tbuckley/cabot-search huggingface dataset:
Genome-wide association analysis of diverticular disease points towards neuromuscular, connective tissue and epithelial pathomechanisms
Authors: Clemens Schafmayer, James William Harrison, Stephan Buch, Christina Lange, Matthias C Reichert, Philipp Hofer, François Cossais, Juozas Kupcinskas, Witigo von Schönfels, Bodo Schniewind, Wolfgang Kruis, Jürgen Tepel, Myrko Zobel, Jonas Rosendahl, Thorsten Jacobi, Andreas Walther-Berends, Michael Schroeder, Ilka Vogel, Petr Sergeev, Hans Boedeker, Holger Hinrichsen, Andreas Volk, Jens-Uwe Erk, Greta Burmeister, Alexander Hendricks, Sebastian Hinz, Sebastian Wolff, Martina Böttner, Andrew R Wood, Jessica Tyrrell, Robin N Beaumont, Melanie Langheinrich, Torsten Kucharzik, Stefanie Brezina, Ursula Huber-Schönauer, Leonora Pietsch, Laura Sophie Noack, Mario Brosch, Alexander Herrmann, Raghavan Veera Thangapandi, Hans Wolfgang Schimming, Sebastian Zeissig, Stefan Palm, Gerd Focke, Anna Andreasson, Peter T Schmidt, Juergen Weitz, Michael Krawczak, Henry Völzke, Gernot Leeb, Patrick Michl, Wolfgang Lieb, Robert Grützmann, Andre Franke, Frank Lammert, Thomas Becker, Limas Kupcinskas, Mauro D’Amato, Thilo Wedel, Christian Datz, Andrea Gsur, Michael N Weedon, Jochen Hampe
Journal: Gut (2019)

Diverticular disease is a common complex disorder characterised by mucosal outpouchings of the colonic wall that manifests through complications such as diverticulitis, perforation and bleeding. We report the to date largest genome-wide association study (GWAS) to identify genetic risk factors for diverticular disease.Discovery GWAS analysis was performed on UK Biobank imputed genotypes using 31 964 cases and 419 135 controls of European descent. Associations were replicated in a European sample of 3893 cases and 2829 diverticula-free controls and evaluated for risk contribution to diverticulitis and uncomplicated diverticulosis. Transcripts at top 20 replicating loci were analysed by real-time quatitative PCR in preparations of the mucosal, submucosal and muscular layer of colon. The localisation of expressed protein at selected loci was investigated by immunohistochemistry.We discovered 48 risk loci, of which 12 are novel, with genome-wide significance and consistent OR in the replication sample. Nominal replication (p<0.05) was observed for 27 loci, and additional 8 in meta-analysis with a population-based cohort. The most significant novel risk variant rs9960286 is located near CTAGE1 with a p value of 2.3×10-10 and 0.002 (ORallelic=1.14 (95% CI 1.05 to 1.24)) in the replication analysis. Four loci showed stronger effects for diverticulitis, PHGR1 (OR 1.32, 95% CI 1.12 to 1.56), FAM155A-2 (OR 1.21, 95% CI 1.04 to 1.42), CALCB (OR 1.17, 95% CI 1.03 to 1.33) and S100A10 (OR 1.17, 95% CI 1.03 to 1.33).In silico analyses point to diverticulosis primarily as a disorder of intestinal neuromuscular function and of impaired connective fibre support, while an additional diverticulitis risk might be conferred by epithelial dysfunction.
