Neoantigen quality predicts immunoediting in survivors of pancreatic cancer
Cancer immunoediting 1 is a hallmark of cancer 2 that predicts that lymphocytes kill more immunogenic cancer cells to cause less immunogenic clones to dominate a population. Although proven in mice 1 , 3 , whether immunoediting occurs naturally in human cancers remains unclear. Here, to address this...
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| Veröffentlicht in: | Nature (London) Jg. 606; H. 7913; S. 389 - 395 |
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| Format: | Journal Article |
| Sprache: | Englisch |
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London
Nature Publishing Group UK
09.06.2022
Nature Publishing Group |
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| ISSN: | 0028-0836, 1476-4687, 1476-4687 |
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| Abstract | Cancer immunoediting
1
is a hallmark of cancer
2
that predicts that lymphocytes kill more immunogenic cancer cells to cause less immunogenic clones to dominate a population. Although proven in mice
1
,
3
, whether immunoediting occurs naturally in human cancers remains unclear. Here, to address this, we investigate how 70 human pancreatic cancers evolved over 10 years. We find that, despite having more time to accumulate mutations, rare long-term survivors of pancreatic cancer who have stronger T cell activity in primary tumours develop genetically less heterogeneous recurrent tumours with fewer immunogenic mutations (neoantigens). To quantify whether immunoediting underlies these observations, we infer that a neoantigen is immunogenic (high-quality) by two features—‘non-selfness’ based on neoantigen similarity to known antigens
4
,
5
, and ‘selfness’ based on the antigenic distance required for a neoantigen to differentially bind to the MHC or activate a T cell compared with its wild-type peptide. Using these features, we estimate cancer clone fitness as the aggregate cost of T cells recognizing high-quality neoantigens offset by gains from oncogenic mutations. With this model, we predict the clonal evolution of tumours to reveal that long-term survivors of pancreatic cancer develop recurrent tumours with fewer high-quality neoantigens. Thus, we submit evidence that that the human immune system naturally edits neoantigens. Furthermore, we present a model to predict how immune pressure induces cancer cell populations to evolve over time. More broadly, our results argue that the immune system fundamentally surveils host genetic changes to suppress cancer.
The human immune system naturally edits cancers of high-quality neoantigens. |
|---|---|
| AbstractList | Cancer immunoediting1 is a hallmark of cancer2 that predicts that lymphocytes kill more immunogenic cancer cells to cause less immunogenic clones to dominate a population. Although proven in mice1,3, whether immunoediting occurs naturally in human cancers remains unclear. Here, to address this, we investigate how 70 human pancreatic cancers evolved over 10 years. We find that, despite having more time to accumulate mutations, rare long-term survivors of pancreatic cancer who have stronger T cell activity in primary tumours develop genetically less heterogeneous recurrent tumours with fewer immunogenic mutations (neoantigens). To quantify whether immunoediting underlies these observations, we infer that a neoantigen is immunogenic (high-quality) by two features-'non-selfness' based on neoantigen similarity to known antigens4,5, and 'selfness' based on the antigenic distance required for a neoantigen to differentially bind to the MHC or activate a T cell compared with its wild-type peptide. Using these features, we estimate cancer clone fitness as the aggregate cost of T cells recognizing high-quality neoantigens offset by gains from oncogenic mutations. With this model, we predict the clonal evolution of tumours to reveal that long-term survivors of pancreatic cancer develop recurrent tumours with fewer high-quality neoantigens. Thus, we submit evidence that that the human immune system naturally edits neoantigens. Furthermore, we present a model to predict how immune pressure induces cancer cell populations to evolve over time. More broadly, our results argue that the immune system fundamentally surveils host genetic changes to suppress cancer.Cancer immunoediting1 is a hallmark of cancer2 that predicts that lymphocytes kill more immunogenic cancer cells to cause less immunogenic clones to dominate a population. Although proven in mice1,3, whether immunoediting occurs naturally in human cancers remains unclear. Here, to address this, we investigate how 70 human pancreatic cancers evolved over 10 years. We find that, despite having more time to accumulate mutations, rare long-term survivors of pancreatic cancer who have stronger