tbuckley/cabot-search huggingface dataset:
Dysbiosis and zonulin upregulation alter gut epithelial and vascular barriers in patients with ankylosing spondylitis
Authors: Francesco Ciccia, Giuliana Guggino, Aroldo Rizzo, Riccardo Alessandro, Michele Maria Luchetti, Simon Milling, Laura Saieva, Heleen Cypers, Tommaso Stampone, Paola Di Benedetto, Armando Gabrielli, Alessio Fasano, Dirk Elewaut, Giovanni Triolo
Journal: Annals of the Rheumatic Diseases (2017)

Dysbiosis has been recently demonstrated in patients with ankylosing spondylitis (AS) but its implications in the modulation of intestinal immune responses have never been studied. The aim of this study was to investigate the role of ileal bacteria in modulating local and systemic immune responses in AS.Ileal biopsies were obtained from 50 HLA-B27+ patients with AS and 20 normal subjects. Silver stain was used to visualise bacteria. Ileal expression of tight and adherens junction proteins was investigated by TaqMan real-time (RT)-PCR and immunohistochemistry. Serum levels of lipopolysaccharide (LPS), LPS-binding protein (LPS-BP), intestinal fatty acid-BP (iFABP) and zonulin were assayed by ELISA. Monocyte immunological functions were studied in in vitro experiments. In addition the effects of antibiotics on tight junctions in human leukocyte antigen (HLA)-B27 transgenic (TG) rats were assessed.Adherent and invasive bacteria were observed in the gut of patients with AS with the bacterial scores significantly correlated with gut inflammation. Impairment of the gut vascular barrier (GVB) was also present in AS, accompanied by significant upregulation of zonulin, and associated with high serum levels of LPS, LPS-BP, iFABP and zonulin. In in vitro studies zonulin altered endothelial tight junctions while its epithelial release was modulated by isolated AS ileal bacteria. AS circulating monocytes displayed an anergic phenotype partially restored by ex vivo stimulation with LPS+sCD14 and their stimulation with recombinant zonulin induced a clear M2 phenotype. Antibiotics restored tight junction function in HLA-B27 TG rats.Bacterial ileitis, increased zonulin expression and damaged intestinal mucosal barrier and GVB, characterises the gut of patients with AS and are associated with increased blood levels of zonulin, and bacterial products. Bacterial products and zonulin influence monocyte behaviour.
P3.04-018 Recurrence Dynamic of Completely Resected Non-Small Cell Lung Cancer in Perspective of Follow-Up Surveillance
Authors: Eung Rae Kim, In Kyu Park, Kwanyong Hyun, Samina Park, Yoohwa Hwang, Chang Hyun Kang, Young Tae Kim
Journal: Journal of Thoracic Oncology (2017)
Financial impact of coverage for zoledronic acid and denosumab in cancer patients with bone metastases.
Authors: M. W. Russell, M. J. Bell, M. Namjoshi, J. D. Miller
Journal: Journal of Clinical Oncology (2011)

e16515 Background: Zoledronic acid (ZA) has been the mainstay for prevention of skeletal related events (SREs) in patients with bone metastases. FDA recently approved denosumab for prevention of SREs in patients with solid-tumor bone metastases. We assessed the financial impact to a managed-care plan of adding denosumab to formulary for this indication. Methods: We modeled change in spending over 1-3 year time horizons in a hypothetical managed care plan with 1 million members (688 having solid-tumor bone metastases). The model addresses drug use and associated costs (including administration), SRE management, and adverse event (AE) treatment under three scenarios: (1) Base Case—ZA-only formulary; (2) Restricted Formulary—denosumab limited to second-line treatment in patients failing ZA; and (3) Open Formulary—unrestricted dispensing of both drugs. SREs included pathologic fracture, therapeutic radiology, spinal cord compression, and orthopedic surgery. AEs included osteonecrosis of the jaw, renal problems, acute phase reactions, and hypocalcemia. Model parameters were derived from published literature, product labels, clinical trial data, and administrative cost databases. Drug costs were published prices minus expected plan copayments. Costs are stated in 2010 US dollars. Results: Base Case total costs were $10.8 million per year. Restricted access to denosumab increased costs to $11.4, $11.6, and $11.7 million over 1, 2, and 3 years (an additional $0.05, $0.06, and $0.08 per-member per-month and $69, $94, and $115 per ZA-treated member per month). Open access to denosumab further increased total costs to $11.8, $12.3, and $12.8 million over 1, 2, and 3 years (an additional $0.09, $0.13, and $0.17 cents per-member per-month, and $125, $183, and $245 per ZA-treated member per month). Conclusions: With an acquisition cost nearly twice that of ZA, restricted and open access to denosumab is expected to add considerably to patient management costs. Incremental benefits should be weighed carefully against these costs before considering coverage.