Predicting Risk of Venous Thromboembolism in Multiple Myeloma: The Impede VTE Score
Authors: Kristen M. Sanfilippo, Suhong Luo, Tzu-Fei Wang, Tanya Wildes, Joseph Mikhael, Jesse W. Keller, Theodore S. Thomas, Kenneth R. Carson, Brian F. Gage
Journal: Blood (2018)
Preliminary Results of the Stapled Peptide ALRN-6924, a Dual Inhibitor of MDMX and MDM2, in Two Phase IIa Dose Expansion Cohorts in Relapsed/Refractory TP53 Wild-Type Peripheral T-Cell Lymphoma
Authors: Andrei R. Shustov, Steven M. Horwitz, Jasmine Zain, Manish R Patel, Sanjay Goel, Lubomir Sokol, Funda Meric-Bernstam, Geoffrey Shapiro, Sunita Dwivedy Nasta, Murali Janakiram, David M Weinstock, Ronald Korn, Marie Payton, D. Allen Annis, Dawn Pinchasik, Manuel Aivado, Amitkumar Mehta
Journal: Blood (2018)
AB0688 Pulmonary and thoracİc vascular findings of behÇet’s disease at computed tomography
Authors: N. Işıksalan Özbülbül, D. Üsküdar Cansu, C. Korkmaz
Journal: Annals of the Rheumatic Diseases (2018)

<h3>Background</h3> Behçet disease is a multisystemic and chronic inflammatory disorder with unknown etiology. Pulmonary involvement is relatively infrequent. <h3>Objectives</h3> To investigate the pulmonary parenchymal changes and thoracic vascular abnormalities due to Behçet's disease at computed tomography. <h3>Methods</h3> 21 patients diagnosed with a diagnosis of Behçet's disease between 2004–2017 were evaluated. Clinical, laboratory, and thoracic computed tomography findings were retrospectively evaluated. Also, the immunsupressive treatments of the patients were documented. <h3>Results</h3> 18 of the patients (85.7%) were male. The mean age of the patients was 44.42±11.7 years, onset age of the disease was 32.4±6.4 years, lenght of follow-up was 8.1±2.3 years. 13 of the patients (61.9%) had hemoptysis at the time of initial diagnosis of Behçet's disease. 14 of the patients (66.6%) showed vascular involvement except pulmonary system. Pulmonary atery aneurysm was observed in 9 patients (%42.8). Pulmonary artery thromboembolism was observed in 15 patients (71.4%). Thoracic computed tomography demonstrated that 5 patients (23.8%) with pulmonary infarct, 4 patients (19%) with pulmonary consolidation, 5 patients (23.8%) with ground-glass opacity in the lung representing pulmonary haemorrhage, 2 patients (9.5%) with pleural effusion, 7 patients (33.3%) with nonspesific parenchymal changes, and one patient with focal atelectasis. Also, one of the patients had intracardiac thrombus. Five of the patients were smokers. <h3>Conclusions</h3> Aneurysm of the pulmonary artery with or without thrombosis is the most common manifestation of Behçet's disease. Pulmonary vasculitis and thrombosis of pulmonary vessels result in infarction, hemorraghe, focal atelectasis. Thoracic computed tomography can clearly demonstrate the pulmonary and vascular abnormalities of Behçet's disease. <h3>References</h3> [1] Emad Y, Abdel-Razek N, Gheita T, el-Wakd M, el-Gohary T, Samadoni A. Multislice CT pulmonary findings in Behçet's disease (report of 16 cases). Clin Rheumatol. 2007Jun;26(6):879–84. Epub 2006 Sep 21. [2] Castañer E, Alguersuari A, Gallardo X, Andreu M, Pallardó Y, Mata JM, Ramírez J. When to suspect pulmonary vasculitis: radiologic and clinical clues. Radiographics. 2010 Jan;30(1):33–53. doi:10.1148/rg.301095103 [3] Hiller N, Lieberman S, Chajek-Shaul T, Bar-Ziv J, Shaham D. Thoracic manifestations of Behçet disease at CT. Radiographics. 2004 May-Jun;24(3):801–8. <h3>Disclosure of Interest</h3> None declared
SAT0020 Impact of il12b single nucleotide polymorphisms on circulating pro-inflammatory cytokines il-12p40 and il-23 in ankylosing spondylitis
Authors: M.G. Ivanova, I. Manolova, R. Stoilov, L. Miteva, S. Stanilova
Journal: Annals of the Rheumatic Diseases (2018)

