Personalized RNA neoantigen vaccines stimulate T cells in pancreatic cancer
Pancreatic ductal adenocarcinoma (PDAC) is lethal in 88% of patients 1 , yet harbours mutation-derived T cell neoantigens that are suitable for vaccines 2 , 3 . Here in a phase I trial of adjuvant autogene cevumeran, an individualized neoantigen vaccine based on uridine mRNA–lipoplex nanoparticles,...
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| Vydáno v: | Nature (London) Ročník 618; číslo 7963; s. 144 - 150 |
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| Médium: | Journal Article |
| Jazyk: | angličtina |
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London
Nature Publishing Group UK
01.06.2023
Nature Publishing Group |
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| ISSN: | 0028-0836, 1476-4687, 1476-4687 |
| On-line přístup: | Získat plný text |
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| Abstract | Pancreatic ductal adenocarcinoma (PDAC) is lethal in 88% of patients
1
, yet harbours mutation-derived T cell neoantigens that are suitable for vaccines
2
,
3
. Here in a phase I trial of adjuvant autogene cevumeran, an individualized neoantigen vaccine based on uridine mRNA–lipoplex nanoparticles, we synthesized mRNA neoantigen vaccines in real time from surgically resected PDAC tumours. After surgery, we sequentially administered atezolizumab (an anti-PD-L1 immunotherapy), autogene cevumeran (a maximum of 20 neoantigens per patient) and a modified version of a four-drug chemotherapy regimen (mFOLFIRINOX, comprising folinic acid, fluorouracil, irinotecan and oxaliplatin). The end points included vaccine-induced neoantigen-specific T cells by high-threshold assays, 18-month recurrence-free survival and oncologic feasibility. We treated 16 patients with atezolizumab and autogene cevumeran, then 15 patients with mFOLFIRINOX. Autogene cevumeran was administered within 3 days of benchmarked times, was tolerable and induced de novo high-magnitude neoantigen-specific T cells in 8 out of 16 patients, with half targeting more than one vaccine neoantigen. Using a new mathematical strategy to track T cell clones (CloneTrack) and functional assays, we found that vaccine-expanded T cells comprised up to 10% of all blood T cells, re-expanded with a vaccine booster and included long-lived polyfunctional neoantigen-specific effector CD8
+
T cells. At 18-month median follow-up, patients with vaccine-expanded T cells (responders) had a longer median recurrence-free survival (not reached) compared with patients without vaccine-expanded T cells (non-responders; 13.4 months,
P
= 0.003). Differences in the immune fitness of the patients did not confound this correlation, as responders and non-responders mounted equivalent immunity to a concurrent unrelated mRNA vaccine against SARS-CoV-2. Thus, adjuvant atezolizumab, autogene cevumeran and mFOLFIRINOX induces substantial T cell activity that may correlate with delayed PDAC recurrence.
