19 results on '"Yearley J"'
Search Results
2. The medieval Latin planctus as a genre
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Yearley, J.
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800 ,Literature - Published
- 1983
3. Infants Who Are Breastfeeding Have Special Needs
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YEARLEY, J.
- Published
- 2000
4. PD-1/PD-L1 expression in mutated ovarian cancers
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Penn, C.A., primary, Lester, J., additional, Bohrer, K., additional, Moon, C., additional, Yearley, J., additional, Karlan, B.Y., additional, and Walsh, C., additional
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- 2019
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5. IFN-gamma-related mRNA profile predicts clinical response to PD-1 blockade
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Ayers, M, Lunceford, J, Nebozhyn, M, Murphy, E, Loboda, A, Kaufman, DR, Albright, A, Cheng, JD, Kang, SP, Shankaran, V, Piha-Paul, SA, Yearley, J, Seiwert, TY, Ribas, A, and McClanahan, TK
- Published
- 2017
6. Analytical validation of quantitative immunohistochemical assays of tumor infiltrating lymphocyte biomarkers
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Singh, U, primary, Cui, Y, additional, Dimaano, N, additional, Mehta, S, additional, Pruitt, SK, additional, Yearley, J, additional, Laterza, OF, additional, Juco, JW, additional, and Dogdas, B, additional
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- 2018
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7. PD-1/PD-L1 expression in BRCA1/2 mutated ovarian cancers
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Penn, C.A., Lester, J., Bohrer, K., Moon, C., Yearley, J., Karlan, B.Y., and Walsh, C.
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- 2019
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8. Abstract P4-04-01: PDL-1 expression in primary breast cancers with germline mutations in BRCA 1 and 2
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Audeh, MW, primary, Dadmanesh, F, additional, and Yearley, J, additional
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- 2016
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9. 18LBA PD-L2 expression in human tumors: relevance to anti-PD-1 therapy in cancer
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Yearley, J., primary, Gibson, C., additional, Yu, N., additional, Moon, C., additional, Murphy, E., additional, and McClanahan, T., additional
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- 2015
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10. Interleukin-23 is sufficient to induce rapid de novo gut tumorigenesis, independent of carcinogens, through activation of innate lymphoid cells
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Chan, I H, primary, Jain, R, additional, Tessmer, M S, additional, Gorman, D, additional, Mangadu, R, additional, Sathe, M, additional, Vives, F, additional, Moon, C, additional, Penaflor, E, additional, Turner, S, additional, Ayanoglu, G, additional, Chang, C, additional, Basham, B, additional, Mumm, J B, additional, Pierce, R H, additional, Yearley, J H, additional, McClanahan, T K, additional, Phillips, J H, additional, Cua, D J, additional, Bowman, E P, additional, Kastelein, R A, additional, and LaFace, D, additional
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- 2014
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11. Biphasic Malignant Testicular Sex Cord-Stromal Tumor in a Cotton-top Tamarin (Saguinus oedipus) with Review of the Literature
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Yearley, J. H., primary, King, N., additional, Liu, X., additional, Curran, E. H., additional, and O'Neil, S. P., additional
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- 2008
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12. Cytokine modulation of the innate immune response in feline immunodeficiency virus-infected cats.