<h3>Background</h3> Ankylosing spondylitis (AS) is an immune-mediated rheumatic disease belonging to the spectrum of axial spondyloarthritides, characterised mainly by chronic inflammatory back pain and radiographic sacroiliitis. Since genetic factors have been shown to be major determinants of susceptibility to the disease and contribute to amplification of immune responses, polymorphic variability in immune response genes are of interest. The interleukin-12p40 gene (IL12B) encodes the p40 polypeptide chain, which, together with p19, composes IL-23, a member of the IL-12 superfamily. <h3>Objectives</h3> In this study, we examined functional association between two <i>IL12B</i> polymorphisms – <i>IL12Bpro</i> (rs17860508) and <i>IL12B 3' UTR</i> A/C (rs3212227), and cytokine production of both pro-inflammatory cytokines IL-12p40 and IL-23 in AS patients. <h3>Methods</h3> A total of 69 AS patients with a mean age 43±16 years and 257 healthy individuals from Bulgarian population were genotyped. Genotyping for the rs3212227 was performed by restriction fragment length polymorphisms-PCR assay and for the rs17860508 by allele specific-PCR. Serum IL-12p40 and IL-23 concentrations measurement was done using ELISA test. <h3>Results</h3> We found significant differences in the genotype (p=0.029) and allele (p=0.006) frequencies of rs17860508 polymorphism between AS patients and controls. An association between AS and the rs17860508 polymorphism was established under the allelic model (allele 2 vs. allele 1; OR=1.698), the dominant model (1.2+2.2 vs. 1.1; OR=2.427), and the co-dominant model (2.2 vs. 1.1; OR=2.812; 1.2 vs. 1.1; OR=2.252). Genotype and allele frequencies of rs3212227 polymorphism of the IL12B were similar in cases and controls. The mean (±SEM) levels of IL-12p40 and IL-23 in AS patients (176.5±20.7 pg/ml; 26.98±3.4 pg/ml, respectively) was significantly higher than in controls (88.8±9.6 pg/ml; 12.1±1.5; respectively) (p&lt;0.001). Stratification based on <i>IL12Bpro</i> revealed significantly higher serum levels of IL-12p40 in AS patients with <i>IL12Bpro</i> 1.1 and 1.2 genotypes than controls. Highest IL-23 serum levels were associated with <i>IL12Bpro</i> 2.2 genotype. With regard of polymorphic variability of <i>IL12B 3' UTR,</i> AC genotype in AS has been linked to a higher IL-12p40 production and lower one of IL-23. <h3>Conclusions</h3> Allelic variants in the <i>IL12B</i> genes have the potential to alter the expression of both IL-12p40 and IL-23 cytokines in specific manner for AS patients. Carriage of the IL12Bpro variant 1-allele and of the 3′-UTR A-allele in the genotype regardless of homo- or heterozygosity could enhance systemic IL-12p40 and IL-23 levels. <h3>Disclosure of Interest</h3> None declared
Optimized FVIII-Domain-Based Chimeric Antigen Receptors to Specifically Target FVIII Inhibitor-Producing B Cells in Hemophilia a
Authors: Vijay Bhoj, Lucy Li, Benjamin J. Samelson-Jones, Bhavya S Doshi, Christoph Ellebrecht, Aimee Payne, Valder R Arruda, Michael C. Milone
Journal: Blood (2018)
AB1040 Is gout a chronic inflammatory disease of a low level of activity?
Authors: M.M. Basaric, N. Damjanov, M. Perovic-Radak
Journal: Annals of the Rheumatic Diseases (2018)

<h3>Objectives</h3> To determine the presence of physical, laboratory and ultrasound (US) signs of inflammation on the affected joints, but also on the joints that in the clinical sense never showed an inflammatory reaction in the intercritical gout period. <h3>Methods</h3> This prospective study included 43 patients (pts.) with diagnosis primary gout (20 with and 23 without acute gout attacks). The research included: demography; medical history; laboratory analyses: sedimentation of erythrocytes (ESR), C reactive proetin (CRP), and serology; physical: detect tender and swollen joint; and US examination detect synovial fluid and hypertrophy, Power Doppler (PD) signal and "double contour" sign on the wrist, first metatarsal joint (MTP1), tibiotalar (TT) joint and knee. <h3>Results</h3> A physical examination showed presence of 78% tender and 43% swollen joints in the group