Adverse drug reactions (ADRs) caused by fluoropyrimidines depend, at least in part, from DPD deficiency resulting from the loss-of-function mutations c.1905+1G > A and c.2846A > T. Moreover, irinotecan ADRs appear frequently in patients bearing the UGT1A1*28 variant, associated with reduced UGT1A1 expression. In this study, we analyse the association between DPYD and UGT variants with ADRs by 5-fluorouracil and irinotecan in subjects enrolled within the phase III TRIBE study, whose final results have been recently reported. Methods: Out of 508 randomized patients, blood samples for pharmacogenetic analyses were available for 440 patients. DNA was extracted from 200 μl of blood and analyses of DPYD c.1905+1G > A, c.2846T > C and UGT1A1*28 was performed by a Pyrosequencing platform (Qiagen, USA). The study was approved by the local Ethics Committee. Results: Each of the DPYD c.1905+1GA and c.2846AT genotypes were found in 5 out of 440 subjects, with a combined frequency of 2.2%. c.1905+1GA and c.2846AT had the same impact on ADRs and, taken together, patients bearing these variants (N = 10) had an increased risk of G3/4 neutropenia (OR: 4.14, p = 0.043) and stomatitis (OR: 10.36, p = 0.003) as compared to wild-type patients. Five out of 10 DPYD mutant patients experienced a G4 ADR after the first cycle of therapy. UGT1A1*28/*28 was found in 39/436 patients (8.9%); these patients had an increased risk of G3/4 neutropenia as compared to both *1/*1 (OR: 3.81, p < 0.001) and *1/*28 (OR: 2.28, p = 0.022) genotypes. Patients bearing DPYD c.1905+1GA, c.2846AT and UGT1A1*28/*28 (N = 49) had an increased risk of G3/4 neutropenia (OR: 2.98, p < 0.001), febrile neutropenia (OR: 2.78, p = 0.023) and G3/4 stomatitis (OR: 6.83, p < 0.001). No significant correlation with G3/4 diarrhea was found. Conclusions: DPYD c.1905+1GA, c.2846AT and UGT1A1*28/*28 are associated with a higher risk of G3/4 ADRs also in the TRIBE trial, underscoring the predictive role of DPYD and UGT1A1 variants across various fluoropyrimidine and irinotecan-containing schedules, and therefore their potential usefulness in treatment tailoring.
Nicotinic Acid in NIDDM
Authors: Yaakov Henkin
Journal: JAMA (1990)

<h3>To the Editor.—</h3> Drs Garg and Grundy<sup>1</sup>continue to enhance our knowledge of the treatment of dyslipidemia in non—insulin-dependent diabetes mellitus (NIDDM) with a systematic evaluation of various treatment modalities for this disease. Their article, "Nicotinic Acid as Therapy for Dyslipidemia in Non—Insulin-Dependent Diabetes Mellitus," provides convincing evidence that nicotinic acid causes a deterioration of the glycemic control in patients with diabetes. Although this has been known for a long time, the well-controlled nature of their study provides insight into the incidence and magnitude of this effect. However, a few comments about their study deserve mention. The dose of nicotinic acid used in this study was rigidly set at 4.5 g/d. This is a high dose, almost certainly higher than the average dose used by most clinicians in nondiabetic subjects. Significant modification in all of the lipoprotein components can often be achieved with nicotinic acid doses of 2 to
Circulating tumor cells as prognostic and predictive markers in metastatic breast cancer patients receiving first-line therapy.
Authors: M. Giuliano, A. Giordano, L. Hsu, B. C. Handy, N. T. Ueno, E. Andreopoulou, R. H. Alvarez, V. Valero, G. N. Hortobagyi, M. Cristofanilli
Journal: Journal of Clinical Oncology (2010)