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Dean GA, Lavoy A, Yearley J, and Stanton C
- Abstract
Background. In vitro data suggest that innate immune function in human immunodeficiency virus type 1-infected patients is compromised; however, in vivo studies are lacking. Feline immunodeficiency virus (FIV) infection in cats provides an excellent model to explore innate immune function in vivo. The innate response against Listeria monocytogenes is well understood, making it a useful immune probe. Methods. Recombinant L. monocytogenes carrying eukaryotic expression plasmids for feline tumor necrosis factor (TNF)-alpha , interleukin (IL)-10, interferon (IFN)-gamma , and IL-15 were created to determine whether specific cytokines would modulate innate immune function. L. monocytogenes was delivered subcutaneously, and local lymph nodes were evaluated for size, cell subpopulations, and L. monocytogenes burden. Two months later, memory responses were evaluated by IFN-gamma enzyme-linked immunospot assay. Results. FIV-positive cats had significantly less lymph-node enlargement and a greater L. monocytogenes burden than FIV-negative control cats. TNF-alpha improved listericidal activity in FIV-negative control cats but not in FIV-positive cats, whereas IL-10 modestly reduced function in FIV-negative control cats. IFN- gamma improved memory responses but not clearance of L. monocytogenes. IL-15 improved innate function in FIV-positive cats and increased the percentage of natural killer cells. Conclusions. Lentivirus infection impairs innate immune function in vivo, and IL-15 can significantly restore function. We hypothesize that altered dendritic-cell function and increased regulatory T cell activity may underlie the innate immune defect in HIV infection. © 2006 by the Infectious Diseases Society of America. All rights reserved. [ABSTRACT FROM AUTHOR]
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- 2006
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13. Association Between Biomarkers and Clinical Outcomes of Pembrolizumab Monotherapy in Patients With Metastatic Triple-Negative Breast Cancer: KEYNOTE-086 Exploratory Analysis.
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Loi S, Salgado R, Schmid P, Cortes J, Cescon DW, Winer EP, Toppmeyer DL, Rugo HS, De Laurentiis M, Nanda R, Iwata H, Awada A, Tan AR, Sun Y, Karantza V, Wang A, Huang L, Saadatpour A, Cristescu R, Yearley J, Lunceford J, Jelinic P, and Adams S
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- Humans, B7-H1 Antigen genetics, Biomarkers, Tumor genetics, Triple Negative Breast Neoplasms drug therapy, Triple Negative Breast Neoplasms genetics, Antineoplastic Agents, Immunological therapeutic use
- Abstract
Purpose: In the two-cohort phase II KEYNOTE-086 study (ClinicalTrials.gov identifier: NCT02447003), first-line and second-line or later pembrolizumab monotherapy demonstrated antitumor activity in metastatic triple-negative breast cancer (mTNBC; N = 254). This exploratory analysis evaluates the association between prespecified molecular biomarkers and clinical outcomes., Methods: Cohort A enrolled patients with disease progression after one or more systemic therapies for metastatic disease irrespective of PD-L1 status; Cohort B enrolled patients with previously untreated PD-L1-positive (combined positive score [CPS] ≥ 1) metastatic disease. The association between the following biomarkers as continuous variables and clinical outcomes (objective response rate [ORR], progression-free survival [PFS], and overall survival [OS]) was evaluated: PD-L1 CPS (immunohistochemistry), cluster of differentiation 8 (CD8; immunohistochemistry), stromal tumor-infiltrating lymphocyte (sTIL; hematoxylin and eosin staining), tumor mutational burden (TMB; whole-exome sequencing [WES]), homologous recombination deficiency-loss of heterozygosity, mutational signature 3 (WES), mutational signature 2 (apolipoprotein B mRNA editing catalytic polypeptide-like; WES), T-cell-inflamed gene expression profile (Tcell
inf GEP; RNA sequencing), and 10 non-Tcellinf GEP signatures (RNA sequencing); Wald test P values were calculated, and significance was prespecified at α = 0.05., Results: In the combined cohorts (A and B), PD-L1 ( P = .040), CD8 ( P < .001), sTILs ( P = .012), TMB ( P = .007), and Tcellinf GEP ( P = .011) were significantly associated with ORR; CD8 ( P < .001), TMB ( P = .034), Signature 3 ( P = .009), and Tcellinf GEP ( P = .002) with PFS; and CD8 ( P < .001), sTILs ( P = .004), TMB ( P = .025), and Tcellinf GEP ( P = .001) with OS. None of the non-Tcellinf GEP signatures were associated with outcomes of pembrolizumab after adjusting for the Tcellinf GEP., Conclusion: In this exploratory biomarker analysis from KEYNOTE-086, baseline tumor PD-L1, CD8, sTILs, TMB, and Tcellinf GEP were associated with improved clinical outcomes of pembrolizumab and may help identify patients with mTNBC who are most likely to respond to pembrolizumab monotherapy.- Published
- 2023
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14. Immune phenotype of patients with stage IV metastatic inflammatory breast cancer.