pts. with acute gout attack, but also 23% pts. had painful and 10% swollen joints in the group without acute gout attack (p&lt;0.001). In the group with acute gout attacks the mean ESR was 32.80 mm/L, value CRP was 8.20 mg/L and leukocytes (Le) (9.09 × 10 9/L), and in the group without acute gout attacks SE was 21.60 mm/L median CRP was 6.40 mg/L and also a higher average Le (8.39 × 10 9/L). So we found that there was no statistical difference (p&gt;0.5) in the laboratory parameters (ESR, CRP and Le) between the groups. There was also no statistically significant difference in the findings of US signs of "double contour" (p&gt;0.5), synovial fluid and hypertrophy(p&gt;0.05), per group, but the presence of PD signal statistics was more often observed in a group of patients in an acute gout attack (p&lt;0.05), table 1. <h3>Conclusions</h3> Our results show the presence of laboratory and ultrasound indicators of joint inflammation in gouty patients at the interclinical stage as well as in patients with acute gout attack. The results of this study show that gout is a chronic inflammatory disease of low activity. <h3>Disclosure of Interest</h3> None declared
Effects of Food on the Pharmacokinetics of Nilotinib in Chronic Myeloid Leukemia: Enabling Significant Dose Reduction and Relief of Treatment Burden: The NIFO-Study
Authors: Christel C. Boons, Yvonne den Hartog, Jeroen J. Janssen, Anthe S. Zandvliet, René Vos, Eleonora L. Swart, N. Harry Hendrikse, Jacqueline G. Hugtenburg
Journal: Blood (2018)
Meta-Analysis Illustrates Role of Interferon-γ Signaling in Multiple Myeloma Pathogenesis
Authors: Jihad Aljabban, Nabeal Aljabban, Mohamad Mukhtar, Saad Syed, Ross Wanner, Francesca Cottini, Tiffany Hughes, Kareem Saleh, Evan C Catton, Taylor Gonzalez, Maryam Panahiazar, Dexter Hadley, Don M. Benson
Journal: Blood (2018)
ATF6α downregulation of PPARα promotes lipotoxicity-induced tubulointerstitial fibrosis
Authors: Tzu-Ming Jao, Masaomi Nangaku, Chia-Hsien Wu, Mai Sugahara, Hisako Saito, Hiroshi Maekawa, Yu Ishimoto, Mari Aoe, Tsuyoshi Inoue, Tetsuhiro Tanaka, Bart Staels, Kazutoshi Mori, Reiko Inagi
Journal: Kidney International (2019)

Tubulointerstitial fibrosis is a strong predictor of progression in patients with chronic kidney disease, and is often accompanied by lipid accumulation in renal tubules. However, the molecular mechanisms modulating the relationship between lipotoxicity and tubulointerstitial fibrosis remain obscure. ATF6α, a transcription factor of the unfolded protein response, is reported to be an upstream regulator of fatty acid metabolism. Owing to their high energy demand, proximal tubular cells (PTCs) use fatty acids as their main energy source. We therefore hypothesized that ATF6α regulates PTC fatty acid metabolism, contributing to lipotoxicity-induced tubulointerstitial fibrosis. Overexpression of activated ATF6α transcriptionally downregulated peroxisome proliferator–activated receptor-α (PPARα), the master regulator of lipid metabolism, leading to reduced activity of fatty acid β-oxidation and cytosolic accumulation of lipid droplets in a human PTC line (HK-2). ATF6α-induced lipid accumulation caused mitochondrial dysfunction, enhanced apoptosis, and increased expression of connective tissue growth factor (CTGF), as well as reduced cell viability. Atf6α-/- mice had sustained expression of PPARα and less tubular lipid accumulation following unilateral ischemia-reperfusion injury (uIRI), resulting in the amelioration of apoptosis; reduced expression of CTGF, α-smooth muscle actin, and collagen I; and less tubulointerstitial fibrosis. Administration of fenofibrate, a PPARα agonist, reduced lipid accumulation and tubulointerstitial fibrosis in the uIRI model. Taken together, these findings suggest that ATF6α deranges fatty acid metabolism in PTCs, which leads to lipotoxicity-mediated apoptosis and CTGF upregulation, both of which promote tubulointerstitial fibrosis.
