How tumours escape mass destruction

It is now well established that the immune system can control neoplastic development and growth in a process termed immunosurveillance. A link between host immunosurveillance and neoplastic progression is revealed in cases where the immune response becomes compromised due to genetic or other patholo...

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Published inOncogene Vol. 27; no. 45; pp. 5894 - 5903
Main Authors Stewart, T J, Abrams, S I
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 06.10.2008
Nature Publishing Group
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Abstract It is now well established that the immune system can control neoplastic development and growth in a process termed immunosurveillance. A link between host immunosurveillance and neoplastic progression is revealed in cases where the immune response becomes compromised due to genetic or other pathological conditions, resulting in a substantially increased incidence and rate of spontaneous tumour formation in both preclinical animal models and patients. It has also been demonstrated in tumour-bearing hosts that the tumorigenic process itself can promote a state of immunosuppression that, in turn, facilitates neoplastic progression. The ability of neoplastic populations to induce a hostile microenvironment through both cell contact-dependent and -independent immunosuppressive networks is a significant barrier to effective cell-mediated immunity and immunotherapy. Thus, a competent immune system is integral for the control of neoplastic disease, and dissecting the plethora of tumour escape mechanisms that disrupt this essential host defense capability is integral for the development of effective immunotherapeutic paradigms.
AbstractList It is now well established that the immune system can control neoplastic development and growth in a process termed immunosurveillance. A link between host immunosurveillance and neoplastic progression is revealed in cases where the immune response becomes compromised due to genetic or other pathological conditions, resulting in a substantially increased incidence and rate of spontaneous tumour formation in both preclinical animal models and patients. It has also been demonstrated in tumour-bearing hosts that the tumorigenic process itself can promote a state of immunosuppression that, in turn, facilitates neoplastic progression. The ability of neoplastic populations to induce a hostile microenvironment through both cell contact-dependent and -independent immunosuppressive networks is a significant barrier to effective cell-mediated immunity and immunotherapy. Thus, a competent immune system is integral for the control of neoplastic disease, and dissecting the plethora of tumour escape mechanisms that disrupt this essential host defense capability is integral for the development of effective immunotherapeutic paradigms.
It is now well established that the immune system can control neoplastic development and growth in a process termed immunosurveillance. A link between host immunosurveillance and neoplastic progression is revealed in cases where the immune response becomes compromised due to genetic or other pathological conditions, resulting in a substantially increased incidence and rate of spontaneous tumour formation in both preclinical animal models and patients. It has also been demonstrated in tumour-bearing hosts that the tumorigenic process itself can promote a state of immunosuppression that, in turn, facilitates neoplastic progression. The ability of neoplastic populations to induce a hostile microenvironment through both cell contact-dependent and -independent immunosuppressive networks is a significant barrier to effective cell-mediated immunity and immunotherapy. Thus, a competent immune system is integral for the control of neoplastic disease, and dissecting the plethora of tumour escape mechanisms that disrupt this essential host defense capability is integral for the development of effective immunotherapeutic paradigms.Oncogene (2008) 27, 5894-5903; doi:10.1038/onc.2008.268
It is now well established that the immune system can control neoplastic development and growth in a process termed immunosurveillance. A link between host immunosurveillance and neoplastic progression is revealed in cases where the immune response becomes compromised due to genetic or other pathological conditions, resulting in a substantially increased incidence and rate of spontaneous tumour formation in both preclinical animal models and patients. It has also been demonstrated in tumour-bearing hosts that the tumorigenic process itself can promote a state of immunosuppression that, in turn, facilitates neoplastic progression. The ability of neoplastic populations to induce a hostile microenvironment through both cell contact-dependent and -independent immunosuppressive networks is a significant barrier to effective cell-mediated immunity and immunotherapy. Thus, a competent immune system is integral for the control of neoplastic disease, and dissecting the plethora of tumour escape mechanisms that disrupt this essential host defense capability is integral for the development of effective immunotherapeutic paradigms. [PUBLICATION ABSTRACT]
Audience Academic
Author Abrams, S I
Stewart, T J
Author_xml – sequence: 1
  givenname: T J
  surname: Stewart