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Fernandez SV, MacFarlane AW 4th, Jillab M, Arisi MF, Yearley J, Annamalai L, Gong Y, Cai KQ, Alpaugh RK, Cristofanilli M, and Campbell KS
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- Adult, Aged, Antigens, CD20 analysis, Antigens, CD20 metabolism, B7-H1 Antigen analysis, B7-H1 Antigen metabolism, Biomarkers, Tumor metabolism, Biopsy, Breast immunology, Breast pathology, CD3 Complex analysis, CD3 Complex metabolism, Carcinoma blood, Carcinoma diagnosis, Carcinoma secondary, Case-Control Studies, Female, Flow Cytometry, Humans, Immunity, Cellular, Immunohistochemistry, Immunophenotyping methods, Inflammatory Breast Neoplasms blood, Inflammatory Breast Neoplasms diagnosis, Inflammatory Breast Neoplasms pathology, Lymphocyte Activation, Lymphocytes, Tumor-Infiltrating immunology, Lymphocytes, Tumor-Infiltrating metabolism, Middle Aged, Neoplasm Staging, Programmed Cell Death 1 Receptor analysis, Programmed Cell Death 1 Receptor metabolism, Retrospective Studies, T-Lymphocytes metabolism, Biomarkers, Tumor analysis, Carcinoma immunology, Inflammatory Breast Neoplasms immunology, T-Lymphocytes immunology
- Abstract
Background: Inflammatory breast cancer (IBC) is a rare but aggressive carcinoma characterized by severe erythema and edema of the breast, with many patients presenting in advanced metastatic disease. The "inflammatory" nature is not due to classic immune-mediated inflammation, but instead results from tumor-mediated blockage of dermal lymphatic ducts. Previous work has shown that expression of PD-L1 on tumor cells can suppress T cell activation in triple-negative (TN) non-IBC breast cancer. In the present work, we investigated immune parameters in peripheral blood of metastatic IBC patients to determine whether cellular components of the immune system are altered, thereby contributing to pathogenesis of the disease. These immune parameters were also compared to PD-1 and PD-L1 expression in IBC tumor biopsies., Methods: Flow cytometry-based immune phenotyping was performed using fresh peripheral blood from 14 stage IV IBC patients and compared to 11 healthy age-similar control women. Immunohistochemistry for CD20, CD3, PD-1, and PD-L1 was performed on tumor biopsies of these metastatic IBC patients., Results: IBC patients with Stage IV disease had lymphopenia with significant reductions in circulating T, B, and NK cells. Reductions were observed in all subsets of CD4
+ T cells, whereas reductions in CD8+ T cells were more concentrated in memory subsets. Immature cytokine-producing CD56bright NK cells expressed higher levels of FcγRIIIa and cytolytic granule components, suggesting accelerated maturation to cytolytic CD56dim cells. Immunohistochemical analysis of tumor biopsies demonstrated moderate to high expression of PD-1 in 18.2% of patients and of PD-L1 in 36.4% of patients. Interestingly, a positive correlation was observed between co-expression levels of PD-L1 and PD-1 in tumor biopsies, and higher expression of PD-L1 in tumor biopsies correlated with higher expression of cytolytic granule components in blood CD4+ T cells and CD56dim NK cells, and higher numbers of CD8+ effector memory T cells in peripheral blood. PD-1 expression in tumor also correlated with increased infiltration of CD20+ B cells in the tumor., Conclusions: Our results suggest that while lymphocyte populations are severely compromised in stage IV IBC patients, an immune response toward the tumor had occurred in some patients, providing biological rationale to evaluate PD-1/PD-L1 immunotherapies for IBC.- Published
- 2020
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15. Collaborative International Research in Clinical and Longitudinal Experience Study in NMOSD.