AB1415-HPR Differences on pain and structural anormalities between patients with rheumatoid arthritis and those with inespecific foot pain: cross sectional study
Authors: G Gijon-Nogueron, A. Reinoso-Cobo, A.B. Ortega-Avila, R. Caliz
Journal: Annals of the Rheumatic Diseases (2018)

<h3>Background</h3> The presence of foot pain and deformity is ubiquitous in Rheumatoid Arthritis (RA). Epidemiological studies consistently suggest a prevalence of foot pain of 90%.<sup>1</sup> Weight gain, high levels of fatigue and deformities such us hallux valgus and metatarsus primus varus, are very frequent too.<sup>2</sup> <h3>Objectives</h3> The aim of this study was to analyse pain levels and structural anormalities among subjects with foot pain and patients with RA. <h3>Methods</h3> A sample comprised of 40 subjects was studied. Participants were recruited from a private podiatry clinic and from the Department of Rheumatology (Granada, Spain). The inclusion criteria were subjects with RA with a duration of at least 10 years according to the American Rheumatism Association criteria for RA, while patients with foot pain seeking podiatry services from April 2017 to January 2018 were used as control group. Outcome measures were as follows: foot pain, activity limitation, disability and foot health status by Foot Function Index questionnaire<sup>3</sup> and Hallux Valgus by Manchester Hallux Valgus Scale.<sup>4</sup> <h3>Results</h3> As shown in Table 1, we found statistical significant differences for the pain scale(p&gt;0.001) and in total score(p&gt;0.001) in the FFI scale between AR group and the control group, but not between group in the Manchester Hallux Scale (p=0.986) <h3>Conclusions</h3> We found higher levels of pain in subjects with RA compared to the control group. Furthermore, although there are clinical differences subjects with RA and with foot pain, we can not conclude strongly that RA increases the possibility of having deformities such as Hallux Valgus. <h3>References</h3> [1] De Mits S, Mielants H, De Clercq D, et al. Quantitative assessment of foot structure in rheumatoid arthritis by a foot digitizer: Detection of deformities even in the absence of erosions. Arthritis Care Res2012;64:1641–8. doi:10.1002/acr.21794 [2] Helliwell P, Reay N, Gilworth G, et al. Development of a foot impact scale for rheumatoid arthritis. Arthritis Care Res2005;53: 418–22. doi:10.1002/art.21176 [3] Paez-Moguer J, Budiman-Mak E, Cuesta-Vargas AI. Cross-cultural adaptation and validation of the Foot Function Index to Spanish. Foot Ankle Surg2014;20:34–9. doi:10.1016/j.fas.2013.09.005 [4] Garrow AP, Papageorgiou A, Silman AJ, et al. The Grading of Hallux Valgus: Manchester Scale. J Am Podiatr Med Assoc2001;91:74–8.http://www.japmaonline.org/doi/abs/10.7547/87507315-91-2-74 <h3>Disclosure of Interest</h3> None declared
FRI0273 Rna sequencing detection of gene dysregulation in epithelial sorted cells from salivary gland tissue reveals interesting pathways involved in sjÖgren’s syndrome pathophysiology
Authors: E. Rivière, N. Tchitchek, G. Nocturne, S. Boudaoud, J. Pascaud, A. Virone, A. Thai, N. Allaire, B. Jagla, M. Mingueneau, X. Mariette
Journal: Annals of the Rheumatic Diseases (2018)

<h3>Background</h3> Primary Sjögren's syndrome (pSS) is a chronic autoimmune disorder characterised by lymphocytic infiltrates and destruction of the salivary glands. Several lines of evidence support the hypothesis that salivary gland epithelial cells (SGECs) are not only the target of autoimmunity in pSS patients but may also play a role for its initiation and maintenance. <h3>Objectives</h3> To establish high-resolution molecular maps of SGEC from pSS patients compared to controls using RNASeq analysis. <h3>Methods</h3> Patients had pSS according to 2016 EULAR/ACR criteria and controls had sicca symptoms without any antibodies and with normal lip biopsy. SGEC, B, T CD4 and CD8 lymphocytes were sorted from salivary gland biopsies from 9 pSS patients and 4 controls, using a FACS ARIA cell sorter. Total RNASeq profiling was performed using MiSeq (Illumina). For SGEC subset, 4 samples were excluded due to a contamination by B lymphocytes, thus analysis was performed on 5 pSS and 4 controls using R software, to identify transcriptional differences between pSS and control SGEC. Functional Enrichment analysis was performed using Ingenuity Pathway Analysis software. <h3>Results</h3> In SGEC, 495 genes were differentially expressed between pSS and controls. 