A phase I clinical trial of an adjuvant personalized mRNA neoantigen vaccine, autogene cevumeran, in patients with pancreatic ductal carcinoma demonstrates that the vaccine can induce T cell activity that may correlate with delayed recurrence of disease. |
|---|---|
| AbstractList | Pancreatic ductal adenocarcinoma (PDAC) is lethal in 88% ofpatients1, yet harbours mutation-derived T cell neoantigens that are suitable for vaccines2,3. Here in a phase I trial of adjuvant autogene cevumeran, an individualized neoantigen vaccine based on uridine mRNA-lipoplex nanoparticles, we synthesized mRNA neoantigen vaccines in real time from surgically resected PDAC tumours. After surgery, we sequentially administered atezolizumab (an anti-PD-Ll immunotherapy), autogene cevumeran (a maximum of20 neoantigens per patient) and a modified version of a four-drug chemotherapy regimen (mFOLFIRINOX, comprising folinic acid, fluorouracil, irinotecan and oxaliplatin). The end points included vaccine-induced neoantigen-specific T cells by highthreshold assays, 18-month recurrence-free survival and oncologic feasibility. We treated 16 patients with atezolizumab and autogene cevumeran, then 15 patients with mFOLFIRINOX. Autogene cevumeran was administered within 3days of benchmarked times, was tolerable and induced de novo high-magnitude neoantigen-specific T cells in 8 out of16 patients, with halftargeting more than one vaccine neoantigen. Using a new mathematical strategy to track T cell clones (CloneTrack) and functional assays, we found that vaccine-expanded Tcells comprised up to 10% ofall blood T cells, re-expanded with a vaccine booster and included long-lived polyfunctional neoantigen-specific effector CD8+ T cells. At 18-month median follow-up, patients with vaccine-expanded T cells (responders) had a longer median recurrence-free survival (not reached) compared with patients without vaccine-expanded T cells (non-responders; 13.4 months, P= 0.003). Differences in the immune fitness ofthe patients did not confound this correlation, as responders and non-responders mounted equivalent immunity to a concurrent unrelated mRNA vaccine against SARS-CoV-2. Thus, adjuvant atezolizumab, autogene cevumeran and mFOLFIRINOX induces substantial T cell activity that may correlate with delayed PDAC recurrence. Pancreatic ductal adenocarcinoma (PDAC) is lethal in 88% of patients , yet harbours mutation-derived T cell neoantigens that are suitable for vaccines . Here in a phase I trial of adjuvant autogene cevumeran, an individualized neoantigen vaccine based on uridine mRNA-lipoplex nanoparticles, we synthesized mRNA neoantigen vaccines in real time from surgically resected PDAC tumours. After surgery, we sequentially administered atezolizumab (an anti-PD-L1 immunotherapy), autogene cevumeran (a maximum of 20 neoantigens per patient) and a modified version of a four-drug chemotherapy regimen (mFOLFIRINOX, comprising folinic acid, fluorouracil, irinotecan and oxaliplatin). The end points included vaccine-induced neoantigen-specific T cells by high-threshold assays, 18-month recurrence-free survival and oncologic feasibility. We treated 16 patients with atezolizumab and autogene cevumeran, then 15 patients with mFOLFIRINOX. Autogene cevumeran was administered within 3 days of benchmarked times, was tolerable and induced de novo high-magnitude neoantigen-specific T cells in 8 out of 16 patients, with half targeting more than one vaccine neoantigen. Using a new mathematical strategy to track T cell clones (CloneTrack) and functional assays, we found that vaccine-expanded T cells comprised up to 10% of all blood T cells, re-expanded with a vaccine booster and included long-lived polyfunctional neoantigen-specific effector CD8 T cells. At 18-month median follow-up, patients with vaccine-expanded T cells (responders) had a longer median recurrence-free survival (not reached) compared with patients without vaccine-expanded T cells (non-responders; 13.4 months, P = 0.003). Differences in the immune fitness