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  1. Article ; Online: Turning a failing PhD around.

    Swanton, Charles

    Nature cancer

    2023  Volume 4, Issue 10, Page(s) 1399–1400

    Language English
    Publishing date 2023-10-25
    Publishing country England
    Document type Journal Article
    ISSN 2662-1347
    ISSN (online) 2662-1347
    DOI 10.1038/s43018-023-00597-w
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  2. Article ; Online: Take lessons from cancer evolution to the clinic.

    Swanton, Charles

    Nature

    2020  Volume 581, Issue 7809, Page(s) 382–383

    MeSH term(s) Aged ; Animals ; Antineoplastic Agents/therapeutic use ; Carcinoma, Non-Small-Cell Lung/genetics ; Carcinoma, Non-Small-Cell Lung/immunology ; Carcinoma, Non-Small-Cell Lung/pathology ; Carcinoma, Non-Small-Cell Lung/therapy ; Disease Models, Animal ; Early Detection of Cancer ; Evolution, Molecular ; Female ; Humans ; Immunotherapy/methods ; Lung Neoplasms/genetics ; Lung Neoplasms/immunology ; Lung Neoplasms/pathology ; Lung Neoplasms/therapy ; Male ; Mice ; Middle Aged ; Neoplasm, Residual/drug therapy ; Smoking/adverse effects ; Smoking Prevention ; State Medicine ; Treatment Outcome ; United Kingdom
    Chemical Substances Antineoplastic Agents
    Language English
    Publishing date 2020-04-29
    Publishing country England
    Document type Journal Article
    ZDB-ID 120714-3
    ISSN 1476-4687 ; 0028-0836
    ISSN (online) 1476-4687
    ISSN 0028-0836
    DOI 10.1038/d41586-020-01347-z
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  3. Article ; Online: Angelika Amon (1967-2020).

    Swanton, Charles

    Cancer cell

    2020  Volume 38, Issue 6, Page(s) 751–752

    MeSH term(s) Aneuploidy ; Austria ; Cell Cycle ; Chromosome Segregation ; Female ; History, 20th Century ; History, 21st Century ; Humans ; Neoplasms/genetics
    Language English
    Publishing date 2020-11-19
    Publishing country United States
    Document type Biography ; Historical Article ; Journal Article ; Portrait
    ZDB-ID 2078448-X
    ISSN 1878-3686 ; 1535-6108
    ISSN (online) 1878-3686
    ISSN 1535-6108
    DOI 10.1016/j.ccell.2020.11.007
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  4. Article ; Online: Distinct Mutagenic Activity of APOBEC3G Cytidine Deaminase Identified in Bladder Cancer.

    Caswell, Deborah / Swanton, Charles

    Cancer research

    2023  Volume 83, Issue 4, Page(s) 487–488

    Abstract: The APOBEC cytidine deaminase enzyme family is linked to mutational signatures identified in cancer. While previous work has provided insights into the role of APOBEC3A and APOBEC3B in mutational processes in cancer, understanding of the mutational ... ...

    Abstract The APOBEC cytidine deaminase enzyme family is linked to mutational signatures identified in cancer. While previous work has provided insights into the role of APOBEC3A and APOBEC3B in mutational processes in cancer, understanding of the mutational signatures induced by other APOBEC family members is limited. In this issue of Cancer Research, Liu and colleagues investigated the role of APOBEC3G (A3G) in bladder cancer. The authors revealed that transgenic expression of A3G in a murine bladder cancer model promotes tumorigenesis and induces a unique mutational signature distinct from previously identified APOBEC signatures. Expression of this A3G-related mutational signature correlated with significantly worse survival in patients with urothelial bladder carcinoma, and A3G expression was identified in 21 different cancer types. These findings suggest that different APOBEC3 enzymes induce unique mutation signatures and play distinct roles in cancer evolution. More complete understanding of the function of each APOBEC3 enzyme will improve anticancer therapy. See related article by Liu et al., p. 506.
    MeSH term(s) Humans ; Animals ; Mice ; Mutagens ; Mutagenesis ; Cytidine Deaminase/genetics ; Urinary Bladder Neoplasms/genetics ; APOBEC-3G Deaminase/genetics ; APOBEC-3G Deaminase/metabolism ; Clonal Evolution ; Minor Histocompatibility Antigens/genetics
    Chemical Substances APOBEC3A protein, human (EC 3.5.4.5) ; Mutagens ; Cytidine Deaminase (EC 3.5.4.5) ; APOBEC-3G Deaminase (EC 3.5.4.5) ; APOBEC3G protein, human (EC 3.5.4.5) ; APOBEC3B protein, human (EC 3.5.4.5) ; Minor Histocompatibility Antigens ; APOBEC3G protein, mouse (EC 3.5.4.5)
    Language English
    Publishing date 2023-02-10
    Publishing country United States
    Document type Editorial ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 1432-1
    ISSN 1538-7445 ; 0008-5472
    ISSN (online) 1538-7445
    ISSN 0008-5472
    DOI 10.1158/0008-5472.CAN-22-3598
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  5. Article ; Online: Tumor heterogeneity impairs immunogenicity in mismatch repair deficient tumors.

