tbuckley/cabot-search huggingface dataset:
PWE-068 Correlation of a patient reported single item global disease rating scale to clinical and biological markers of disease activity: Abstract PWE-068 Table 1
Authors: M Rimmer, R Asher, R Jackson, G Race, P Collins, M Dibb, C Probert, J Rhodes, S Subramanian
Journal: Gut (2015)

<h3>Introduction</h3> Multiple instruments exist to assess disease activity in inflammatory bowel disease (IBD). However, several factors preclude routine clinical use of these instruments. These include time limitations, need for separate tools in Crohn’s disease (CD) and ulcerative colitis (UC) and finally the inability to fully capture the burden of disease from a patient’s perspective. A simple easy to use patient reported outcome measure will help inform clinical decision making. We evaluated the correlation of a single item patient reported disease control scale to physician assessment, clinical and biological markers of disease activity. <h3>Method</h3> We conducted a single centre prospective cross-sectional study. Patients with IBD (with the exception of ostomy patients) attending clinic at the Royal Liverpool University Hospital were eligible for inclusion. Disease activity was assessed using Harvey-Bradshaw Index (HBI) for CD or simple clinical colitis activity index (SCCAI) for UC. Patients were asked to rate the control of CD or UC on a numerical scale verbally in response to ‘How do you rate the control of your CD or UC today on a scale of 0–10, 10 being the best?’. Information on blood tests including C-reactive protein (CRP) was collected if these were requested as part of routine clinical care. The study was approved by Liverpool Research Ethics Committee as part of an on-going prospective IBD registry study. <h3>Results</h3> A total of 176 observations, median age 38.5 (IQR 25–53) were included. 98 patients (56%) had CD and 72 had UC (44%). Both HBI and SCCAI showed a significant association with the single item patient-reported score (Kruskall-Wallis, p &lt; 0.001). Across all patients a score of at least 8 (IQR 8–10) corresponded to remission on HBI and SCCAI (Table 1). The degree of agreement between patient scoring and activity index was substantially better for UC/SCCAI (kappa score 0.65) than for CD/HBI (kappa 0.39), possibly reflecting the emphasis of CD activity scores (HBI and CDAI) on diarrhoea rather than other symptoms such as fatigue. There was no significant association between CRP and patient reported global rating scale for both CD and UC (p = 0.7). <h3>Conclusion</h3> A simple “instant” patient reported score for disease control can be readily obtained in the clinic and shows good correlation with more complex scores. In Crohn’s disease, particularly, it might give a fairer reflection of the patient’s wellbeing than conventional more complex scores. <h3>Disclosure of interest</h3> None Declared.
Direct Antiviral Agent Treatment of Chronic HCV Infection Results in Rapid Regression of Transient Elastography (Fibroscan®) and Validated Fibrosis Markers FIB-4 and APRI
Authors: J.A. Bachofner, P.V. Valli, A. Kröger, B. Müllhaupt, J.C. Mertens
Journal: Journal of Hepatology (2016)
How Azobenzene Photoswitches Restore Visual Responses to the Blind Retina
Authors: Ivan Tochitsky, Zachary Helft, Victor Meseguer, Russell B. Fletcher, Kirstan A. Vessey, Michael Telias, Bristol Denlinger, Jonatan Malis, Erica L. Fletcher, Richard H. Kramer
Journal: Neuron (2016)
Monitoring of Wilms’ Tumor 1 (WT1) Expression in Peripheral Blood (PB) of Patients with Myelodysplastic Syndromes (MDS) By a Standardized European Leukemia Net (ELN)-Certified Assay to Detect Minimal Residual Disease (MRD) and Guide Therapeutic Interventions Following Allogeneic Transplantation