of the patients did not confound this correlation, as responders and non-responders mounted equivalent immunity to a concurrent unrelated mRNA vaccine against SARS-CoV-2. Thus, adjuvant atezolizumab, autogene cevumeran and mFOLFIRINOX induces substantial T cell activity that may correlate with delayed PDAC recurrence. Pancreatic ductal adenocarcinoma (PDAC) is lethal in 88% of patients 1 , yet harbours mutation-derived T cell neoantigens that are suitable for vaccines 2 , 3 . Here in a phase I trial of adjuvant autogene cevumeran, an individualized neoantigen vaccine based on uridine mRNA–lipoplex nanoparticles, we synthesized mRNA neoantigen vaccines in real time from surgically resected PDAC tumours. After surgery, we sequentially administered atezolizumab (an anti-PD-L1 immunotherapy), autogene cevumeran (a maximum of 20 neoantigens per patient) and a modified version of a four-drug chemotherapy regimen (mFOLFIRINOX, comprising folinic acid, fluorouracil, irinotecan and oxaliplatin). The end points included vaccine-induced neoantigen-specific T cells by high-threshold assays, 18-month recurrence-free survival and oncologic feasibility. We treated 16 patients with atezolizumab and autogene cevumeran, then 15 patients with mFOLFIRINOX. Autogene cevumeran was administered within 3 days of benchmarked times, was tolerable and induced de novo high-magnitude neoantigen-specific T cells in 8 out of 16 patients, with half targeting more than one vaccine neoantigen. Using a new mathematical strategy to track T cell clones (CloneTrack) and functional assays, we found that vaccine-expanded T cells comprised up to 10% of all blood T cells, re-expanded with a vaccine booster and included long-lived polyfunctional neoantigen-specific effector CD8 + T cells. At 18-month median follow-up, patients with vaccine-expanded T cells (responders) had a longer median recurrence-free survival (not reached) compared with patients without vaccine-expanded T cells (non-responders; 13.4 months, P = 0.003). Differences in the immune fitness of the patients did not confound this correlation, as responders and non-responders mounted equivalent immunity to a concurrent unrelated mRNA vaccine against SARS-CoV-2. Thus, adjuvant atezolizumab, autogene cevumeran and mFOLFIRINOX induces substantial T cell activity that may correlate with delayed PDAC recurrence. A phase I clinical trial of an adjuvant personalized mRNA neoantigen vaccine, autogene cevumeran, in patients with pancreatic ductal carcinoma demonstrates that the vaccine can induce T cell activity that may correlate with delayed recurrence of disease. Pancreatic ductal adenocarcinoma (PDAC) is lethal in 88% of patients1, yet harbours mutation-derived T cell neoantigens that are suitable for vaccines 2,3. Here in a phase I trial of adjuvant autogene cevumeran, an individualized neoantigen vaccine based on uridine mRNA–lipoplex nanoparticles, we synthesized mRNA neoantigen vaccines in real time from surgically resected PDAC tumours. After surgery, we sequentially administered atezolizumab (an anti-PD-L1 immunotherapy), autogene cevumeran (a maximum of 20 neoantigens per patient) and a modified version of a four-drug chemotherapy regimen (mFOLFIRINOX, comprising folinic acid, fluorouracil, irinotecan and oxaliplatin). The end points included vaccine-induced neoantigen-specific T cells by high-threshold assays, 18-month recurrence-free survival and oncologic feasibility. We treated 16 patients with atezolizumab and autogene cevumeran, then 15 patients with mFOLFIRINOX. Autogene cevumeran was administered within 3 days of benchmarked times, was tolerable and induced de novo high-magnitude neoantigen-specific T cells in 8 out of 16 patients, with half targeting more than one vaccine neoantigen. Using a new mathematical strategy to track T cell clones (CloneTrack) and functional assays, we found that vaccine-expanded T cells comprised up to 10% of all blood T cells, re-expanded with a vaccine booster and included long-lived polyfunctional