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23 results on '"Weirather, Jason L"'

1. Cancer-specific innate and adaptive immune rewiring drives resistance to PD-1 blockade in classic Hodgkin lymphoma

Author

Paczkowska, Julia, Tang, Ming, Wright, Kyle T., Song, Li, Luu, Kelsey, Shanmugam, Vignesh, Welsh, Emma L., Weirather, Jason L., Besson, Naomi, Olszewski, Harrison, Porter, Billie A., Pfaff, Kathleen L., Redd, Robert A., Cader, Fathima Zumla, Mandato, Elisa, Ouyang, Jing, Calabretta, Eleonora, Bai, Gali, Lawton, Lee N., Armand, Philippe, Rodig, Scott J., Liu, Xiaole Shirley, and Shipp, Margaret A.

Published
2024
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4. Combined protein and nucleic acid imaging reveals virus-dependent B cell and macrophage immunosuppression of tissue microenvironments

Author

Jiang, Sizun, Chan, Chi Ngai, Rovira-Clavé, Xavier, Chen, Han, Bai, Yunhao, Zhu, Bokai, McCaffrey, Erin, Greenwald, Noah F., Liu, Candace, Barlow, Graham L., Weirather, Jason L., Oliveria, John Paul, Nakayama, Tsuguhisa, Lee, Ivan T., Matter, Matthias S., Carlisle, Anne E., Philips, Darci, Vazquez, Gustavo, Mukherjee, Nilanjan, Busman-Sahay, Kathleen, Nekorchuk, Michael, Terry, Margaret, Younger, Skyler, Bosse, Marc, Demeter, Janos, Rodig, Scott J., Tzankov, Alexandar, Goltsev, Yury, McIlwain, David Robert, Angelo, Michael, Estes, Jacob D., and Nolan, Garry P.

Published
2022
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5. Durvalumab plus tremelimumab alone or in combination with low-dose or hypofractionated radiotherapy in metastatic non-small-cell lung cancer refractory to previous PD(L)-1 therapy: an open-label, multicentre, randomised, phase 2 trial

Author

Schoenfeld, Jonathan D, Giobbie-Hurder, Anita, Ranasinghe, Srinika, Kao, Katrina Z, Lako, Ana, Tsuji, Junko, Liu, Yang, Brennick, Ryan C, Gentzler, Ryan D, Lee, Carrie, Hubbard, Joleen, Arnold, Susanne M, Abbruzzese, James L, Jabbour, Salma K, Uboha, Nataliya V, Stephans, Kevin L, Johnson, Jennifer M, Park, Haeseong, Villaruz, Liza C, Sharon, Elad, Streicher, Howard, Ahmed, Mansoor M, Lyon, Hayley, Cibuskis, Carrie, Lennon, Niall, Jhaveri, Aashna, Yang, Lin, Altreuter, Jennifer, Gunasti, Lauren, Weirather, Jason L, Mak, Raymond H, Awad, Mark M, Rodig, Scott J, Chen, Helen X, Wu, Catherine J, Monjazeb, Arta M, and Hodi, F Stephen

Published
2022
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6. A randomized phase 2 study of neoadjuvant carboplatin and paclitaxel with or without atezolizumab in triple negative breast cancer (TNBC) - NCI 10013

Author

Ademuyiwa, Foluso O., Gao, Feng, Street, Cherease R., Chen, Ina, Northfelt, Donald W., Wesolowski, Robert, Arora, Mili, Brufsky, Adam, Dees, E. Claire, Santa-Maria, Cesar A., Connolly, Roisin M., Force, Jeremy, Moreno-Aspitia, Alvaro, Herndon, John M., Carmody, Madelyn, Davies, Sherri R., Larson, Sarah, Pfaff, Kathleen L., Jones, Stephanie M., Weirather, Jason L., Giobbie-Hurder, Anita, Rodig, Scott J., Liu, Zheng, Hagemann, Ian S., Sharon, Elad, and Gillanders, William E.