T cell activity in primary tumours develop genetically less heterogeneous recurrent tumours with fewer immunogenic mutations (neoantigens). To quantify whether immunoediting underlies these observations, we infer that a neoantigen is immunogenic (high-quality) by two features-'non-selfness' based on neoantigen similarity to known antigens4,5, and 'selfness' based on the antigenic distance required for a neoantigen to differentially bind to the MHC or activate a T cell compared with its wild-type peptide. Using these features, we estimate cancer clone fitness as the aggregate cost of T cells recognizing high-quality neoantigens offset by gains from oncogenic mutations. With this model, we predict the clonal evolution of tumours to reveal that long-term survivors of pancreatic cancer develop recurrent tumours with fewer high-quality neoantigens. Thus, we submit evidence that that the human immune system naturally edits neoantigens. Furthermore, we present a model to predict how immune pressure induces cancer cell populations to evolve over time. More broadly, our results argue that the immune system fundamentally surveils host genetic changes to suppress cancer. Cancer immunoediting is a hallmark of cancer that predicts that lymphocytes kill more immunogenic cancer cells to cause less immunogenic clones to dominate a population. Although proven in mice , whether immunoediting occurs naturally in human cancers remains unclear. Here, to address this, we investigate how 70 human pancreatic cancers evolved over 10 years. We find that, despite having more time to accumulate mutations, rare long-term survivors of pancreatic cancer who have stronger T cell activity in primary tumours develop genetically less heterogeneous recurrent tumours with fewer immunogenic mutations (neoantigens). To quantify whether immunoediting underlies these observations, we infer that a neoantigen is immunogenic (high-quality) by two features-'non-selfness' based on neoantigen similarity to known antigens , and 'selfness' based on the antigenic distance required for a neoantigen to differentially bind to the MHC or activate a T cell compared with its wild-type peptide. Using these features, we estimate cancer clone fitness as the aggregate cost of T cells recognizing high-quality neoantigens offset by gains from oncogenic mutations. With this model, we predict the clonal evolution of tumours to reveal that long-term survivors of pancreatic cancer develop recurrent tumours with fewer high-quality neoantigens. Thus, we submit evidence that that the human immune system naturally edits neoantigens. Furthermore, we present a model to predict how immune pressure induces cancer cell populations to evolve over time. More broadly, our results argue that the immune system fundamentally surveils host genetic changes to suppress cancer. Cancer immunoediting 1 is a hallmark of cancer 2 that predicts that lymphocytes kill more immunogenic cancer cells to cause less immunogenic clones to dominate a population. Although proven in mice 1,3 , whether immunoediting occurs naturally in human cancers remains unclear. Here, to address this, we investigate how 70 human pancreatic cancers evolved over 10 years. We find that, despite having more time to accumulate mutations, rare long-term survivors of pancreatic cancer who have stronger T cell activity in primary tumours develop genetically less heterogeneous recurrent tumours with fewer immunogenic mutations (neoantigens). To quantify whether immunoediting underlies these observations, we infer that a neoantigen is immunogenic (high-quality) by two features—‘non-selfness’ based on neoantigen similarity to known antigens 4,5 , and ‘selfness’ based on the antigenic distance required for a neoantigen to differentially bind to the MHC or activate a T cell compared with its wild-type peptide. Using these features, we estimate cancer clone fitness as the aggregate cost of T cells recognizing high-quality neoantigens offset by gains from oncogenic mutations. With this model, we predict the clonal evolution of tumours to reveal that long-term survivors of pancreatic cancer develop recurrent tumours with fewer high-quality neoantigens. Thus, we submit evidence that that the human immune system naturally edits neoantigens. Furthermore, we present a model to predict how immune pressure induces cancer cell populations to evolve over time. More broadly, our results argue that the immune system fundamentally surveils host genetic changes to suppress cancer. Cancer immunoediting 1 is a hallmark of cancer 2 that predicts that lymphocytes kill more immunogenic cancer cells to cause less immunogenic clones to dominate a population. Although proven in mice 1,3 , whether immunoediting occurs naturally in human cancers remains unclear. Here, to address this, we investigate how 70 