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Cook LJ, Rose JW, Alvey JS, Jolley AM, Kuhn R, Marron B, Pederson M, Enriquez R, Yearley J, McKechnie S, Han MH, Tomczak AJ, Levy M, Mealy MA, Coleman J, Bennett JL, Johnson R, Barnes-Garcia M, Traboulsee AL, Carruthers RL, Lee LE, Schubert JJ, McMullen K, Kister I, Rimler Z, Reid A, Sicotte NL, Planchon SM, Cohen JA, Ivancic D, Sedlak JL, Sand IK, Repovic P, Amezcua L, Pruitt A, Amundson E, Chitnis T, Mullin DS, Klawiter EC, Russo AW, Riley CS, Onomichi KB, Levine L, Nelson KE, Nealon NM, Engel C, Kruse-Hoyer M, Marcille M, Tornes L, Rumpf A, Greer A, Kenneally Behne M, Rodriguez RR, Behne DW, Blackway DW, Coords B, Blaschke TF, Sheard J, Smith TJ, Behne JM, and Yeaman MR
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- Adult, Biomedical Research methods, Cohort Studies, Female, Humans, Longitudinal Studies, Male, Middle Aged, Neuromyelitis Optica blood, Biomedical Research trends, Internationality, Intersectoral Collaboration, Neuromyelitis Optica diagnosis, Neuromyelitis Optica ethnology
- Abstract
Objective: To develop a resource of systematically collected, longitudinal clinical data and biospecimens for assisting in the investigation into neuromyelitis optica spectrum disorder (NMOSD) epidemiology, pathogenesis, and treatment., Methods: To illustrate its research-enabling purpose, epidemiologic patterns and disease phenotypes were assessed among enrolled subjects, including age at disease onset, annualized relapse rate (ARR), and time between the first and second attacks., Results: As of December 2017, the Collaborative International Research in Clinical and Longitudinal Experience Study (CIRCLES) had enrolled more than 1,000 participants, of whom 77.5% of the NMOSD cases and 71.7% of the controls continue in active follow-up. Consanguineous relatives of patients with NMOSD represented 43.6% of the control cohort. Of the 599 active cases with complete data, 84% were female, and 76% were anti-AQP4 seropositive. The majority were white/Caucasian (52.6%), whereas blacks/African Americans accounted for 23.5%, Hispanics/Latinos 12.4%, and Asians accounted for 9.0%. The median age at disease onset was 38.4 years, with a median ARR of 0.5. Seropositive cases were older at disease onset, more likely to be black/African American or Hispanic/Latino, and more likely to be female., Conclusions: Collectively, the CIRCLES experience to date demonstrates this study to be a useful and readily accessible resource to facilitate accelerating solutions for patients with NMOSD.
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- 2019
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16. Pan-tumor genomic biomarkers for PD-1 checkpoint blockade-based immunotherapy.
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Cristescu R, Mogg R, Ayers M, Albright A, Murphy E, Yearley J, Sher X, Liu XQ, Lu H, Nebozhyn M, Zhang C, Lunceford JK, Joe A, Cheng J, Webber AL, Ibrahim N, Plimack ER, Ott PA, Seiwert TY, Ribas A, McClanahan TK, Tomassini JE, Loboda A, and Kaufman D
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- Cell Cycle Checkpoints, Genetic Markers, Humans, Immunotherapy, Inflammation genetics, Mutation, T-Lymphocytes immunology, Transcriptome, Tumor Burden genetics, Antibodies, Monoclonal, Humanized therapeutic use, Antineoplastic Agents, Immunological therapeutic use, Biomarkers, Tumor genetics, Molecular Targeted Therapy methods, Neoplasms genetics, Neoplasms therapy, Programmed Cell Death 1 Receptor antagonists & inhibitors
- Abstract
Programmed cell death protein-1 (PD-1) and programmed cell death ligand-1 (PD-L1) checkpoint blockade immunotherapy elicits durable antitumor effects in multiple cancers, yet not all patients respond. We report the evaluation of >300 patient samples across 22 tumor types from four KEYNOTE clinical trials. Tumor mutational burden (TMB) and a T cell-inflamed gene expression profile (GEP) exhibited joint predictive utility in identifying responders and nonresponders to the PD-1 antibody pembrolizumab. TMB and GEP were independently predictive of response and demonstrated low correlation, suggesting that they capture distinct features of neoantigenicity and T cell activation. Analysis of The Cancer Genome Atlas database showed TMB and GEP to have a low correlation, and analysis by joint stratification revealed biomarker-defined patterns of targetable-resistance biology. These biomarkers may have utility in clinical trial design by guiding rational selection of anti-PD-1 monotherapy and combination immunotherapy regimens., (Copyright © 2018 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works.)