Authors: Thomas Schroeder, Sabrina Pechtel, Marius Lamers, Ariane Dienst, Esther Schuler, Elena Rachlis, Nadija Wegener, Andrea Kündgen, Mustafa Kondakci, Roland Fenk, Norbert Gattermann, Rainer Haas, Ulrich Germing, Guido Kobbe
Journal: Blood (2014)
Pregnancy and Complications in Tetralogy of Fallot; 204 Patients
Authors: Ali Balci, Willem Drenthen, Barbara J. M. Mulder, Jolien W. Roos-Hesselink, Adriaan A. Voors, Hubert W. Vliegen, Werner Budts, Arie P. J. van Dijk, Dirk J. van Veldhuisen, Petronella G. Pieper
Journal: Journal of the American College of Cardiology (2009)
Ledipasvir/Sofosbuvir for Recurrent Hepatitis C in Liver Transplant Recipients: A Real-Life Spanish Multicentre Experience
Authors: M. Prieto, I. Fernández, M.-C. Londoño, M. Abradelo, J.M. Pascasio, F. Gea, D. Rincón, V. Cuervas-Mons, G. Crespo, J.L. Montero, V. Hontangas, C. Baliellas, J.M. Sousa, M. García, S. Pascual, J.A. Pons, L. Castells, M. Testillano, M. Jimenez, A. Otero, E. Molina, A. González, F. Nogueras, L. González-Dieguez, S. Lorente, G. Sánchez-Antolín, J.I. Herrero, F. Casafont
Journal: Journal of Hepatology (2016)
RNA Interference Mediated Suppression of HBV Transcripts Restores HBV-Specific Immunity and Enhances the Efficacy of Therapeutic Vaccination
Authors: T. Michler, A. Kosinska, C. Jäger, N. Röder, D. Grimm, M. Heikenwälder, M. Roggendorf, U. Protzer
Journal: Journal of Hepatology (2016)
Induction treatment in first-line with chemotherapy + bevacizumab (bev) in metastatic colorectal cancer: Results from the gercor-DREAM phase III study.
Authors: Christophe Tournigand, Werner Scheithauer, Benoit Samson, Gérard Lledo, Frédéric Viret, Thierry Andre, Jean François Ramée, Nicole Tubiana-Mathieu, Jérôme Dauba, Olivier Dupuis, Yves Rinaldi, May Mabro, Nathalie Aucoin, Ahmed Khalil, Jean Latreille, Christophe Louvet, David Brusquant, Franck Bonnetain, Benoist Chibaudel, Aimery De Gramont
Journal: Journal of Clinical Oncology (2013)

457 Background: the DREAM study compares a maintenance therapy with bevacizumab (bev) alone or with the erlotinib after a bev-based induction therapy with FOLFOX, or biweekly XELOX or FOLFIRI. Efficacy of the induction treatment is reported here. Methods: Patients (pts) with previously untreated metastatic colorectal cancer received one of the following regimen (investigator’s choice): mFOLFOX7-bev, biweekly mXELOX-bev or FOLFIRI-bev. Oxaliplatin was administered no more than 6 cycles. In the 1st cohort, pts received 3 months (m) of FOLFOX-bev or mXELOX-bev before randomization. In the 2nd cohort, pts received 3m of FOLFOX-bev or mXELOX-bev then 3 m of fluoropyrimidine-bev, or 6 m of FOLFIRI-bev before randomization. Pts with disease control were then randomized between bev alone or with erlotinib until progression. Results: FOLFOX-bev was administered in 424 pts, mXELOX-bev in 203 pts and FOLFIRI-bev in 67 pts. Pts characteristics for the whole population are: median age 63 yrs (26-80), male/female 59.8%/40.2%, synchronous mets/metachronous 82.6%/17.4%, PS 0/1/2 58%/39%/3%, LDH&gt;UNL 53%, platelets &gt;400000/mm3 27%. Patients received a median nb of 6 cycles of oxaliplatin for FOLFOX-bev and mXELOX-bev, and a median nb of 12 cycles of irinotecan with FOLFIRI-bev. Response rates are respectively 48%, 50% and 63%. Median PFS are respectively 8.61m, 8.97m and 9m. Severe toxicity profiles (grade 3-4) appear to be different according to the schedule : more neutropenia and diarrhea with FOLFIRI-bev, HFS and diarrhea with mXELOX-bev and neuropathy with FOLFOX-bev. Conclusions: Modified biweekly XELOX-bev provides similar efficacy results with FOLFOX-bev, and FOLFIRI-bev as induction therapy in first-line. Clinical trial information: NCT00265824.