Published
2022
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7. Spatial signatures identify immune escape via PD-1 as a defining feature of T-cell/histiocyte-rich large B-cell lymphoma

Author

Griffin, Gabriel K., Weirather, Jason L., Roemer, Margaretha G.M., Lipschitz, Mikel, Kelley, Alyssa, Chen, Pei-Hsuan, Gusenleitner, Daniel, Jeter, Erin, Pak, Christine, Gjini, Evisa, Chapuy, Bjoern, Rosenthal, Michael H., Xu, Jie, Chen, Benjamin J., Sohani, Aliyah R., Lovitch, Scott B., Abramson, Jeremy S., Ishizuka, Jeffrey J., Kim, Austin I., Jacobson, Caron A., LaCasce, Ann S., Fletcher, Christopher D., Neuberg, Donna, Freeman, Gordon J., Hodi, F. Stephen, Wright, Kyle, Ligon, Azra H., Jacobsen, Eric D., Armand, Philippe, Shipp, Margaret A., and Rodig, Scott J.

Published
2021
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18. Characterization of genetics in patients with mucosal melanoma treated with immune checkpoint blockade.

Author

Buchbinder, Elizabeth I., Weirather, Jason L., Manos, Michael, Quattrochi, Brian J., Sholl, Lynette M., Brennick, Ryan C., Bowling, Peter, Bailey, Nancy, Magarace, Lisa, Ott, Patrick A., Haq, Rizwan, Izar, Benjamin, Giobbie‐Hurder, Anita, and Hodi, F. Stephen

Subjects
*GENETICS, *MUCOUS membranes, *GENES, *GENETIC testing, *MELANOCYTES, *MELANOMA
Abstract

Mucosal melanoma is a rare form of melanoma which arises from melanocytes in the mucosal membranes and can be effectively treated with immune checkpoint blockade (ICB). However, response rates in mucosal melanoma are lower than those observed for cutaneous melanomas. Targeted sequencing of up to 447 genes (OncoPanel) was performed on tumors from all mucosal melanoma patients seen at the Dana‐Farber Cancer Institute from 2011 until March 2019. We identified a total of 46 patients who received ICB with both tumor‐genotype and ICB response data available. Within this cohort of patients, 16 (35%) had durable clinical benefit (DCB) to their first line of ICB. The average mutational burden/megabase was 6.23 and did not correlate with tumor response to ICB. Patients with KIT aberrations had a higher DCB rate compared with patients with wildtype KIT (71 vs. 28%), but this was not found to be statistically significant. For comparison, we analyzed tumor genotypes from an additional 50 mucosal melanoma tumors and 189 cutaneous melanoma tumors. The most frequent mutations in mucosal melanoma were in SF3B1 (27%), KIT (18%), and NF1 (17%), a pattern that is distinct from cutaneous melanomas. In addition, there were genetic differences observed based upon the site of origin of the mucosal melanoma. Our findings explore clinical features of response in patients with mucosal melanoma treated with ICB and demonstrate a low mutational burden that does not correlate with response. In addition, the lack of significant association between the genetic aberrations tested and response to ICB indicates the need for further exploration in this patient population. [ABSTRACT FROM AUTHOR]

Published
2021
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19. Neoadjuvant Nivolumab or Nivolumab Plus Ipilimumab in Untreated Oral Cavity Squamous Cell Carcinoma: A Phase 2 Open-Label Randomized Clinical Trial.

Author

Schoenfeld, Jonathan D., Hanna, Glenn J., Jo, Vickie Y., Rawal, Bhupendra, Chen, Yu-Hui, Catalano, Paul S., Lako, Ana, Ciantra, Zoe, Weirather, Jason L., Criscitiello, Shana, Luoma, Adrienne, Chau, Nicole, Lorch, Jochen, Kass, Jason I., Annino, Donald, Goguen, Laura, Desai, Anupam, Ross, Brendan, Shah, Hina J., and Jacene, Heather A.

Published
2020
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20. MHC proteins confer differential sensitivity to CTLA-4 and PD-1 blockade in untreated metastatic melanoma.

Author

Rodig, Scott J., Gusenleitner, Daniel, Jackson, Donald G., Gjini, Evisa, Giobbie-Hurder, Anita, Jin, Chelsea, Chang, Han, Lovitch, Scott B., Horak, Christine, Weber, Jeffrey S., Weirather, Jason L., Wolchok, Jedd D., Postow, Michael A., Pavlick, Anna C., Chesney, Jason, and Hodi, F. Stephen

Subjects
MAJOR histocompatibility complex, APOPTOSIS, MELANOMA, IMMUNOHISTOCHEMISTRY, NUCLEOTIDE sequence, EXOMES, ANTIGENS, PATIENTS
Abstract