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- 2018
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17. Patterns of PD-1, PD-L1, and PD-L2 expression in pediatric solid tumors.
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Pinto N, Park JR, Murphy E, Yearley J, McClanahan T, Annamalai L, Hawkins DS, and Rudzinski ER
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- B7-H1 Antigen genetics, Biomarkers, Tumor genetics, Child, Humans, Immunoenzyme Techniques, Neoplasm Staging, Neoplasms pathology, Prognosis, Programmed Cell Death 1 Ligand 2 Protein genetics, Programmed Cell Death 1 Receptor genetics, RNA, Messenger analysis, RNA, Messenger genetics, B7-H1 Antigen metabolism, Biomarkers, Tumor metabolism, Neoplasms metabolism, Programmed Cell Death 1 Ligand 2 Protein metabolism, Programmed Cell Death 1 Receptor metabolism
- Abstract
Background: Significant antitumor effects have been observed in a variety of malignancies via blockade of immune checkpoints. Interaction of programmed death 1 (PD-1) with its ligands PD-L1 and PD-L2 suppresses T-cell function and restricts immune-mediated tumor killing. We examined expression of these proteins in children with solid tumors, as expression may serve as biomarkers of response to this class of drugs., Methods: Sections cut from formalin-fixed paraffin-embedded (FFPE) tissue blocks were processed and evaluated for PD-1, PD-L1, and PD-L2 by immunohistochemistry (IHC) as well as by mRNA expression. A semiquantitative 0-5 IHC scoring system (0 = negative to 5 = very high) was applied, with scores incorporating combined prevalence of tumor cell and nontumor cell labeling. Expression profiling was performed using the NanoString nCounter™ system. Data analysis was performed using quantile normalization. All quantile-normalized data underwent subsequent log10 transformation., Results: One hundred twenty-four FFPE blocks were included in the analysis. PD-1, PD-L1, and PD-L2 IHC were not evaluable in 8, 0, and 12 blocks, respectively. PD-1, PDL-1, and PDL-2 expression was negative to moderate by both IHC (range 0-3) and mRNA expression (range 0-2.62). Correlation between IHC score and mRNA expression was poor for all three tested proteins (PD-1, r
2 = 0.06; PDL-1, r2 = 0.007; and PDL-2, r2 = 0.15)., Conclusions: Expression of PD-1, PD-L1, and PD-L2 is low in pediatric solid tumors. At low levels of expression, IHC score and mRNA expression correlate poorly. Current and planned clinical trials will determine whether this low level of expression predicts limited response to immune checkpoint inhibitors., (© 2017 Wiley Periodicals, Inc.)- Published
- 2017
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18. IFN-γ-related mRNA profile predicts clinical response to PD-1 blockade.