Therapeutic Options for Low Dose Proleukin in Autoimmune Liver Diseases through Selective Induction of Phospho-STAT5, Regulatory Phenotype and Prosurvival BCL-2 in TREG
Authors: H. Jeffery, L. Jeffery, J. Birtwistle, D. Adams, Y.H. Oo
Journal: Journal of Hepatology (2016)
Modeling Early HCV Kinetics to Individualize Direct Acting Antivirals Treatment Duration in Patients with Advanced Cirrhosis
Authors: M. Gambato, L. Canini, S. Lens, F. Graw, M.C. Londoño, S.L. Uprichard, Z. Mariño, E. Reverter, C. Bartres, P. González, S.J. Cotler, X. Forns, H. Dahari
Journal: Journal of Hepatology (2016)
NCCTG phase II trial of CCI-779 in recurrent glioblastoma multiforme (GBM)
Authors: E. Galanis, J. C. Buckner, M. Maurer, K. Ballman, M. Hidalgo, J. I. Kreisberg, J. Boni, C. D. D. James, R. B. Jenkins, D. J. Walsh
Journal: Journal of Clinical Oncology (2004)

1503 Background: CCI-779 is a small molecule inhibitor of the mammalian target of rapamycin (mTOR). mTOR is a rational therapeutic target in GBM, being downstream from important pathways such as EGFR and PTEN. Study aims: to determine the efficacy of CCI-779 in recurrent GBM, to assess toxicity, to evaluate the pharmacokinetics (PK) of CCI-779 for pts on p450 inducing anticonvulsants (EIAC), to define the pt population most likely to benefit from treatment (Rx), and to determine whether CCI-779 successfully interacts with the target pathway. Methods: Recurrent GBM pts with ≤ 1 chemo regimen for progressive disease, stable steroid dose for ≥ 1 wk prior to baseline scan, acceptable hematologic, renal, liver function, cholesterol and triglyceride levels were eligible. CCI-779 dose was 250 mg iv q wk. Results: 41 pts were treated. Rx was well tolerated: grade 3+ hematologic toxicity was observed in 12 %, and grade 3+ non-hematologic toxicity in 51%, and consisted mostly of hypercholesterolemia (15%), hypertriglyceridemia (12%), hyperglycemia (10%), rash (5%), stomatitis (5%), fatigue (2%). Sirolimus metabolite trough concentration, AUC and AUC sum (CCI+sirolimus) were decreased in EIAC pts by 65%, 50%, and 40% respectively, but they were still within the therapeutic range of preclinical models. Assessment of tumor Akt and p70s6 kinase phosphorylation (PHOS) pre-Rx, demonstrated activation of the Akt and p70s6k in the majority of pts (14/17 and 11/17 pts respectively). Analysis of p70s6k PHOS in peripheral blood mononuclear cells (PMBC), showed post-Rx inhibition in 7/10 pts. Although there were no objective partial responses in the first 31 pts, evidence of antitumor activity was observed, with significant decrease in T2 signal abnormality in 5 pts and modest decrease in T1 Gad enhancement in 3 pts. Conclusions: CCI-779 is well tolerated in recurrent GBM pts. Despite the impact of EIAC on CCI-779 metabolism, therapeutic levels were achieved. There is preliminary evidence of antitumor activity, as well as inhibition of the target pathway in post-Rx PBMCs. Assessment of the PTEN and EGFR tumor status, Akt and p70s6k PHOS pre- and post-Rx and correlation with response and toxicity is ongoing. No significant financial relationships to disclose.
Treatment of Chronically HBV-Infected Chimpanzees with RNA Interference Therapeutic ARC-520 LED to Potent Reduction of Viral MRNA, DNA and Proteins without Observed Drug Resistance
Authors: Z. Xu, D. Chavez, B. Guerra, M. Littlejohn, R. Peterson, S. Locarnini, R. Gish, C. Anzalone, S. Kanner, J. Goetzmann, R. Lanford, D. Lewis, C. Wooddell
Journal: Journal of Hepatology (2016)
Deep Sequencing Results from the Phase 2 Impact Study of Simeprevir in Combination with Daclatasvir and Sofosbuvir in Treatment-Naïve and -Experienced Patients with Chronic Hepatitis C Virus Genotype 1 or 4 Infection and Decompensated Liver Disease
Authors: C. Sarrazin, V. Van Eygen, L. Vijgen, M. Gamil, M. Beumont, E. Lawitz, S. De Meyer
Journal: Journal of Hepatology (2016)
Response to tyrosine kinase inhibitors in advanced non-small-cell lung cancer with concomitant c-MET overexpression and EGFR mutation.