Loss of membrane MHC class I protein expression in most of tumor cells in advanced melanomas predicts primary resistance to anti–CTLA-4, but not anti-PD1, treatment. MHC-ing immunotherapy response: Currently, there is no way to predict response to anti–CTLA-4 cancer immunotherapy. Using data from two published independent phase 2 clinical trials, Rodig et al. showed that MHC class I expression in advanced melanoma predicted resistance to anti–CTLA-4, but not anti-PD-1, treatment, which may need MHC class II to be effective. These results may explain why patients on combined therapy do better on average, with one drug overcoming the limitations of the other. The combination is also more toxic than single agents; knowing which drug to administer to which patients could make melanoma immunotherapy less taxing without sacrificing efficacy. Combination anti–cytotoxic T lymphocyte antigen 4 (CTLA-4) and anti–programmed cell death protein 1 (PD-1) therapy promotes antitumor immunity and provides superior benefit to patients with advanced-stage melanoma compared with either therapy alone. T cell immunity requires recognition of antigens in the context of major histocompatibility complex (MHC) class I and class II proteins by CD8+ and CD4+ T cells, respectively. We examined MHC class I and class II protein expression on tumor cells from previously untreated melanoma patients and correlated the results with transcriptional and genomic analyses and with clinical response to anti–CTLA-4, anti–PD-1, or combination therapy. Most (>50% of cells) or complete loss of melanoma MHC class I membrane expression was observed in 78 of 181 cases (43%), was associated with transcriptional repression of HLA-A, HLA-B, HLA-C, and B2M, and predicted primary resistance to anti–CTLA-4, but not anti–PD-1, therapy. Melanoma MHC class II membrane expression on >1% cells was observed in 55 of 181 cases (30%), was associated with interferon-γ (IFN-γ) and IFN-γ–mediated gene signatures, and predicted response to anti–PD-1, but not anti–CTLA-4, therapy. We conclude that primary response to anti–CTLA-4 requires robust melanoma MHC class I expression. In contrast, primary response to anti–PD-1 is associated with preexisting IFN-γ–mediated immune activation that includes tumor-specific MHC class II expression and components of innate immunity when MHC class I is compromised. The benefits of combined checkpoint blockade may be attributable, in part, to distinct requirements for melanoma-specific antigen presentation to initiate antitumor immunity. [ABSTRACT FROM AUTHOR]

Published
2018
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21. Fine mapping under linkage peaks for symptomatic or asymptomatic outcomes of Leishmania infantum infection in Brazil.

Author

Weirather, Jason L., Duggal, Priya, Nascimento, Eliana L., Monteiro, Gloria R., Martins, Daniella R., Lacerda, Henio G., Fakiola, Michaela, Blackwell, Jenefer M., Jeronimo, Selma M.B., and Wilson, Mary E.

Subjects
*LEISHMANIA infantum, *GENE mapping, *LINKAGE (Genetics), *PHENOTYPES
Abstract

Infection with the protozoan Leishmania infantum can lead to asymptomatic infection and protective immunity, or to the progressive and potentially fatal disease visceral leishmaniasis (VL). Published studies show host genetic background determines in part whether infected individuals will develop a symptomatic or asymptomatic outcome. The purpose of the current study was to fine map chromosome regions previously linked with risk for symptomatic (chromosome 9) or asymptomatic (chromosomes 15 and 19) manifestations of L. infantum infection. We conducted a family-based genetic study of VL and asymptomatic infection (detected by a DTH skin test) with a final post quality control sample of 961 individuals with full genotype and phenotype information from highly endemic neighborhoods of northeast Brazil. A total of 5485 SNPs under the linkage peaks on chromosomes 9, 15 and 19 were genotyped. No strong SNP associations were observed for the DTH phenotype. The most significant associations with the VL phenotype were with SNP rs1470217 (p = 5.9e − 05; p corrected = 0.057) on chromosome 9, and with SNP rs8107014 (p = 1.4e − 05; p corrected = 0.013) on chromosome 19. SNP rs1470217 is situated in a 180 kb intergenic region between TMEM215 (Transmembrane protein 215) and APTX (Aprataxin). SNP rs8107014 lies in the intron between exons 26 and 27 of a 34 exon transcript (ENST00000204005) of LTBP4 , (Latent transforming growth factor-beta-binding protein 4a). The latter supports growing evidence that the transforming growth factor-beta pathway is important in the immunopathogenesis of VL. [ABSTRACT FROM AUTHOR]

Published
2016
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