Abstract A19: Identification of Heregulin (HRG) expression as a driver of a difficult-to-treat cancer phenotype and development of a companion diagnostic for the HRG-ErbB3 targeting drug seribantumab
Authors: Sara Mathews, Gregory Finn, Arthur J. Kudla, Victoria Rimkunas, Peter Laivins, Gavin MacBeath, Akos Czibere, Jason Baum
Journal: Clinical Cancer Research (2017)

Abstract Heregulin (HRG) is the cognate ligand of the ErbB3 receptor and has been identified as a potent driver of a distinct tumor cell phenotype characterized by enhanced survival that appears to be inherently more resistant to standard of care therapies. Seribantumab (MM-121) is a fully human monoclonal antibody designed to block HRG from binding to ErbB3 and to prevent the establishment of HRG-driven cancer cell survival in response to cytotoxic therapies. Clinical evidence from randomized studies suggests that patients who receive standard therapy have shorter progression-free survival (PFS) when their tumors are positive for HRG RNA expression compared to patients receiving standard therapy with HRG-negative tumors. The addition of seribantumab was able to enhance the anti-tumor effect of these respective standard therapies and prolong PFS in patients with HRG-positive tumors. Profiling data indicates that positive HRG expression can be found in more than a third of most solid tumors identifying a high unmet medical need. In order to identify HRG-driven tumors with a more difficult-to-treat phenotype, an RNA in situ hybridization (ISH) diagnostic assay has been developed. Details will be presented illustrating the benefits of RNA ISH over alternate detection methods for HRG. This includes the visualization of tumor cell HRG expression with high sensitivity and specificity in small tissue specimens such as fine needle aspirates and core needle biopsies. This assay is currently being used to select patients for inclusion into diagnostic-driven clinical studies. Citation Format: Sara Mathews, Gregory Finn, Arthur J. Kudla, Victoria Rimkunas, Peter Laivins, Gavin MacBeath, Akos Czibere, Jason Baum. Identification of Heregulin (HRG) expression as a driver of a difficult-to-treat cancer phenotype and development of a companion diagnostic for the HRG-ErbB3 targeting drug seribantumab. [abstract]. In: Proceedings of the AACR Precision Medicine Series: Targeting the Vulnerabilities of Cancer; May 16-19, 2016; Miami, FL. Philadelphia (PA): AACR; Clin Cancer Res 2017;23(1_Suppl):Abstract nr A19.
APC/C Dysfunction Limits Excessive Cancer Chromosomal Instability
Authors: Laurent Sansregret, James O. Patterson, Sally Dewhurst, Carlos López-García, André Koch, Nicholas McGranahan, William Chong Hang Chao, David J. Barry, Andrew Rowan, Rachael Instrell, Stuart Horswell, Michael Way, Michael Howell, Martin R. Singleton, René H. Medema, Paul Nurse, Mark Petronczki, Charles Swanton
Journal: Cancer Discovery (2017)

Abstract Intercellular heterogeneity, exacerbated by chromosomal instability (CIN), fosters tumor heterogeneity and drug resistance. However, extreme CIN correlates with improved cancer outcome, suggesting that karyotypic diversity required to adapt to selection pressures might be balanced in tumors against the risk of excessive instability. Here, we used a functional genomics screen, genome editing, and pharmacologic approaches to identify CIN-survival factors in diploid cells. We find partial anaphase-promoting complex/cyclosome (APC/C) dysfunction lengthens mitosis, suppresses pharmacologically induced chromosome segregation errors, and reduces naturally occurring lagging chromosomes in cancer cell lines or following tetraploidization. APC/C impairment caused adaptation to MPS1 inhibitors, revealing a likely resistance mechanism to therapies targeting the spindle assembly checkpoint. Finally, CRISPR-mediated introduction of cancer somatic mutations in the APC/C subunit cancer driver gene CDC27 reduces chromosome segregation errors, whereas reversal of an APC/C subunit nonsense mutation increases CIN. Subtle variations in mitotic duration, determined by APC/C activity, influence the extent of CIN, allowing cancer cells to dynamically optimize fitness during tumor evolution. Significance: We report a mechanism whereby cancers balance the evolutionary advantages associated with CIN against the fitness costs caused by excessive genome instability, providing insight into the consequence of CDC27 APC/C subunit driver mutations in cancer. Lengthening of mitosis through APC/C modulation may be a common mechanism of resistance to cancer therapeutics that increase chromosome segregation errors. Cancer Discov; 7(2); 218–33. ©2017 AACR. See related commentary by Burkard and Weaver, p. 134. This article is highlighted in the In This Issue feature, p. 115