280 genes were up-regulated, and 215 genes were down-regulated. Enrichment analysis (table<b> 1</b>) highlighted IL-7 signalling pathways (including IL-7, STAT5A, STAT1 genes) and interferon signalling (including OAS1, IFIT3, IFI6, TAP1 genes). Other genes potentially involved in immune responses and interactions between SGEC and lymphocytes were significantly up-regulated, including bone marrow stromal cell antigen 2, HLA-DRA, BAFF-R and IL-23 A (table <b>2</b>). These results need to be confirmed by RT qPCR. However, consistent results have already been obtained in our laboratory, showing that IL-7 serum level is increased in pSS patients compared to controls and that SGECs produce IL-7 after interferon stimulation. The analysis of the non-coding RNA part and the other sorted cells subtypes is ongoing. <h3>Conclusions</h3> Immune interactions between SGEC and B or T lymphocytes could represent a key in the understanding of the initiation and/or maintenance of autoimmunity in pSS. Our study highlights the key role of epithelial cells in activation of immune cells. <i>In vitro</i> experiments are needed to confirm these results and elucidate the molecular mechanisms. <h3>Acknowledgements</h3> Arthritis Fondation Courtin, Arthritis R and D for providing a PhD fellowship <h3>Disclosure of Interest</h3> None declared
Tocilizumab to Prevent Infusion-Related Events in Patients with Chronic Lymphocytic Leukemia and Co-Morbidities Treated with Obinutuzumab and Chlorambucil: Results from the Randomized Phase Ib GALACTA Trial
Authors: Ciara Louise Freeman, Sebastian Böttcher, Javier De la Serna, Julio Delgado, Franca Falzetti, Marco Gobbi, Sandra Lejniece, Maria Chiara Di Bernardo, Navita L Mallalieu, Tina Nielsen, Andrea Knapp, John G. Gribben
Journal: Blood (2018)
Growth hormone administration influence on soleus muscle of heart failure rats
Authors: A. R. R. Lima, R. L. Damatto, L. U. Pagan, M. J. Gomes, C. Bonomo, M. D. M. Cezar, F. C. Damatto, P. F. Martinez, K. Okoshi, M. P. Okoshi
Journal: European Journal of Heart Failure (2015)
The First-week Proliferative Response of Peripheral Blood PD-1+CD8+ T Cells Predicts the Response to Anti-PD-1 Therapy in Solid Tumors
Authors: Kyung Hwan Kim, Jinhyun Cho, Bo Mi Ku, Jiae Koh, Jong-Mu Sun, Se-Hoon Lee, Jin Seok Ahn, Jaekyung Cheon, Young Joo Min, Su-Hyung Park, Keunchil Park, Myung-Ju Ahn, Eui-Cheol Shin
Journal: Clinical Cancer Research (2019)

Abstract Purpose: To investigate blood-based dynamic biomarkers that predict responses to anti–programmed cell death protein 1 (PD-1) therapy in solid tumors. Experimental Design: Preplanned biomarker analysis was performed as part of a phase II clinical trial (NCT02607631) in patients with metastatic or refractory thymic epithelial tumors (TETs; n = 31) who received pembrolizumab. The biomarker was further tested in an independent cohort of prospectively recruited patients with metastatic non–small cell lung cancer (NSCLC) who received pembrolizumab or nivolumab (NSCLC cohort 1; n = 33) and validated in an independent cohort of patients with NSCLC (NSCLC cohort 2; n = 46). Peripheral blood samples were obtained immediately before treatment (D0) and 7 days after the first dose (D7) and analyzed using multi-color flow cytometry. Results: A higher fold-change in the percentage of Ki-67+ cells among PD-1+CD8+ T cells 7 days after the first dose (Ki-67D7/D0) significantly predicted durable clinical benefit (DCB; P &amp;lt; 0.001) and prolonged progression-free survival (PFS; P = 0.027) in patients with TETs. Ki-67D7/D0 ≥ 2.8 was also associated with better DCB, PFS, and overall survival (OS) in NSCLC cohort 1 (all P &amp;lt; 0.05). Ki-67D7/D0 was subsequently validated in NSCLC cohort 2, and Ki-67D7/D0 ≥ 2.8 significantly predicted better DCB (P = 0.001), PFS (P = 0.002), and OS (P = 0.037). Ki-67D7/D0 had a low correlation with tumor PD-L1 expression and combining both factors did not improve the predictive power of Ki-67D7/D0. Conclusions: The proliferative response of peripheral blood PD-1+CD8+ T cells, measured as the fold-change in the percentage of Ki-67+ cells 7 days after treatment (Ki-67D7/D0), may be a useful surrogate biomarker for predicting the response and prognosis to anti-PD-1 therapy in solid tumors.