    Reading, James L / Caswell, Deborah R / Swanton, Charles

    Nature genetics

    2024  Volume 55, Issue 10, Page(s) 1610–1612

    MeSH term(s) Humans ; DNA Mismatch Repair/genetics ; Colorectal Neoplasms/genetics ; Colorectal Neoplasms/pathology ; Brain Neoplasms/pathology ; Neoplastic Syndromes, Hereditary
    Language English
    Publishing date 2024-02-23
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1108734-1
    ISSN 1546-1718 ; 1061-4036
    ISSN (online) 1546-1718
    ISSN 1061-4036
    DOI 10.1038/s41588-023-01492-x
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  6. Article ; Online: Cancer therapeutics through an evolutionary lens.

    Swanton, Charles

    Journal of the Royal Society of Medicine

    2018  Volume 111, Issue 1, Page(s) 8–14

    MeSH term(s) Biological Evolution ; Chromosomal Instability ; Drug Resistance, Neoplasm/genetics ; Humans ; Mutation ; Neoplasms/drug therapy ; Neoplasms/genetics ; Neoplasms/immunology
    Language English
    Publishing date 2018-02-08
    Publishing country England
    Document type Journal Article ; Lecture
    ZDB-ID 6731-3
    ISSN 1758-1095 ; 0141-0768 ; 0035-9157
    ISSN (online) 1758-1095
    ISSN 0141-0768 ; 0035-9157
    DOI 10.1177/0141076817742096
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  7. Article ; Online: Cancer cell-intrinsic mechanisms driving acquired immune tolerance.

    Ghorani, Ehsan / Swanton, Charles / Quezada, Sergio A

    Immunity

    2023  Volume 56, Issue 10, Page(s) 2270–2295

    Abstract: Immune evasion is a hallmark of cancer, enabling tumors to survive contact with the host immune system and evade the cycle of immune recognition and destruction. Here, we review the current understanding of the cancer cell-intrinsic factors driving ... ...

    Abstract Immune evasion is a hallmark of cancer, enabling tumors to survive contact with the host immune system and evade the cycle of immune recognition and destruction. Here, we review the current understanding of the cancer cell-intrinsic factors driving immune evasion. We focus on T cells as key effectors of anti-cancer immunity and argue that cancer cells evade immune destruction by gaining control over pathways that usually serve to maintain physiological tolerance to self. Using this framework, we place recent mechanistic advances in the understanding of cancer immune evasion into broad categories of control over T cell localization, antigen recognition, and acquisition of optimal effector function. We discuss the redundancy in the pathways involved and identify knowledge gaps that must be overcome to better target immune evasion, including the need for better, routinely available tools that incorporate the growing understanding of evasion mechanisms to stratify patients for therapy and trials.
    MeSH term(s) Humans ; Neoplasms ; Immune Tolerance ; T-Lymphocytes ; Immunotherapy ; Immune Evasion
    Language English
    Publishing date 2023-10-11
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 1217235-2
    ISSN 1097-4180 ; 1074-7613
    ISSN (online) 1097-4180
    ISSN 1074-7613
    DOI 10.1016/j.immuni.2023.09.004
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  8. Article ; Online: Placing the patient at the heart of discovery science.