Authors: Na Na Lou, Yi-Long Wu, Jin-Ji Yang, Xu-Chao Zhang, Qing Zhou, Jian Su, Hua-Jun Chen, Zhen Wang, Xiao-Yan Bai, Bin-Chao Wang
Journal: Journal of Clinical Oncology (2016)

9054 Background: The common driver genes in non-small-cell lung cancer (NSCLC) include EGFR, ALK, KRAS and so on. MET amplification coexisting with EGFR mutation is recognized as intrinsic resistance to EGFR tyrosine kinase inhibitors (EGFR TKIs). We investigate the frequency of MET overexpression coexisting with EGFRmutation, response to EGFR TKIs and survival in advanced NSCLC patients with such co-alterations. Methods: From Jan 1st 2014 to Dec 31st 2015, we screened 149 consecutive NSCLC patients for the presence of MET overexpression concomitant EGFR mutation. MET overexpression was detected by immunohistochemistry (IHC), in which ≥ 50% tumor cells with moderate to high intensity staining were defined as MET positive. MET amplification was detected by fluorescence in situ hybridization (FISH), and FISH positive was defined as gene focal amplification or high polysomy (at least 15% cells with ≥ 5 copy numbers). Meanwhile, EGFRmutations were tested by DNA sequencing or Scorpion amplification refractory mutation system (ARMS). Results: The frequency of concomitant MET overexpression and EGFR mutation was 38.9% (58/149) in advanced NSCLC. However, the frequency of MET amplification was 13.6% (6/44). The frequency of primary resistance to EGFR TKIs was 24.1% (14/58) in EGFR/MET-coexisted patients and 14.2% (13/91) in those with only EGFR mutations, P= 0.13. Response rate (RR) of EGFR-TKIs was 48.3% (28/58), and 71.4% (65/91) in these two arms respectively, P= 0.004. Median PFS was 10.7 vs 11.2 months, Hazard ratio (HR) = 1.05, 95% CI 0.69~1.60, P = 0.82. Primary resistance to EGFR TKIs were found in 2 cases with concomitant MET amplification and EGFRmutations, but they responded to combination of EGFR and MET inhibitors. Conclusions: Advanced NSCLC patients with concomitant EGFR mutation and MET overexpression have relatively low RR with EGFR-TKIs, indicating that MET overexpression potentially causes primary resistance to EGFR-TKIs which might be overcome by combination of EGFR and MET inhibitors.
Multi-Center Study on Myelodysplastic Syndromes with Isolated Partial or Total Loss of Chromosome 7
Authors: Elena Crisà, Esperanza Such, Steven Best, Austin Kulasekararaj, José Cervera, Vera Adema, Nicholas Lea, Dario Ferrero, Bernardino Allione, Julie Schanz, Detlef Haase, Guillermo F. Sanz, Francesco Sole, Ghulam J. Mufti
Journal: Blood (2014)
Multiplexed, targeted profiling of single-cell proteomes and transcriptomes in a single reaction
Authors: Alex S Genshaft, Shuqiang Li, Caroline J. Gallant, Spyros Darmanis, Sanjay M. Prakadan, Carly G. K. Ziegler, Martin Lundberg, Simon Fredriksson, Joyce Hong, Aviv Regev, Kenneth J. Livak, Ulf Landegren, Alex K. Shalek
Journal: Genome biology (2016)

We present a scalable, integrated strategy for coupled protein and RNA detection from single cells. Our approach leverages the DNA polymerase activity of reverse transcriptase to simultaneously perform proximity extension assays and complementary DNA synthesis in the same reaction. Using the Fluidigm C1™ system, we profile the transcriptomic and proteomic response of a human breast adenocarcinoma cell line to a chemical perturbation, benchmarking against in situ hybridizations and immunofluorescence staining, as well as recombinant proteins, ERCC Spike-Ins, and population lysate dilutions. Through supervised and unsupervised analyses, we demonstrate synergies enabled by simultaneous measurement of single-cell protein and RNA abundances. Collectively, our generalizable approach highlights the potential for molecular metadata to inform highly-multiplexed single-cell analyses.
A comparison of efficacy and toxicity between never-smokers and smokers with lung adenocarcinoma after concurrent gefitinib and thoracic radiotherapy.