neoantigen-specific effector CD8+ T cells. At 18-month median follow-up, patients with vaccine-expanded T cells (responders) had a longer median recurrence-free survival (not reached) compared with patients without vaccine-expanded T cells (non-responders; 13.4 months, P = 0.003). Differences in the immune fitness of the patients did not confound this correlation, as responders and non-responders mounted equivalent immunity to a concurrent unrelated mRNA vaccine against SARS-CoV-2. Thus, adjuvant atezolizumab, autogene cevumeran and mFOLFIRINOX induces substantial T cell activity that may correlate with delayed PDAC recurrence. A phase I clinical trial of an adjuvant personalized mRNA neoantigen vaccine, autogene cevumeran, in patients with pancreatic ductal carcinoma demonstrates that the vaccine can induce T cell activity that may correlate with delayed recurrence of disease. Pancreatic ductal adenocarcinoma (PDAC) is lethal in 88% of patients1, yet harbours mutation-derived T cell neoantigens that are suitable for vaccines 2,3. Here in a phase I trial of adjuvant autogene cevumeran, an individualized neoantigen vaccine based on uridine mRNA-lipoplex nanoparticles, we synthesized mRNA neoantigen vaccines in real time from surgically resected PDAC tumours. After surgery, we sequentially administered atezolizumab (an anti-PD-L1 immunotherapy), autogene cevumeran (a maximum of 20 neoantigens per patient) and a modified version of a four-drug chemotherapy regimen (mFOLFIRINOX, comprising folinic acid, fluorouracil, irinotecan and oxaliplatin). The end points included vaccine-induced neoantigen-specific T cells by high-threshold assays, 18-month recurrence-free survival and oncologic feasibility. We treated 16 patients with atezolizumab and autogene cevumeran, then 15 patients with mFOLFIRINOX. Autogene cevumeran was administered within 3 days of benchmarked times, was tolerable and induced de novo high-magnitude neoantigen-specific T cells in 8 out of 16 patients, with half targeting more than one vaccine neoantigen. Using a new mathematical strategy to track T cell clones (CloneTrack) and functional assays, we found that vaccine-expanded T cells comprised up to 10% of all blood T cells, re-expanded with a vaccine booster and included long-lived polyfunctional neoantigen-specific effector CD8+ T cells. At 18-month median follow-up, patients with vaccine-expanded T cells (responders) had a longer median recurrence-free survival (not reached) compared with patients without vaccine-expanded T cells (non-responders; 13.4 months, P = 0.003). Differences in the immune fitness of the patients did not confound this correlation, as responders and non-responders mounted equivalent immunity to a concurrent unrelated mRNA vaccine against SARS-CoV-2. Thus, adjuvant atezolizumab, autogene cevumeran and mFOLFIRINOX induces substantial T cell activity that may correlate with delayed PDAC recurrence.Pancreatic ductal adenocarcinoma (PDAC) is lethal in 88% of patients1, yet harbours mutation-derived T cell neoantigens that are suitable for vaccines 2,3. Here in a phase I trial of adjuvant autogene cevumeran, an individualized neoantigen vaccine based on uridine mRNA-lipoplex nanoparticles, we synthesized mRNA neoantigen vaccines in real time from surgically resected PDAC tumours. After surgery, we sequentially administered atezolizumab (an anti-PD-L1 immunotherapy), autogene cevumeran (a maximum of 20 neoantigens per patient) and a modified version of a four-drug chemotherapy regimen (mFOLFIRINOX, comprising folinic acid, fluorouracil, irinotecan and oxaliplatin). The end points included vaccine-induced neoantigen-specific T cells by high-threshold assays, 18-month recurrence-free survival and oncologic feasibility. We treated 16 patients with atezolizumab and autogene cevumeran, then 15 patients with mFOLFIRINOX. Autogene cevumeran was administered within 3 days of benchmarked times, was tolerable and induced de novo high-magnitude neoantigen-specific T cells in 8 out of 16 