human pancreatic cancers evolved over 10 years. We find that, despite having more time to accumulate mutations, rare long-term survivors of pancreatic cancer who have stronger T cell activity in primary tumours develop genetically less heterogeneous recurrent tumours with fewer immunogenic mutations (neoantigens). To quantify whether immunoediting underlies these observations, we infer that a neoantigen is immunogenic (high-quality) by two features—‘non-selfness’ based on neoantigen similarity to known antigens 4,5 , and ‘selfness’ based on the antigenic distance required for a neoantigen to differentially bind to the MHC or activate a T cell compared with its wild-type peptide. Using these features, we estimate cancer clone fitness as the aggregate cost of T cells recognizing high-quality neoantigens offset by gains from oncogenic mutations. With this model, we predict the clonal evolution of tumours to reveal that long-term survivors of pancreatic cancer develop recurrent tumours with fewer high-quality neoantigens. Thus, we submit evidence that that the human immune system naturally edits neoantigens. Furthermore, we present a model to predict how immune pressure induces cancer cell populations to evolve over time. More broadly, our results argue that the immune system fundamentally surveils host genetic changes to suppress cancer. Cancer immunoediting1 is a hallmark of cancer2 that predicts that lymphocytes kill more immunogenic cancer cells to cause less immunogenic clones to dominate a population. Although proven in mice1,3, whether immunoediting occurs naturally in human cancers remains unclear. Here, to address this, we investigate how 70 human pancreatic cancers evolved over 10 years. We find that, despite having more time to accumulate mutations, rare long-term survivors of pancreatic cancer who have stronger T cell activity in primary tumours develop genetically less heterogeneous recurrent tumours with fewer immunogenic mutations (neoantigens). To quantify whether immunoediting underlies these observations, we infer that a neoantigen is immunogenic (high-quality) by two features-'non-selfness' based on neoantigen similarity to known antigens4,5, and 'selfness' based on the antigenic distance required for a neoantigen to differentially bind to the MHC or activate a T cell compared with its wild-type peptide. Using these features, we estimate cancer clone fitness as the aggregate cost of T cells recognizing high-quality neoantigens offset by gains from oncogenic mutations. With this model, we predict the clonal evolution of tumours to reveal that long-term survivors of pancreatic cancer develop recurrent tumours with fewer high-quality neoantigens. Thus, we submit evidence that that the human immune system naturally edits neoantigens. Furthermore, we present a model to predict how immune pressure induces cancer cell populations to evolve over time. More broadly, our results argue that the immune system fundamentally surveils host genetic changes to suppress cancer. Cancer immunoediting 1 is a hallmark of cancer 2 that predicts that lymphocytes kill more immunogenic cancer cells to cause less immunogenic clones to dominate a population. Although proven in mice 1 , 3 , whether immunoediting occurs naturally in human cancers remains unclear. Here, to address this, we investigate how 70 human pancreatic cancers evolved over 10 years. We find that, despite having more time to accumulate mutations, rare long-term survivors of pancreatic cancer who have stronger T cell activity in primary tumours develop genetically less heterogeneous recurrent tumours with fewer immunogenic mutations (neoantigens). To quantify whether immunoediting underlies these observations, we infer that a neoantigen is immunogenic (high-quality) by two features—‘non-selfness’ based on neoantigen similarity to known antigens 4 , 5 , and ‘selfness’ based on the antigenic distance required for a neoantigen to differentially bind to the MHC or activate a T cell compared with its wild-type peptide. Using these features, we estimate cancer clone fitness as the aggregate cost of T cells recognizing high-quality neoantigens offset by gains from oncogenic mutations. With this model, we predict the clonal evolution of tumours to reveal that long-term survivors of pancreatic cancer develop recurrent tumours with fewer high-quality neoantigens. Thus, we submit evidence that that the human immune system naturally edits neoantigens. Furthermore, we present a model to predict how immune pressure induces cancer cell populations to evolve over time. More broadly, our results argue that the immune system fundamentally surveils host genetic changes to suppress cancer. The human immune system naturally edits cancers of high-quality neoantigens. Cancer immunoediting1 is a hallmark of cancer2 that predicts