Frequency and Prognostic Relevance of Cancer Testis Antigen 45 Expression in Multiple Myeloma
Authors: Valeria C.C. Andrade, Gisele W. B. Colleoni, Andre Luiz Vettore, Maria R. R. Silva, Roberta Spetic Felix, Manuella Sampaio Almeida, Fabricio Carvalho, Marco A. Zago, Otavia L. Caballero, Andrew J. Simpson
Journal: Blood (2008)
Everolimus (EVE) for relapsed/refractory classical Hodgkin lymphoma (cHL): Open-label, single-arm, phase II study.
Authors: Patrick B. Johnston, Lauren C. Pinter-Brown, Jaqueline Willemann Rogerio, Ghulam Warsi, Quincy Chau, Rod Ramchandren
Journal: Journal of Clinical Oncology (2012)

8028 Background: Effective treatment for relapsed/refractory cHL is lacking. The oral mammalian target of rapamycin inhibitor EVE showed promising efficacy and acceptable toxicity in cHL. We conducted a study to confirm EVE safety and efficacy in relapsed/refractory cHL. Methods: In this multicenter, open-label, 2-step, phase 2 study, adults with cHL that progressed after high-dose chemotherapy with autologous hematopoietic stem cell transplant (AHSCT) or a gemcitabine-, vinorelbine-, or vinblastine-containing regimen received EVE 10 mg/d until disease progression or unacceptable toxicity. Response was assessed every 12 wk via integrated positron emission tomography/computed tomography (CT) with contrast or CT with contrast. Primary endpoint was overall response rate (ORR) per modified response criteria for malignant lymphoma. Adverse events (AEs) were assessed during, and for ≥4 wk after, EVE treatment. Results: 55 patients were enrolled. Of the 38 currently evaluable patients, 37% were men, median age was 32.5 y, 53% were pretreated with AHSCT, and 95% were pretreated with gemcitabine, vinorelbine, or vinblastine; 71% had disease progression during previous therapies or discontinued previous treatment due to progression. 23 patients discontinued treatment, most commonly due to disease progression (n = 11). ORR was 37% (Table). Median progression-free survival (PFS) was 7.2 mo. The most common hematologic AEs were thrombocytopenia (39%) and anemia (24%); the most common nonhematologic AEs were fatigue (47%), cough (29%), dyspnea (26%), headache (21%), and rash (21%). Grade 3/4 AEs, most commonly thrombocytopenia (18%), were observed in 45% of patients. Conclusions: EVE showed a favorable ORR and median PFS in the first 38 evaluable patients with highly pretreated, relapsed/refractory cHL. The AE profile was consistent with that previously observed for EVE. These preliminary results confirm those of an earlier study and support further evaluation of EVE in cHL. [Table: see text]
Association of Delayed Adjuvant Chemotherapy With Survival After Lung Cancer Surgery
Authors: Michelle C. Salazar, Joshua E. Rosen, Zuoheng Wang, Brian N. Arnold, Daniel C. Thomas, Roy S. Herbst, Anthony W. Kim, Frank C. Detterbeck, Justin D. Blasberg, Daniel J. Boffa
Journal: JAMA Oncology (2017)

<h3>Importance</h3> Adjuvant chemotherapy offers a survival benefit to a number of staging scenarios in non–small-cell lung cancer. Variable recovery from lung cancer surgery may delay a patient’s ability to tolerate adjuvant chemotherapy, yet the urgency of chemotherapy initiation is unclear. <h3>Objective</h3> To assess differences in survival according to the time interval between non–small-cell lung cancer resection and the initiation of postoperative chemotherapy to determine the association between adjuvant treatment timing and efficacy. <h3>Design, Setting, and Participants</h3> This retrospective observational study examined treatment-naive patients with completely resected non–small-cell lung cancer who received postoperative multiagent chemotherapy between 18 and 127 days after resection between