patients, with half targeting more than one vaccine neoantigen. Using a new mathematical strategy to track T cell clones (CloneTrack) and functional assays, we found that vaccine-expanded T cells comprised up to 10% of all blood T cells, re-expanded with a vaccine booster and included long-lived polyfunctional neoantigen-specific effector CD8+ T cells. At 18-month median follow-up, patients with vaccine-expanded T cells (responders) had a longer median recurrence-free survival (not reached) compared with patients without vaccine-expanded T cells (non-responders; 13.4 months, P = 0.003). Differences in the immune fitness of the patients did not confound this correlation, as responders and non-responders mounted equivalent immunity to a concurrent unrelated mRNA vaccine against SARS-CoV-2. Thus, adjuvant atezolizumab, autogene cevumeran and mFOLFIRINOX induces substantial T cell activity that may correlate with delayed PDAC recurrence. Pancreatic ductal adenocarcinoma (PDAC) is lethal in 88% of patients 1 , yet harbours mutation-derived T cell neoantigens that are suitable for vaccines 2,3 . Here in a phase I trial of adjuvant autogene cevumeran, an individualized neoantigen vaccine based on uridine mRNA–lipoplex nanoparticles, we synthesized mRNA neoantigen vaccines in real time from surgically resected PDAC tumours. After surgery, we sequentially administered atezolizumab (an anti-PD-L1 immunotherapy), autogene cevumeran (a maximum of 20 neoantigens per patient) and a modified version of a four-drug chemotherapy regimen (mFOLFIRINOX, comprising folinic acid, fluorouracil, irinotecan and oxaliplatin). The end points included vaccine-induced neoantigen-specific T cells by high-threshold assays, 18-month recurrence-free survival and oncologic feasibility. We treated 16 patients with atezolizumab and autogene cevumeran, then 15 patients with mFOLFIRINOX. Autogene cevumeran was administered within 3 days of benchmarked times, was tolerable and induced de novo high-magnitude neoantigen-specific T cells in 8 out of 16 patients, with half targeting more than one vaccine neoantigen. Using a new mathematical strategy to track T cell clones (CloneTrack) and functional assays, we found that vaccine-expanded T cells comprised up to 10% of all blood T cells, re-expanded with a vaccine booster and included long-lived polyfunctional neoantigen-specific effector CD8 + T cells. At 18-month median follow-up, patients with vaccine-expanded T cells (responders) had a longer median recurrence-free survival (not reached) compared with patients without vaccine-expanded T cells (non-responders; 13.4 months, P = 0.003). Differences in the immune fitness of the patients did not confound this correlation, as responders and non-responders mounted equivalent immunity to a concurrent unrelated mRNA vaccine against SARS-CoV-2. Thus, adjuvant atezolizumab, autogene cevumeran and mFOLFIRINOX induces substantial T cell activity that may correlate with delayed PDAC recurrence. |
| Author | Rhee, Ina Dobrin, Anton Odgerel, Zagaa Yu, Rebecca Patterson, Erin Ceglia, Nicholas Epstein, Andrew S. Zebboudj, Abderezak Tang, Laura Basturk, Olca Chandra, Adrienne Kaya Ruan, Jennifer Olcese, Cristina Merghoub, Taha Wolchok, Jedd D. Guasp, Pablo Mellman, Ira Türeci, Özlem Chu, Alexander Cohen, Noah Sethna, Zachary Wei, Alice C. Soares, Kevin C. D’Angelica, Michael I. Sugarman, Ryan Balachandran, Vinod P. Derhovanessian, Evelyna Greenbaum, Benjamin D. Yadav, Mahesh Lihm, Jayon Waters, Theresa O’Reilly, Eileen M. Pang, Nan Park, Wungki Jarnagin, William R. Won, Elizabeth Łuksza, Marta Katz, Seth Varghese, Anna M. Momtaz, Parisa Müller, Felicitas Do, Richard Kinh Gönen, Mithat Desai, Avni Kingham, T. Peter Drebin, Jeffrey Sahin, Ugur Rojas, Luis A. Amisaki, Masataka Sadelain, Michel Payne, George |