that lymphocytes kill more immunogenic cancer cells to cause less immunogenic clones to dominate a population. Although proven in mice1,3, whether immunoediting occurs naturally in human cancers remains unclear. Here, to address this, we investigate how 70 human pancreatic cancers evolved over 10 years. We find that, despite having more time to accumulate mutations, rare long-term survivors of pancreatic cancer who have stronger T cell activity in primary tumours develop genetically less heterogeneous recurrent tumours with fewer immunogenic mutations (neoantigens). To quantify whether immunoediting underlies these observations, we infer that a neoantigen is immunogenic (high-quality) by two features—‘non-selfness’ based on neoantigen similarity to known antigens4,5, and ‘selfness’ based on the antigenic distance required for a neoantigen to differentially bind to the MHC or activate a T cell compared with its wild-type peptide. Using these features, we estimate cancer clone fitness as the aggregate cost of T cells recognizing high-quality neoantigens offset by gains from oncogenic mutations. With this model, we predict the clonal evolution of tumours to reveal that long-term survivors of pancreatic cancer develop recurrent tumours with fewer high-quality neoantigens. Thus, we submit evidence that that the human immune system naturally edits neoantigens. Furthermore, we present a model to predict how immune pressure induces cancer cell populations to evolve over time. More broadly, our results argue that the immune system fundamentally surveils host genetic changes to suppress cancer. The human immune system naturally edits cancers of high-quality neoantigens. |
| Author | Iacobuzio-Donahue, Christine Hoyos, David Balachandran, Vinod P. Sethna, Zachary M. Dobrin, Anton Odgerel, Zagaa Greenbaum, Benjamin D. Wolchok, Jedd Walczak, Aleksandra M. Yu, Rebecca Lihm, Jayon Patterson, Erin Gigoux, Mathieu Leung, Joanne Bravi, Barbara Waters, Theresa Zebboudj, Abderezak Monasson, Remi Kappagantula, Rajya Chandra, Adrienne Kaya Łuksza, Marta Merghoub, Taha Cocco, Simona Soares, Kevin Makohon-Moore, Alvin Guasp, Pablo Gill, Anthony Rojas, Luis A. Elhanati, Yuval Mora, Thierry Johns, Amber Amisaki, Masataka Sadelain, Michel |
| Author_xml | – sequence: 1 givenname: Marta surname: Łuksza fullname: Łuksza, Marta email: marta.luksza@mssm.edu organization: Tisch Cancer Institute, Departments of Oncological Sciences and Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai – sequence: 2 givenname: Zachary M. surname: Sethna fullname: Sethna, Zachary M. organization: Computational Oncology Service, Department of Biostatistics, Memorial Sloan Kettering Cancer Center, 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: Luis A. 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: 4 givenname: Jayon orcidid: 0000-0002-1308-6507 surname: Lihm fullname: Lihm, Jayon organization: Computational Oncology Service, Department of Biostatistics, Memorial Sloan Kettering Cancer Center – sequence: 5 givenname: Barbara orcidid: 0000-0003-4860-7584 surname: Bravi fullname: Bravi, Barbara organization: Laboratoire de Physique de l’Ecole Normale Supérieure, ENS, Université PSL, CNRS, Sorbonne Université, Université de Paris, Department of Mathematics, Imperial College London – sequence: 6 givenname: Yuval surname: Elhanati fullname: Elhanati, Yuval organization: Computational Oncology Service, Department of Biostatistics, Memorial Sloan Kettering Cancer Center – sequence: 7 givenname: Kevin orcidid: 0000-0002-0406-017X surname: Soares fullname: Soares, Kevin 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: 8 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: 9 givenname: Anton 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: 10 givenname: David surname: Hoyos fullname: Hoyos, David organization: Computational Oncology Service, Department of Biostatistics, Memorial Sloan Kettering Cancer Center – sequence: 11 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: 12 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: 13 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: 14 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: 15 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: 16 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: 17 givenname: Joanne surname: Leung fullname: Leung, Joanne organization: Hepatopancreatobiliary Service, Department of Surgery, Memorial Sloan Kettering Cancer Center – sequence: 18 givenname: Rajya surname: Kappagantula fullname: Kappagantula, Rajya organization: David M. Rubenstein Center for Pancreatic Cancer Research, Memorial Sloan Kettering Cancer Center, Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center – sequence: 19 givenname: Alvin orcidid: 0000-0002-4781-3565 surname: Makohon-Moore fullname: Makohon-Moore, Alvin