1033 Background: The detection of ≥5 circulating tumor cells (CTC)/7.5 ml of blood in patients (pts) with metastatic breast cancer (MBC) predicts worse progression-free survival (PFS) and overall survival (OS). In this retrospective study we confirmed the prognostic role of CTC and hypothesized a potential predictive value of this marker. Methods: We enumerated CTC by CellSearch in a cohort of 235 newly diagnosed pts with MBC prior to receiving first-line therapy, between September 2004 and November 2009. We compared with log-rank test PFS and OS according to CTC count defined groups (<5 vs. ≥5) and type of systemic therapies: endocrine therapy or different regimens of chemotherapy (CTx). Results: At a median follow-up of 12.5 months (range, 1-59), 69 pts (29%) had died. The prognostic value of CTC was confirmed in the overall population survival analysis. Median PFS was 11.4 months for subjects with CTC<5 and 7.3 months for those with CTC≥5 (p=0.002), median OS was 40.1 and 23.1 months, respectively (p<0.001). These findings were confirmed in the multivariate analysis. Furthermore, in 47 pts receiving endocrine therapy, a count of CTC <5 was associated with better PFS (14.1 vs. 3.5 months; p=0.006) and OS (p=0.002). Of the 109 HER2-negative pts treated with CTx, 64 (59%) received poly-CTx, and 45 (41%) received mono-CTx. Pts receiving poly-CTx had a better PFS than those receiving mono-CTx, independently of CTC count, while a significant improvement in OS was only seen in the CTC≥5 group (p=0.001). Moreover, the addition of bevacizumab to taxane- based mono-CTx (n=33) showed a therapeutic advantage over mono-CTx (n=45), only in pts with CTC≥5 (median PFS: 7.4 vs. 3.6 months respectively, p=.002). Conclusions: Baseline CTC count was confirmed to be a strong prognostic factor in MBC patients receiving first-line systemic therapy. This analysis suggests the prognostic information could be particularly useful in managing pts with ≥5 CTC in which various therapeutic choices (endocrine therapy, poly-CTx and bevacizumab-based therapies) may provide differential palliative benefit. Future prospective trials should investigate the role of CTC in defining personalized therapies in MBC. No significant financial relationships to disclose.
Lineage-specific and single-cell chromatin accessibility charts human hematopoiesis and leukemia evolution
Authors: M Ryan Corces, Jason D Buenrostro, Beijing Wu, Peyton G Greenside, Steven M Chan, Julie L Koenig, Michael P Snyder, Jonathan K Pritchard, Anshul Kundaje, William J Greenleaf, Ravindra Majeti, Howard Y Chang
Journal: Nature Genetics (2016)
Agonistic CD40 mAb-Driven IL12 Reverses Resistance to Anti-PD1 in a T-cell–Rich Tumor
Authors: Shin Foong Ngiow, Arabella Young, Stephen J. Blake, Geoffrey R. Hill, Hideo Yagita, Michele W. L. Teng, Alan J. Korman, Mark J. Smyth
Journal: Cancer Research (2016)

The durability and efficacy of anti-human PD1 monoclonal antibodies (PD1 mAb) vary across different malignancies. Although an absence of tumor-infiltrating cytotoxic T lymphocytes has been identified as a cause for resistance to PD1 mAb, the presence of intratumor exhausted PD1hi T cells also contributes to insensitivity to this immune checkpoint therapy. In this study, we used mouse tumor models of PD1 mAb resistance that harbored PD1hi T cells and flow cytometry analysis of tumor-infiltrating leukocytes immediately post-therapy as a screening platform to identify agents that could resensitize T cells to PD1 blockade. We showed that an agonistic anti-CD40 mAb converted PD1hi T cells into PD1lo T cells, reversing phenotypic T-cell exhaustion and allowing the anti-PD1 refractory tumors to respond to anti-PD1 therapy. PD1 downmodulation by anti-CD40 mAb relied upon IL12 but not IL23, CD80/CD86/CD28, or CD70/CD27. Consistent with a role for regulatory T cells (Treg) in promoting T-cell exhaustion, we also showed that intratumor Treg presented with a less activated and attenuated suppressive phenotype, marked by reductions in CTLA4 and PD1. Similar to anti-CD40 mAb, anti-CTLA4 mAb also lowered intratumor T-cell PD1 expression. Our study provides a proof-of-principle framework to systematically identify immune conditioning agents able to convert PD1hi T cells to PD1lo T cells, with clinical implications in the management of anti-PD1 refractory patients. Cancer Res; 76(21); 6266-77. ©2016 AACR.
EANO guidelines for the diagnosis and treatment of meningiomas
Authors: Roland Goldbrunner, Giuseppe Minniti, Matthias Preusser, Michael D Jenkinson, Kita Sallabanda, Emmanuel Houdart, Andreas von Deimling, Pantelis Stavrinou, Florence Lefranc, Morten Lund-Johansen, Elizabeth Cohen-Jonathan Moyal, Dieta Brandsma, Roger Henriksson, Riccardo Soffietti, Michael Weller
Journal: The Lancet Oncology (2016)
A comparison of clofarabine with ara-C, each in combination with daunorubicin as induction treatment in older patients with acute myeloid leukaemia
Authors: A K Burnett, N H Russell, R K Hills, J Kell, O J Nielsen, M Dennis, P Cahalin, C Pocock, S Ali, S Burns, S Freeman, D Milligan, R E Clark
Journal: Leukemia (2016)