| Author_xml | – sequence: 1 givenname: Luis A. orcidid: 0000-0001-9218-4086 surname: Rojas fullname: Rojas, Luis A. organization: Immuno-Oncology Service, Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, Hepatopancreatobiliary Service, Department of Surgery, Memorial Sloan Kettering Cancer Center – sequence: 2 givenname: Zachary surname: Sethna fullname: Sethna, Zachary organization: Immuno-Oncology Service, Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, Hepatopancreatobiliary Service, Department of Surgery, Memorial Sloan Kettering Cancer Center – sequence: 3 givenname: Kevin C. orcidid: 0000-0002-0406-017X surname: Soares fullname: Soares, Kevin C. organization: Hepatopancreatobiliary Service, Department of Surgery, Memorial Sloan Kettering Cancer Center, David M. Rubenstein Center for Pancreatic Cancer Research, Memorial Sloan Kettering Cancer Center – sequence: 4 givenname: Cristina surname: Olcese fullname: Olcese, Cristina organization: Hepatopancreatobiliary Service, Department of Surgery, Memorial Sloan Kettering Cancer Center – sequence: 5 givenname: Nan surname: Pang fullname: Pang, Nan organization: Hepatopancreatobiliary Service, Department of Surgery, Memorial Sloan Kettering Cancer Center – sequence: 6 givenname: Erin surname: Patterson fullname: Patterson, Erin organization: Hepatopancreatobiliary Service, Department of Surgery, Memorial Sloan Kettering Cancer Center – sequence: 7 givenname: Jayon surname: Lihm fullname: Lihm, Jayon organization: Computational Oncology Service, Department of Epidemiology and Biostatistics, Memorial Sloan Kettering Cancer Center – sequence: 8 givenname: Nicholas surname: Ceglia fullname: Ceglia, Nicholas organization: Computational Oncology Service, Department of Epidemiology and Biostatistics, Memorial Sloan Kettering Cancer Center – sequence: 9 givenname: Pablo orcidid: 0000-0002-3655-916X surname: Guasp fullname: Guasp, Pablo organization: Immuno-Oncology Service, Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, Hepatopancreatobiliary Service, Department of Surgery, Memorial Sloan Kettering Cancer Center – sequence: 10 givenname: Alexander surname: Chu fullname: Chu, Alexander organization: Computational Oncology Service, Department of Epidemiology and Biostatistics, Memorial Sloan Kettering Cancer Center – sequence: 11 givenname: Rebecca surname: Yu fullname: Yu, Rebecca organization: Immuno-Oncology Service, Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, Hepatopancreatobiliary Service, Department of Surgery, Memorial Sloan Kettering Cancer Center – sequence: 12 givenname: Adrienne Kaya surname: Chandra fullname: Chandra, Adrienne Kaya organization: Immuno-Oncology Service, Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, Hepatopancreatobiliary Service, Department of Surgery, Memorial Sloan Kettering Cancer Center – sequence: 13 givenname: Theresa surname: Waters fullname: Waters, Theresa organization: Immuno-Oncology Service, Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, Hepatopancreatobiliary Service, Department of Surgery, Memorial Sloan Kettering Cancer Center – sequence: 14 givenname: Jennifer surname: Ruan fullname: Ruan, Jennifer organization: Immuno-Oncology Service, Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, Hepatopancreatobiliary Service, Department of Surgery, Memorial Sloan Kettering Cancer Center – sequence: 15 givenname: Masataka orcidid: 0000-0003-4153-4036 surname: Amisaki fullname: Amisaki, Masataka organization: Immuno-Oncology Service, Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, Hepatopancreatobiliary Service, Department of Surgery, Memorial Sloan Kettering Cancer Center – sequence: 16 givenname: Abderezak orcidid: 0000-0002-4708-5211 surname: Zebboudj fullname: Zebboudj, Abderezak organization: Immuno-Oncology Service, Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, Hepatopancreatobiliary Service, Department of Surgery, Memorial Sloan Kettering Cancer Center – sequence: 17 givenname: Zagaa surname: Odgerel fullname: Odgerel, Zagaa organization: Immuno-Oncology Service, Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, Hepatopancreatobiliary Service, Department of Surgery, Memorial Sloan Kettering Cancer Center – sequence: 18 givenname: George surname: Payne fullname: Payne, George organization: Immuno-Oncology Service, Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, Hepatopancreatobiliary Service, Department of Surgery, Memorial Sloan Kettering Cancer Center – sequence: 19 givenname: Evelyna surname: Derhovanessian fullname: Derhovanessian, Evelyna organization: BioNTech – sequence: 20 givenname: Felicitas surname: Müller fullname: Müller, Felicitas organization: BioNTech – sequence: 21 givenname: Ina surname: Rhee fullname: Rhee, Ina organization: Genentech – sequence: 22 givenname: Mahesh surname: Yadav fullname: Yadav, Mahesh organization: Genentech – sequence: 23 givenname: Anton orcidid: 0000-0002-9751-0677 surname: Dobrin fullname: Dobrin, Anton organization: Center for Cell Engineering, Memorial Sloan Kettering Cancer Center, Immunology Program, Sloan Kettering Institute, Memorial Sloan Kettering Cancer Center – sequence: 24 givenname: Michel orcidid: 0000-0002-9031-8025 surname: Sadelain fullname: Sadelain, Michel organization: Center for Cell Engineering, Memorial Sloan Kettering Cancer Center, Immunology Program, Sloan Kettering Institute, Memorial Sloan Kettering Cancer Center – sequence: 25 givenname: Marta surname: Łuksza fullname: Łuksza, Marta organization: Department of Oncological Sciences, Tisch Cancer Institute, Icahn School of Medicine at Mount Sinai – sequence: 26 givenname: Noah orcidid: 0000-0003-3947-2585 surname: Cohen fullname: Cohen, Noah organization: Department of Surgery, Icahn School of Medicine at Mount Sinai – sequence: 27 givenname: Laura surname: Tang fullname: Tang, Laura organization: Department of Pathology, Memorial Sloan Kettering Cancer Center – sequence: 28 givenname: Olca orcidid: 0000-0003-2747-1366 surname: Basturk fullname: Basturk, Olca organization: Department of Pathology, Memorial Sloan Kettering Cancer Center – sequence: 29 givenname: Mithat surname: Gönen fullname: Gönen, Mithat organization: Department of Epidemiology and Biostatistics, Memorial Sloan Kettering Cancer Center – sequence: 30 givenname: Seth surname: Katz fullname: Katz, Seth organization: Department of Radiology, Memorial Sloan Kettering Cancer Center – sequence: 31 givenname: Richard Kinh surname: Do fullname: Do, Richard Kinh organization: Department of Radiology, Memorial Sloan Kettering Cancer Center – sequence: 32 givenname: Andrew S. surname: Epstein fullname: Epstein, Andrew S. organization: Department of Medicine, Memorial Sloan Kettering Cancer Center – sequence: 33 givenname: Parisa surname: Momtaz fullname: Momtaz, Parisa organization: Department of Medicine, Memorial Sloan Kettering Cancer Center – sequence: 34 givenname: Wungki orcidid: 0000-0002-8006-3102 surname: Park fullname: Park, Wungki organization: David M. Rubenstein Center for Pancreatic Cancer Research, Memorial Sloan Kettering Cancer Center, Department of Medicine, Memorial Sloan Kettering Cancer Center – sequence: 35 givenname: Ryan surname: Sugarman fullname: Sugarman, Ryan organization: Department of Medicine, Memorial Sloan Kettering Cancer Center – sequence: 36 givenname: Anna M. surname: Varghese fullname: Varghese, Anna M. organization: Department of Medicine, Memorial Sloan Kettering Cancer Center – sequence: 37 givenname: Elizabeth surname: Won fullname: Won, Elizabeth organization: Department of Medicine, Memorial Sloan Kettering Cancer Center – sequence: 38 givenname: Avni surname: Desai fullname: Desai, Avni organization: Department of Medicine, Memorial Sloan Kettering Cancer Center – sequence: 39 givenname: Alice C. orcidid: 0000-0002-2505-959X surname: Wei fullname: Wei, Alice C. organization: Hepatopancreatobiliary Service, Department of Surgery, Memorial Sloan Kettering Cancer Center, David M. Rubenstein Center for Pancreatic Cancer Research, Memorial Sloan Kettering Cancer Center – sequence: 40 givenname: Michael I. surname: D’Angelica fullname: D’Angelica, Michael I. organization: Hepatopancreatobiliary Service, Department of Surgery, Memorial Sloan Kettering Cancer Center, David