    Aldea, Mihaela / Bernard, Elsa / Swanton, Charles / Andre, Fabrice

    European journal of cancer (Oxford, England : 1990)

    2023  Volume 193, Page(s) 113306

    MeSH term(s) Humans ; Research ; Heart ; Patients
    Language English
    Publishing date 2023-09-22
    Publishing country England
    Document type Editorial ; Research Support, Non-U.S. Gov't
    ZDB-ID 82061-1
    ISSN 1879-0852 ; 0277-5379 ; 0959-8049 ; 0964-1947
    ISSN (online) 1879-0852
    ISSN 0277-5379 ; 0959-8049 ; 0964-1947
    DOI 10.1016/j.ejca.2023.113306
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  9. Article ; Online: ctDNA: An emerging neoadjuvant biomarker in resectable solid tumors.

    Abbosh, Christopher / Swanton, Charles

    PLoS medicine

    2021  Volume 18, Issue 10, Page(s) e1003771

    Abstract: Christopher Abbosh and Charles Swanton discuss circulating tumor DNA as a potential biomarker for neoadjuvant treatment response in solid tumors. ...

    Abstract Christopher Abbosh and Charles Swanton discuss circulating tumor DNA as a potential biomarker for neoadjuvant treatment response in solid tumors.
    MeSH term(s) Biomarkers, Tumor/blood ; Biomarkers, Tumor/genetics ; Circulating Tumor DNA/genetics ; Colorectal Neoplasms/pathology ; Humans ; Kinetics ; Liver Neoplasms/secondary ; Neoadjuvant Therapy ; Neoplasms/genetics ; Neoplasms/therapy
    Chemical Substances Biomarkers, Tumor ; Circulating Tumor DNA
    Language English
    Publishing date 2021-10-12
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2185925-5
    ISSN 1549-1676 ; 1549-1277
    ISSN (online) 1549-1676
    ISSN 1549-1277
    DOI 10.1371/journal.pmed.1003771
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  10. Article ; Online: Clonal Evolution in Healthy and Premalignant Tissues: Implications for Early Cancer Interception Strategies.

    Rane, Jayant K / Frankell, Alexander M / Weeden, Clare E / Swanton, Charles

    Cancer prevention research (Philadelphia, Pa.)

    2023  Volume 16, Issue 7, Page(s) 369–378

    Abstract: Histologically normal human tissues accumulate significant mutational burden with age. The extent and spectra of mutagenesis are comparable both in rapidly proliferating and post-mitotic tissues and in stem cells compared with their differentiated ... ...

    Abstract Histologically normal human tissues accumulate significant mutational burden with age. The extent and spectra of mutagenesis are comparable both in rapidly proliferating and post-mitotic tissues and in stem cells compared with their differentiated progeny. Some of these mutations provide increased fitness, giving rise to clones which, at times, can replace the entire surface area of tissues. Compared with cancer, somatic mutations in histologically normal tissues are primarily single-nucleotide variations. Interestingly though, the presence of these mutations and positive clonal selection in isolation remains a poor indicator of potential future cancer transformation in solid tissues. Common clonally expanded mutations in histologically normal tissues also do not always represent the most frequent early mutations in cancers of corresponding tissues, indicating differences in selection pressures. Preliminary evidence implies that stroma and immune system co-evolve with age, which may impact selection dynamics. In this review, we will explore the mutational landscape of histologically normal and premalignant human somatic tissues in detail and discuss cell-intrinsic and environmental factors that can determine the fate of positively selected mutations within them. Precisely pinpointing these determinants of cancer transformation would aid development of early cancer interventional and prevention strategies.
    MeSH term(s) Humans ; Precancerous Conditions/genetics ; Precancerous Conditions/pathology ; Mutation ; Clone Cells/pathology ; Cell Transformation, Neoplastic/genetics ; Clonal Evolution/genetics
    Language English
    Publishing date 2023-03-17
    Publishing country United States
    Document type Review ; Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2434717-6
    ISSN 1940-6215 ; 1940-6207
    ISSN (online) 1940-6215
    ISSN 1940-6207
    DOI 10.1158/1940-6207.CAPR-22-0469
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