organization: David M. Rubenstein Center for Pancreatic Cancer Research, Memorial Sloan Kettering Cancer Center, Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center – sequence: 20 givenname: Amber surname: Johns fullname: Johns, Amber organization: The Kinghorn Cancer Centre, Garvan Institute of Medical Research – sequence: 21 givenname: Anthony surname: Gill fullname: Gill, Anthony organization: The Kinghorn Cancer Centre, Garvan Institute of Medical Research, University of Sydney – sequence: 22 givenname: Mathieu orcidid: 0000-0002-1831-7597 surname: Gigoux fullname: Gigoux, Mathieu organization: Immuno-Oncology Service, Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, Swim Across America and Ludwig Collaborative Laboratory, Parker Institute for Cancer Immunotherapy, Memorial Sloan Kettering Cancer Center – sequence: 23 givenname: Jedd orcidid: 0000-0001-6718-2222 surname: Wolchok fullname: Wolchok, Jedd organization: Immuno-Oncology Service, Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, Swim Across America and Ludwig Collaborative Laboratory, Parker Institute for Cancer Immunotherapy, Memorial Sloan Kettering Cancer Center – sequence: 24 givenname: Taha orcidid: 0000-0002-1518-5111 surname: Merghoub fullname: Merghoub, Taha organization: Immuno-Oncology Service, Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, Swim Across America and Ludwig Collaborative Laboratory, Parker Institute for Cancer Immunotherapy, Memorial Sloan Kettering Cancer Center – sequence: 25 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: 26 givenname: Erin surname: Patterson fullname: Patterson, Erin organization: Hepatopancreatobiliary Service, Department of Surgery, Memorial Sloan Kettering Cancer Center – sequence: 27 givenname: Remi surname: Monasson fullname: Monasson, Remi organization: Laboratoire de Physique de l’Ecole Normale Supérieure, ENS, Université PSL, CNRS, Sorbonne Université, Université de Paris – sequence: 28 givenname: Thierry surname: Mora fullname: Mora, Thierry organization: Laboratoire de Physique de l’Ecole Normale Supérieure, ENS, Université PSL, CNRS, Sorbonne Université, Université de Paris – sequence: 29 givenname: Aleksandra M. surname: Walczak fullname: Walczak, Aleksandra M. organization: Laboratoire de Physique de l’Ecole Normale Supérieure, ENS, Université PSL, CNRS, Sorbonne Université, Université de Paris – sequence: 30 givenname: Simona orcidid: 0000-0002-1852-7789 surname: Cocco fullname: Cocco, Simona organization: Laboratoire de Physique de l’Ecole Normale Supérieure, ENS, Université PSL, CNRS, Sorbonne Université, Université de Paris – sequence: 31 givenname: Christine orcidid: 0000-0002-4672-3023 surname: Iacobuzio-Donahue fullname: Iacobuzio-Donahue, Christine organization: David M. Rubenstein Center for Pancreatic Cancer Research, Memorial Sloan Kettering Cancer Center, Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center – sequence: 32 givenname: Benjamin D. orcidid: 0000-0001-6153-8793 surname: Greenbaum fullname: Greenbaum, Benjamin D. email: greenbab@mskcc.org organization: Computational Oncology Service, Department of Biostatistics, Memorial Sloan Kettering Cancer Center, Physiology, Biophysics & Systems Biology, Weill Cornell Medicine, Weill Cornell Medical College – sequence: 33 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, Parker Institute for Cancer Immunotherapy, Memorial Sloan Kettering Cancer Center |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/35589842$$D View this record in MEDLINE/PubMed https://hal.science/hal-04331950$$DView record in HAL |
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that predicts that lymphocytes kill more immunogenic cancer cells to cause less immunogenic clones to dominate... Cancer immunoediting is a hallmark of cancer that predicts that lymphocytes kill more immunogenic cancer cells to cause less immunogenic clones to dominate a... Cancer immunoediting1 is a hallmark of cancer2 that predicts that lymphocytes kill more immunogenic cancer cells to cause less immunogenic clones to dominate a... Cancer immunoediting 1 is a hallmark of cancer 2 that predicts that lymphocytes kill more immunogenic cancer cells to cause less immunogenic clones to dominate... |
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| SubjectTerms | 631/57/2266 631/67/580/1884 631/67/69 Antigens Cancer Cloning Discrimination Evolution Humanities and Social Sciences Hypotheses Immune system Immunogenicity Life Sciences Lymphocytes Lymphocytes T Major histocompatibility complex multidisciplinary Mutation Neoantigens Pancreatic cancer Peptides Physics Science Science (multidisciplinary) Survival T cell receptors Thymus gland Tumors |
| Title | Neoantigen quality predicts immunoediting in survivors of pancreatic cancer |
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