M. Rubenstein Center for Pancreatic Cancer Research, Memorial Sloan Kettering Cancer Center – sequence: 41 givenname: T. Peter surname: Kingham fullname: Kingham, T. Peter organization: Hepatopancreatobiliary Service, Department of Surgery, Memorial Sloan Kettering Cancer Center, David M. Rubenstein Center for Pancreatic Cancer Research, Memorial Sloan Kettering Cancer Center – sequence: 42 givenname: Ira orcidid: 0000-0002-6132-7299 surname: Mellman fullname: Mellman, Ira organization: Genentech – sequence: 43 givenname: Taha orcidid: 0000-0002-1518-5111 surname: Merghoub fullname: Merghoub, Taha organization: Meyer Cancer Center, Weill Cornell Medicine, Weill Cornell Medical College – sequence: 44 givenname: Jedd D. surname: Wolchok fullname: Wolchok, Jedd D. organization: Meyer Cancer Center, Weill Cornell Medicine, Weill Cornell Medical College – sequence: 45 givenname: Ugur orcidid: 0000-0003-0363-1564 surname: Sahin fullname: Sahin, Ugur organization: BioNTech – sequence: 46 givenname: Özlem surname: Türeci fullname: Türeci, Özlem organization: BioNTech, HI-TRON, Helmholtz Institute for Translational Oncology – sequence: 47 givenname: Benjamin D. orcidid: 0000-0001-6153-8793 surname: Greenbaum fullname: Greenbaum, Benjamin D. email: greenbab@mskcc.org organization: Computational Oncology Service, Department of Epidemiology and Biostatistics, Memorial Sloan Kettering Cancer Center, Physiology, Biophysics and Systems Biology, Weill Cornell Medicine, Weill Cornell Medical College – sequence: 48 givenname: William R. surname: Jarnagin fullname: Jarnagin, William R. organization: Hepatopancreatobiliary Service, Department of Surgery, Memorial Sloan Kettering Cancer Center, David M. Rubenstein Center for Pancreatic Cancer Research, Memorial Sloan Kettering Cancer Center – sequence: 49 givenname: Jeffrey surname: Drebin fullname: Drebin, Jeffrey organization: Hepatopancreatobiliary Service, Department of Surgery, Memorial Sloan Kettering Cancer Center, David M. Rubenstein Center for Pancreatic Cancer Research, Memorial Sloan Kettering Cancer Center – sequence: 50 givenname: Eileen M. orcidid: 0000-0002-8076-9199 surname: O’Reilly fullname: O’Reilly, Eileen M. organization: David M. Rubenstein Center for Pancreatic Cancer Research, Memorial Sloan Kettering Cancer Center, Department of Medicine, Memorial Sloan Kettering Cancer Center – sequence: 51 givenname: Vinod P. orcidid: 0000-0002-2956-223X surname: Balachandran fullname: Balachandran, Vinod P. email: balachav@mskcc.org organization: Immuno-Oncology Service, Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, Hepatopancreatobiliary Service, Department of Surgery, Memorial Sloan Kettering Cancer Center, David M. Rubenstein Center for Pancreatic Cancer Research, Memorial Sloan Kettering Cancer Center |
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| Copyright | The Author(s) 2023 2023. The Author(s). Copyright Nature Publishing Group Jun 1, 2023 |
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| Snippet | Pancreatic ductal adenocarcinoma (PDAC) is lethal in 88% of patients
1
, yet harbours mutation-derived T cell neoantigens that are suitable for vaccines
2
,
3... Pancreatic ductal adenocarcinoma (PDAC) is lethal in 88% of patients 1 , yet harbours mutation-derived T cell neoantigens that are suitable for vaccines 2,3 .... Pancreatic ductal adenocarcinoma (PDAC) is lethal in 88% of patients , yet harbours mutation-derived T cell neoantigens that are suitable for vaccines . Here... Pancreatic ductal adenocarcinoma (PDAC) is lethal in 88% ofpatients1, yet harbours mutation-derived T cell neoantigens that are suitable for vaccines2,3. Here... Pancreatic ductal adenocarcinoma (PDAC) is lethal in 88% of patients1, yet harbours mutation-derived T cell neoantigens that are suitable for vaccines 2,3.... |
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| Title | Personalized RNA neoantigen vaccines stimulate T cells in pancreatic cancer |
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