Authors: J. Chen, M. Fan, G. Jiang, X. Fu, L. Xie, X. Xu, G. Zhang
Journal: Journal of Clinical Oncology (2010)

e13586 Background: There is limited data on the outcomes of Asian smoker or never-smoker lung adenocarcinoma patients treated with concurrent gefitinib and radiotherapy. We herein report our observations from a phase I trial (NCT 00497250). Methods: Patients with stage IIIB or selected stage IV, failure of platinum-based chemotherapy regimen NSCLC were eligible. Four cohorts of eight patients each were planned to be treated with escalating doses from 54 to 60 Gy of conformal or intensity-modulated radiotherapy administered in combination with gefitinib 250 mg daily during and 60 days after the completion of RT. To December 2009, a total of 28 patients were eligible for this analysis. Among them, there were 8 stage IIIb and 20 stage IV, 17 were never-smokers, and 11 smokers. Results: After a median follow-up time of 9 months (95% CI: 1.6-21.2) for the entire group, the median survival was 17 months (95% CI: 12-24) and 14 months (95% CI: 6-22), and 1-yr survival was 76% and 61%, respectively for never-smokers and smokers (p=0.250). In never-smokers, three (18%) achieved PR and 13 (77%) had SD as their best response accessed by RECIST, while there were 3 (27%) PR and 7 (64%) SD in smokers. One male smoker with 50 pack-years smoking history developed bilateral interstitial pneumonia one week after 60Gy and died of respiratory failure one month late. Other adverse events were generally mild or moderate (Table). There were no significant differences between never-smokers or smokers. Conclusions: There was no excessive toxicity in Chinese never-smoker patients with lung adenocarcinoma treated with concurrent radiotherapy and daily gefitinib. The life-threatening toxicity (interstitial pneumonia) was seen in a male smoker. There was a trend toward a longer median survival time in never-smokers. Biomarker studies are warranted. Toxicity CTCAE 3.0 grade Never-smokers Smokers Rash 1/2 12 (71%) 8 (73%) >3 0 0 Pulmonary 1/2 14 (82%) 9 (82%) >3 0 1 (G5)(9%) Esophageal 1/2 9 (53%) 6 (55%) >3 0 0 Hematological 1/2 9 (53%) 7 (64%) >3 0 0 No significant financial relationships to disclose.
Update analysis: Prospective observational study for the impact of short-term periodic steroid premedication for cancer chemotherapy on bone metabolism—ESPRESSO-01 study.
Authors: Michio Nakamura, Atsushi Ishiguro, Tetsuhito Muranaka, Satoshi Yuki, Taichi Murai, Chika Matsuda, Ayane Oba, Kazufumi Itaya, Taku Shigesawa, Yuta Koike, Yomo Fujita, Ayana Endo, Yoko Tsukuda, Yuji Ono, Takahiko Kudo, Atsushi Nagasaka, Shuji Nishikawa, Yoshito Komatsu
Journal: Journal of Clinical Oncology (2016)

e18145 Background: Although glucocorticoid (GC) premedication (GCP) before chemotherapy (CTx) are frequently used to prevent nausea and vomiting for continuing comfortable CTx, the side effects of intermittent GCs on bone health have not yet been reported. We previously reported that GCP caused the reduction of bone mineral densities at lumbar spine (BMD-LS) and the increase of bone turnover markers, such as cross-linked N-telopeptide of type I collagen (NTX) and bone alkaline phosphatase (BAP) (ASCO-GI 2016 Abst.523). We now report the updated results about secondary endpoints of this study (ESPRESSO-01 study). Methods: The eligibility criteria were as the follows: (i) histologically proven gastrointestinal cancer (GIC). ; (ii) The duration of periodical GCP is weekly, biweekly, and triweekly. ; (iii) age over 20. The primary endpoint was to investigate the variations of BMD-LS by dual energy x-ray absorptiometry (DXA), NTX, and BAP, between baseline (BL) and 16 weeks after starting CTx (16w). Secondary endpoints were the influence of GCs dose intensity, treatment duration, regimens, primary site, and so on. Results: From June 2013 to April 2015, 98 pts were enrolled, and 74 pts comprised the full analysis set (FAS). Not only the levels of BMD-LS but also those of total hip and femoral neck BMD at 16w were decreased compared with BL and the average percent changes were -1.9% (n = 74, 95% CI: -2.7% to -1.1%, p < 0.0001), -2.2% (n = 73, 95% CI: -3.6% to -0.9%, p = 0.002), and -2.0% (n = 73, 95% CI:-3.1% to -1.0%, p < 0.0001), respectively. Regard to secondary endpoints, there was no significant correlation between BMD change level and primary site, treatment regimens, durations, and additive oral steroid usage. Conclusions: We found that periodic GCP in GIC pts caused the reduction of BMD and the increase of NTX and BAP independent of treatment regimens, independent of treatment regimens, durations, and additive steroid usage. Now we plan the further study ESPRESSO-02 to investigate the efficacy of prevention GCP induced osteoporosis. Clinical trial information: UMIN000011054.