The study was designed to compare clofarabine plus daunorubicin vs daunorubicin/ara-C in older patients with acute myeloid leukaemia (AML) or high-risk myelodysplastic syndrome (MDS). Eight hundred and six untreated patients in the UK NCRI AML16 trial with AML/high-risk MDS (median age, 67 years; range 56–84) and normal serum creatinine were randomised to two courses of induction chemotherapy with either daunorubicin/ara-C (DA) or daunorubicin/clofarabine (DClo). Patients were also included in additional randomisations; ± one dose of gemtuzumab ozogamicin in course 1; 2v3 courses and ± azacitidine maintenance. The primary end point was overall survival. The overall response rate was 69% (complete remission (CR) 60%; CRi 9%), with no difference between DA (71%) and DClo (66%). There was no difference in 30-/60-day mortality or toxicity: significantly more supportive care was required in the DA arm even though platelet and neutrophil recovery was significantly slower with DClo. There were no differences in cumulative incidence of relapse (74% vs 68%; hazard ratio (HR) 0.93 (0.77–1.14), P=0.5); survival from relapse (7% vs 9%; HR 0.96 (0.77–1.19), P=0.7); relapse-free (31% vs 32%; HR 1.02 (0.83–1.24), P=0.9) or overall survival (23% vs 22%; HR 1.08 (0.93–1.26), P=0.3). Clofarabine 20 mg/m2 given for 5 days with daunorubicin is not superior to ara-C+daunorubicin as induction for older patients with AML/high-risk MDS.
CD146-targeted immunoPET and NIRF Imaging of Hepatocellular Carcinoma with a Dual-Labeled Monoclonal Antibody
Authors: Reinier Hernandez, Haiyan Sun, Christopher G. England, Hector F. Valdovinos, Emily B. Ehlerding, Todd E. Barnhart, Yunan Yang, Weibo Cai
Journal: Theranostics (2016)

Overexpression of CD146 has been correlated with aggressiveness, recurrence rate, and poor overall survival in hepatocellular carcinoma (HCC) patients.In this study, we set out to develop a CD146-targeting probe for high-contrast noninvasive in vivo positron emission tomography (PET) and near-infrared fluorescence (NIRF) imaging of HCCs.YY146, an anti-CD146 monoclonal antibody, was employed as a targeting molecule to which we conjugated the zwitterionic near-infrared fluorescence (NIRF) dye ZW800-1 and the chelator deferoxamine (Df).This enabled labeling of Df-YY146-ZW800 with 89 Zr and its subsequent detection using PET and NIRF imaging, all without compromising antibody binding properties.Two HCC cell lines expressing high (HepG2) and low (Huh7) levels of CD146 were employed to generate subcutaneous (s.c.) and orthotopic xenografts in athymic nude mice.Sequential PET and NIRF imaging performed after intravenous injection of 89 Zr-Df-YY146-ZW800 into tumor-bearing mice unveiled prominent and persistent uptake of the tracer in HepG2 tumors that peaked at 31.65 ± 7.15 percentage of injected dose per gram (%ID/g; n=4) 72 h post-injection.Owing to such marked accumulation, tumor delineation was successful by both PET and NIRF, which facilitated the fluorescence image-guided resection of orthotopic HepG2 tumors, despite the relatively high liver background.CD146-negative Huh7 and CD146-blocked HepG2 tumors exhibited significantly lower 89 Zr-Df-YY146-ZW800 accretion (6.1 ± 0.5 and 8.1 ± 1.0 %ID/g at 72 h p.i., respectively; n=4), demonstrating the CD146-specificity of the tracer in vivo.Ex vivo biodistribution and immunofluorescent staining corroborated the accuracy of the imaging data and correlated tracer uptake with in situ CD146 expression.Overall, 89 Zr-Df-YY146-ZW800 showed excellent properties as a PET/NIRF imaging agent, including high in vivo affinity and specificity for CD146-expressing HCC.CD146-targeted molecular imaging using dual-labeled YY146 has great potential for early detection, prognostication, and image-guided surgical resection of liver malignancies.
Cardiac Toxicity Of High Dose Cyclophosphamide Post T Cell Replete HLA Haploidentical Hematopoietic Stem Cell Transplantation
Authors: Laetitia Souchet, Julien Mayaux, Damien Roosweil, Madalina Uzunov, Alfred Le, Charles-Edouard Luyt, Jean Paul Vernant, Françoise Norol, Hélène Treberden-Negre, Nabih Azar, Bénédicte Lebrun-Vigne, Delphine Callot, Ali Boudifa, Veronique Leblond, Stéphanie Nguyen
Journal: Blood (2013)