January 2004 and December 2012. The study population was limited to patients with lymph node metastases, tumors 4 cm or larger, or local extension. Patients were identified from the National Cancer Database, a hospital-based tumor registry that captures more than 70% of incident lung cancer cases in the United States. The association between time to initiation of adjuvant chemotherapy and survival was evaluated using Cox models with restricted cubic splines. <h3>Exposures</h3> Adjuvant chemotherapy administered at different time points after surgery. <h3>Main Outcomes and Measures</h3> Effectiveness of adjuvant chemotherapy according to time to initiation after surgery. <h3>Results</h3> A total of 12 473 patients (median [interquartile range] age, 64 [57-70] years) were identified: 3073 patients (25%) with stage I disease; 5981 patients (48%), stage II; and 3419 patients (27%), stage III. A Cox model with restricted cubic splines identified the lowest mortality risk when chemotherapy was started 50 days postoperatively (95% CI, 39-56 days). Initiation of chemotherapy after this interval (57-127 days; ie, the later cohort) did not increase mortality (hazard ratio [HR], 1.037; 95% CI, 0.972-1.105;<i>P</i> = .27). Furthermore, in a Cox model of 3976 propensity-matched pairs, patients who received chemotherapy during the later interval had a lower mortality risk than those treated with surgery only (HR, 0.664; 95% CI, 0.623-0.707;<i>P</i> &lt; .001). <h3>Conclusions and Relevance</h3> In the National Cancer Database, adjuvant chemotherapy remained efficacious when started 7 to 18 weeks after non–small-cell lung cancer resection. Patients who recover slowly from non–small-cell lung cancer surgery may still benefit from delayed adjuvant chemotherapy started up to 4 months after surgery.
P2.01-002 Serum Protein Signature in Lung Cancer Patients and in Patients with Chronic Obstructive Pulmonary Disease
Authors: Janna Berg, Ann Halvorsen, May-Bente Bengtson, Kristin A. Taskén, Gunhild Mælandsmo, Arne Yndestad, Bente Halvorsen, Odd Terje Brustugun, Pål Aukrust, Thor Ueland, Åslaug Helland
Journal: Journal of Thoracic Oncology (2017)
P2.02-062 Alterations in Pulmonary Function Tests Predict the Development of Radiation-Induced Pneumonitis in Advanced NSCLC
Authors: Oscar Arrieta, Rosario Fernandez Plata, Wendy Muñoz Montaño, David Martínez Briseño, Juan Beck Magaña, Cecilia García-Sancho, Francisco Lozano Ruiz, Abigail Guzmán Barragán, Monika Blake Cerda, Luis Torre Bouscoulet
Journal: Journal of Thoracic Oncology (2017)
Detection of B-Cell Clonality in Bone Marrow Is Independent Predictor of Outcome in De Novo Diffuse Large B-Cell Lymphoma Patients Treated with High-Dose Chemotherapy
Authors: Olga A. Gavrilina, Eugene E. Zvonkov, Elena N. Parovichnikova, Andrey B. Sudarikov, Alla M. Kovrigina, Sergey K. Kravchenko, Nelly G. Gabeeva, Aminat U. Magomedova, Valeri G. Savchenko, Sergey M. Kulikov
Journal: Blood (2014)
Treatment of AML with Myelodysplasia Related Changes(AML-MRC) By Sequential Therapy of Azacitidine (AZA) and Intensive Chemotherapy
Authors: Taiichi Kyo, Kouhei Kyo, Kayo Toishikawa, Ryota Imanaka, Tetsuro Ochi, Yuta Katayama, Takeshi Okatani, Mitsuhiro Itagaki, Koji Iwato, Hideki Asaoku
Journal: Blood (2014)
MA07.02 Updated Efficacy and Safety Data from the Phase 2 NP28761 Study of Alectinib in ALK-Positive Non-Small-Cell Lung Cancer
Authors: D. Ross Camidge, Shirish Gadgeel, Sai-Hong Ou, Leena Gandhi, Gregory Riely, Jeremy Cetnar, Howard West, Mark Socinski, Alberto Chiappori, Tarek Mekhail, Bo Chao, Hossein Borghaei, Kathryn Gold, Walter Bordogna, Bogdana Balas, Johannes Noe, Sophie Golding, Ali Zeaiter, Alice Shaw
Journal: Journal of Thoracic Oncology (2017)
Infusion of CD19-Directed and Multivirus Specific Cytotoxic T Lymphocytes After Allogeneic Hematopoietic Stem Cell Transplantation for B Cell Malignancies,
Authors: Conrad Russell Y. Cruz, Kenneth P. Micklethwaite, Barbara Savoldo, Stephanie Ku, Robert A. Krance, Oumar Diouf, Rammurti Kamble, A. John Barrett, Elizabeth J. Shpall, Helen E. Heslop, Cliona M. Rooney, Malcolm K. Brenner, Catherine M. Bollard, Gianpietro Dotti
Journal: Blood (2011)