PLPNA3 Status in Nash is Associated with Increased Histological Severity at Baseline but Not with Response to Therapy in the Golden-505 Elafibranor Trial
Authors: V. Ratziu, S. Francque, S. Harrison, A. Sanyal, P. Bedossa, L. Serfaty, M. Romero-Gomez, J. Boursier, M. Abdelmalek, S. Caldwell, J. Drenth, D. Hum, R. Hanf, A. Roudot, S. Megnien, B. Staels, Q. Anstee
Journal: Journal of Hepatology (2016)
The Molecular Characteristics in CDR3 of TCR Vα and Vβ Genes Associated with cGVHD in Patients after Allogeneic Hematopoietic Stem Cell Transplantation.
Authors: Xiuli Wu, Yangqiu Li, Kanger Zhu, Xin Du, Shaohua Chen, Lijian Yang, Suxia Geng, Yuhong Lu, Jie Chen
Journal: Blood (2007)
A Post-Hoc Analysis ofthe Golden505 Trial Demonstrates Histological and Cardiometabolic Efficacy of Elafibranor-120 Mg in Patients with Moderate or Severe Nash That Are Eligible for Pharmacotherapy
Authors: V. Ratziu, S. Harrison, S. Francque, P. Bedossa, Q. Anstee, L. Serfaty, M. Romero-Gomez, J. Boursier, M. Abdelmalek, S. Caldwell, J. Drenth, D. Hum, R. Hanf, A. Roudot, S. Megnien, A. Sanyal, B. Staels
Journal: Journal of Hepatology (2016)
Enhancement of DC-based immunotherapy using a small molecule TGF-β inhibitor
Authors: Matthew P. Rausch, Emmanuel T. Akporiaye, Daruka Mahadevan
Journal: Cancer Research (2005)

Proc Amer Assoc Cancer Res, Volume 46, 2005

5310 

The limited clinical efficacy of existing dendritic cell (DC)-based cancer vaccines can be attributed in part to suppressive factors produced by the growing tumor that inhibit the ability of the immune system to mount an effective anti-tumor response. One of these factors is transforming growth factor-beta (TGF-β). We have previously shown that TGF-β directly contributes to the invasive and metastatic potential of 4T1 breast cancer cells by inducing morphological changes indicative of epithelial to mesenchymal transition (EMT). In addition, this cytokine may further promote tumor progression in vivo by inhibiting the antigen presenting and immunostimulatory activities of DCs. Strategies that neutralize the effects of TGF-β may therefore lead to more effective DC-based cancer therapies by controlling tumor spread and permitting the successful induction of the anti-tumor response. HTS466284 is a potent small molecule inhibitor of TGF-β that has been shown to selectively bind to the TGF-β receptor type I (TGF-βRI), stabilizing this receptor in an inactive conformation that subsequently inhibits downstream signaling events. In this study, we employed HTS466284, a novel TGF-βRI kinase inhibitor, to render DCs resistant to the deleterious effects of tumor-derived TGF-β in order to more effectively treat established 4T1 tumors. Our results show that HTS466284 blocked gene transcription in a dose dependant manner following TGF-β exposure in mink lung epithelial cells transfected with the TGF-β responsive 3TP-Lux reporter construct. In addition, HTS466284 prevented Smad2 phosphorylation, an early step in the TGF-β signaling cascade, in both DCs and 4T1 cells. Blockade of TGF-β signal transduction in 4T1 cells by HTS466284 treatment prevented TGF-β-induced EMT and inhibited the in vitro migration of these cells. Finally, treatment of mice bearing established 4T1 tumors with the combination of DC and HTS466284 significantly delayed tumor growth and inhibited surface lung metastasis formation. These results demonstrate that HTS466284 treatment may represent a viable strategy to bolster the efficacy of DC-based anti-cancer vaccines.