  fullname: Stewart, T J
  organization: Laboratory of Tumor Immunology and Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, 2Current address: Cancer Immunology Research Program, The Peter MacCallum Cancer Institute, Level 2, Smorgon Family Building, St Andrews Place, East Melbourne, Victoria 3002, Australia
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  email: scott.abrams@roswellpark.org
  organization: Laboratory of Tumor Immunology and Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, 3Current address: Department of Immunology, Roswell Park Cancer Institute, Elm and Carlton Streets, Buffalo, NY 14263, USA
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Copyright Macmillan Publishers Limited 2008
COPYRIGHT 2008 Nature Publishing Group
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IsDoiOpenAccess true
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Issue 45
Keywords tumour escape
immunosuppression
tumour microenvironment
tumour immunity
immunosurveillance
Language English
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OpenAccessLink http://dx.doi.org/10.1038/onc.2008.268
PMID 18836470
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PublicationTitle Oncogene
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Publisher Nature Publishing Group UK
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Liu, Caldwell, Greeneltch, Yang, Abrams (CR56) 2006; 176
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Dunn, Koebel, Schreiber (CR16) 2006; 6
Krambeck, Thompson, Dong, Lohse, Park, Kuntz (CR41) 2006; 103
Sica, Choi, Zhu, Tamada, Wang, Tamura (CR82) 2003; 18
Bron, Scolyer, Thompson, Hersey (CR6) 2004; 36
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Schmielau, Finn (CR79) 2001; 61
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Kusmartsev, Gabrilovich (CR44) 2006; 55
Vogelstein, Kinzler (CR97) 2004; 10
Liu, Caldwell, Abrams (CR55) 2005; 65
Curiel (CR11) 2007; 117
Gordon, Arndt, Hawkins, Doherty, Inwards, Munsell (CR26) 2005; 27
Flies, Chen (CR21) 2007; 30
Stewart, Greeneltch, Lutsiak, Abrams (CR87) 2007; 9
Kortylewski, Kujawski, Wang, Wei, Zhang, Pilon-Thomas (CR40) 2005; 11
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Chang, Ferrone (CR9) 2007; 56
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Bosque, Pardo, Martinez-Lorenzo, Lasierra, Larrad, Marzo (CR5) 2005; 35
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Suzuki, Kapoor, Jassar, Kaiser, Albelda (CR89) 2005; 11
Whiteside (CR100) 2006; 16
Ichihara, Kono, Takahashi, Kawaida, Sugai, Fujii (CR33) 2003; 9
Ohigashi, Sho, Yamada, Tsurui, Hamada, Ikeda (CR65) 2005; 11
Zamanakou, Germenis, Karanikas (CR107) 2007; 111
Dudley, Wunderlich, Robbins, Yang, Hwu, Schwartzentruber (CR15) 2002; 298
Espana, Fernandez, Rubio, Torregrosa, Blanco, Sierra (CR18) 2004; 87
Kim, Emi, Tanabe, Uchida, Toge (CR37) 2004; 100
Ferris, Whiteside, Ferrone (CR19) 2006; 12
Smyth, Thia, Street, MacGregor, Godfrey, Trapani (CR85) 2000; 192
Sinha, Clements, Fulton, Ostrand-Rosenberg (CR83) 2007; 67
Yang, Thangaraju, Greeneltch, Browning, Schoenlein, Tamura (CR104) 2007; 67
Li, Wan, Sanjabi, Robertson, Flavell (CR49) 2006; 24
Takeda, Hayakawa, Smyth, Kayagaki, Yamaguchi, Kakuta (CR90) 2001; 7
Jung, Kim, Park (CR35) 2004; 13
Abrams (CR1) 2004; 6
Nagaraj, Gabrilovich (CR61) 2007; 601
Zhou, Drake, Levitsky (CR109) 2006; 107
Liyanage, Moore, Joo, Tanaka, Herrmann, Doherty (CR58) 2002; 169
Bui, Schreiber (CR8) 2007; 19
Lee, Yee, Savage, Fong, Brockstedt, Weber (CR48) 1999; 5
Ochoa, Zea, Hernandez, Rodriguez (CR63) 2007; 13
Yu, Kortylewski, Pardoll (CR106) 2007; 7
Cuenca, Cheng, Wang, Brayer, Horna, Gu (CR10) 2003; 63
Korman, Peggs, Allison (CR39) 2006; 90
Gallimore, Sakaguchi (CR24) 2002; 107
Giovarelli, Musiani, Garotta, Ebner, Di Carlo, Kim (CR25) 1999; 163
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Hanahan, Weinberg (CR28) 2000; 100
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PP Lee (BFonc2008268_CR48) 1999; 5
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Snippet It is now well established that the immune system can control neoplastic development and growth in a process termed immunosurveillance. A link between host...
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SubjectTerms Animal models
Animals
Apoptosis
Cancer cells
Carcinogenesis
Cell Adhesion - immunology
Cell Adhesion - physiology
Cell Biology
Cell Communication - immunology
Cell Communication - physiology
Cell-mediated immunity
Cellular biology
Cellular immunity
Control
Genetic aspects
Genetics
Health aspects
Human Genetics
Humans
Immune response
Immune system
Immune Tolerance - immunology
Immune Tolerance - physiology
Immunology
Immunosuppression
Immunosurveillance
Immunotherapy
Internal Medicine
Medicine
Medicine & Public Health
Microenvironments
Models, Biological
Neoplasms - immunology
Oncology
review
Tumor Escape - immunology
Tumor Escape - physiology
Tumors
Title How tumours escape mass destruction
URI http://dx.doi.org/10.1038/onc.2008.268
https://link.springer.com/article/10.1038/onc.2008.268
https://www.ncbi.nlm.nih.gov/pubmed/18836470
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https://www.proquest.com/docview/2641386572
https://search.proquest.com/docview/19748898
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Volume 27
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