Co-Acquisition of RUNX1 and CSF3R Mutations Transforms Hematopoietic Progenitor Cells of CN Patients into More Primitive Highly Proliferative Blasts: Evidence in CN Patients and in a Mouse Model
Authors: Olga Klimenkova, Maksim Klimiankou, Amy Schmidt, Carol Stocking, Cornelia Zeidler, Daniel C. Link, Karl Welte, Julia Skokowa
Journal: Blood (2014)
OA02.06 Converting Tumor-Mediated PD-L1 Inhibition into CAR T-Cell Costimulation to Potentiate Thoracic Cancers Immunotherapy
Authors: Aurore Morello, Nan Chen, Leonid Cherkassky, Michel Sadelain, David Jones, Prasad Adusumilli
Journal: Journal of Thoracic Oncology (2017)
P2.02-036 Double Plasty Operation; A Procedure with Pulmonary Arterioplasty and Bronchoplasty against Centrally Located Non-Small Cell Lung Cancer
Authors: Koji Takahashi, Makoto Sonobe, Ryo Miyata, Shigeto Nishikawa, Hiroyuki Cho, Shinya Neri, Takao Nakanishi, Toshi Menju, Hiroshi Date
Journal: Journal of Thoracic Oncology (2017)
PUB095 Computed Tomography Imaging of Superior Vena Cava Involvement in T4-Classed Lung Cancer
Authors: Henda Neji, Salma Jebri, Monia Attia, Ines Baccouche, Mahdi Afrit, Houda Elbanna, Soumaya Laabidi, Saoussen Hantous, Amel Mekkaoui, Khaoula Ben Miled-M'Rad
Journal: Journal of Thoracic Oncology (2017)
Masked Chimeric Antigen Receptor for Tumor-Specific Activation
Authors: Xiaolu Han, Paul D. Bryson, Yifan Zhao, Gunce E. Cinay, Si Li, Yunfei Guo, Natnaree Siriwon, Pin Wang
Journal: Molecular Therapy (2017)

Adoptive cellular therapy based on chimeric antigen receptor (CAR)-engineered T (CAR-T) cells is a powerful form of cancer immunotherapy. CAR-T cells can be redirected to specifically recognize tumor-associated antigens (TAAs) and induce high levels of antitumor activity. However, they may also display "on-target off-tumor" toxicities, resulting from low-level expression of TAAs in healthy tissues. These adverse effects have raised considerable safety concerns and limited the clinical application of this otherwise promising therapeutic modality. To minimize such side effects, we have designed an epidermal growth factor receptor (EGFR)-specific masked CAR (mCAR), which consists of a masking peptide that blocks the antigen-binding site and a protease-sensitive linker. Proteases commonly active in the tumor microenvironment can cleave the linker and disengage the masking peptide, thereby enabling CAR-T cells to recognize target antigens only at the tumor site. In vitro mCAR showed dramatically reduced antigen binding and antigen-specific activation in the absence of proteases, but normal levels of binding and activity upon treatment with certain proteases. Masked CAR-T cells also showed antitumor efficacy in vivo comparable to that of unmasked CAR. Our study demonstrates the feasibility of improving the safety profile of conventional CARs and may also inspire future design of CAR molecules targeting broadly expressed TAAs. Adoptive cellular therapy based on chimeric antigen receptor (CAR)-engineered T (CAR-T) cells is a powerful form of cancer immunotherapy. CAR-T cells can be redirected to specifically recognize tumor-associated antigens (TAAs) and induce high levels of antitumor activity. However, they may also display "on-target off-tumor" toxicities, resulting from low-level expression of TAAs in healthy tissues. These adverse effects have raised considerable safety concerns and limited the clinical application of this otherwise promising therapeutic modality. To minimize such side effects, we have designed an epidermal growth factor receptor (EGFR)-specific masked CAR (mCAR), which consists of a masking peptide that blocks the antigen-binding site and a protease-sensitive linker. Proteases commonly active in the tumor microenvironment can cleave the linker and disengage the masking peptide, thereby enabling CAR-T cells to recognize target antigens only at the tumor site. In vitro mCAR showed dramatically reduced antigen binding and antigen-specific activation in the absence of proteases, but normal levels of binding and activity upon treatment with certain proteases. Masked CAR-T cells also showed antitumor efficacy in vivo comparable to that of unmasked CAR. Our study demonstrates the feasibility of improving the safety profile of conventional CARs and may also inspire future design of CAR molecules targeting broadly expressed TAAs.