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Ayers M, Lunceford J, Nebozhyn M, Murphy E, Loboda A, Kaufman DR, Albright A, Cheng JD, Kang SP, Shankaran V, Piha-Paul SA, Yearley J, Seiwert TY, Ribas A, and McClanahan TK
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- B7-H1 Antigen metabolism, Biopsy, Carcinoma drug therapy, Carcinoma immunology, Carcinoma, Non-Small-Cell Lung drug therapy, Carcinoma, Non-Small-Cell Lung immunology, Gene Expression Regulation, Neoplastic, Humans, Immune System, Immunohistochemistry, Lung Neoplasms drug therapy, Lung Neoplasms immunology, Melanoma drug therapy, Melanoma immunology, Pilot Projects, Programmed Cell Death 1 Receptor metabolism, ROC Curve, Sequence Analysis, RNA, Signal Transduction, Skin Neoplasms drug therapy, Skin Neoplasms immunology, Stomach Neoplasms drug therapy, Treatment Outcome, Tumor Microenvironment, Antibodies, Monoclonal, Humanized therapeutic use, Antineoplastic Agents therapeutic use, Gene Expression Profiling, Interferon-gamma metabolism, Programmed Cell Death 1 Receptor antagonists & inhibitors, Stomach Neoplasms immunology
- Abstract
Programmed death-1-directed (PD-1-directed) immune checkpoint blockade results in durable antitumor activity in many advanced malignancies. Recent studies suggest that IFN-γ is a critical driver of programmed death ligand-1 (PD-L1) expression in cancer and host cells, and baseline intratumoral T cell infiltration may improve response likelihood to anti-PD-1 therapies, including pembrolizumab. However, whether quantifying T cell-inflamed microenvironment is a useful pan-tumor determinant of PD-1-directed therapy response has not been rigorously evaluated. Here, we analyzed gene expression profiles (GEPs) using RNA from baseline tumor samples of pembrolizumab-treated patients. We identified immune-related signatures correlating with clinical benefit using a learn-and-confirm paradigm based on data from different clinical studies of pembrolizumab, starting with a small pilot of 19 melanoma patients and eventually defining a pan-tumor T cell-inflamed GEP in 220 patients with 9 cancers. Predictive value was independently confirmed and compared with that of PD-L1 immunohistochemistry in 96 patients with head and neck squamous cell carcinoma. The T cell-inflamed GEP contained IFN-γ-responsive genes related to antigen presentation, chemokine expression, cytotoxic activity, and adaptive immune resistance, and these features were necessary, but not always sufficient, for clinical benefit. The T cell-inflamed GEP has been developed into a clinical-grade assay that is currently being evaluated in ongoing pembrolizumab trials.
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- 2017
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19. A diet high in saturated fat and cholesterol accelerates simian immunodeficiency virus disease progression.
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Mansfield KG, Carville A, Wachtman L, Goldin BR, Yearley J, Li W, Woods M, Gualtieri L, Shannon R, and Wanke C
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- Animals, Cholesterol, Dietary immunology, Coronary Vessels pathology, Coronary Vessels virology, Disease Progression, Inflammation, Kaplan-Meier Estimate, Macaca mulatta, Receptors, Tumor Necrosis Factor, Type II blood, Simian Acquired Immunodeficiency Syndrome immunology, Viral Load, Cholesterol, Dietary adverse effects, Diet, Atherogenic, Interleukin-18 blood, Simian Acquired Immunodeficiency Syndrome physiopathology, Simian Immunodeficiency Virus pathogenicity
- Abstract
Several lines of evidence suggest that dietary fat and cholesterol may play a role in the pathogenesis of human immunodeficiency virus (HIV) infection and disease progression. We examined the effect that an atherogenic diet (AD) high in saturated fatty acids and cholesterol has on disease progression and systemic inflammation in the simian immunodeficiency virus (SIV)-infected macaque model of acquired immunodeficiency syndrome. Macaques fed an AD had significantly more rapid disease progression, resulting in an increased risk of SIV-related death compared with that in control macaques (hazard ratio, 5.4 [95% confidence interval, 1.7-17.0]; P<.001). Peak viral load was higher in the AD group compared with control values, but further statistically significant differences were not detected at viral set point. The baseline plasma interleukin-18 level after 6 months of the AD was predictive of disease progression. Our findings may have important implications for HIV-infected individuals, because they suggest that dietary changes and manipulation of lipid metabolism could offer potential benefits by slowing disease progression.
- Published
- 2007
- Full Text
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