P3.02b-026 Association of EGFR Exon 19 Deletion and EGFR-TKI treatment duration with Frequency of T790M Mutation in EGFR-Mutant Lung Cancer Patients
Authors: Norikazu Matsuo, Koichi Azuma, Kazuko Sakai, Akihiko Kawahara, Hidenobu Ishii, Takaaki Tokito, Takashi Kinoshita, Kazuhiko Yamada, Kazuto Nishio, Tomoaki Hoshino
Journal: Journal of Thoracic Oncology (2017)
Immune Reconstitution and Immune Correlates of Clinical Outcome IN Acute LEUKEMIA PATIENTS Treated with Haploidentical STEM CELL TRANSPLANTATION.
Authors: Alessandra Forcina, Maddalena Noviello, Veronica Valtolina, Attilio Bondanza, Daniela Clerici, Luca Vago, Sara Mastaglio, Maria Teresa Lupo-Stanghellini, Katharina Fleischhauer, Consuelo Corti, Massimo Bernardi, Jacopo Peccatori, Claudio Bordignon, Fabio Ciceri, Chiara Bonini
Journal: Blood (2009)
Serum Uric Acid Is a Novel Prognostic Factor in Patients with Primary Systemic Amyloidosis.
Authors: Shaji K. Kumar, Angela Dispenzieri, Martha Q. Lacy, Suzanne R. Hayman, Nelson Leung, Steven R. Zeldenrust, Francis K. Buadi, Robert A. Kyle, Vincent Rajkumar, Morie A. Gertz
Journal: Blood (2007)
Dual Antiplatelet Therapy Versus Aspirin Monotherapy in Diabetics With Multivessel Disease Undergoing CABG
Authors: Sean van Diepen, Valentin Fuster, Subodh Verma, Taye H. Hamza, F. Sandra Siami, Shaun G. Goodman, Michael E. Farkouh
Journal: Journal of the American College of Cardiology (2017)
Recombinant FVIII and FVIIa Added to Flowing Hemophiliac Blood Co-Localize with Platelet Aggregates Adherent to a Collagen Surface, Promoting Local Fibrin Deposition in Wake-like Patterns Around the Aggregates
Authors: Eric F. Grabowski, Bohan Liu, Matthew Gerace, Paul E. Grabowski, Peter Gunnarsson, Mirella Ezban
Journal: Blood (2015)
Distinctive Hematological Abnormalities and GATA1 Mutation Spectra In East Asian Neonates and Children with Down Syndrome
Authors: Hye-Ran Kim, Da-Woon Kim, Hee-Jo Baek, Hoon Kook, Tai- Ju Hwang, Jong-Hee Shin, Soon-Pal Suh, Dong-Wook Ryang, Myung-Geun Shin
Journal: Blood (2010)
P3.02c-040 Checkmate 384: A Phase 3B/4 Dose-Frequency Optimization Trial of Nivolumab in Advanced or Metastatic Non-Small Cell Lung Cancer (NSCLC)
Authors: Ronald Harris, Niels Reinmuth, Paul Mitchell, Jin Zhu, I-Fen Chang, Eric Pichon
Journal: Journal of Thoracic Oncology (2017)