Cancer resistance of SR/CR mice in the genetic knockout backgrounds of leukocyte effector mechanisms: determinations for functional requirements

Background Spontaneous Regression/Complete Resistant (SR/CR) mice are a colony of cancer-resistant mice that can detect and rapidly destroy malignant cells with innate cellular immunity, predominately mediated by granulocytes. Our previous studies suggest that several effector mechanisms, such as perforin, granzymes, or complements, may be involved in the killing of cancer cells. However, none of these effector mechanisms is known as critical for granulocytes. Additionally, it is unclear which effector mechanisms are required for the cancer killing activity of specific leukocyte populations and the survival of SR/CR mice against the challenges of lethal cancer cells. We hypothesized that if any of these effector mechanisms was required for the resistance to cancer cells, its functional knockout in SR/CR mice should render them sensitive to cancer challenges. This was tested by cross breeding SR/CR mice into the individual genetic knockout backgrounds of perforin ($ Prf^{-/-} $), superoxide ($ Cybb^{-/} $), or inducible nitric oxide ($ Nos2^{-/} $). Methods SR/CR mice were bred into individual $ Prf^{-/-} $, $ Cybb^{-/-} $, or $ Nos2^{-/-} $ genetic backgrounds and then challenged with sarcoma 180 (S180). Their overall survival was compared to controls. The cancer killing efficiency of purified populations of macrophages and neutrophils from these immunodeficient mice was also examined. Results When these genetically engineered mice were challenged with cancer cells, the knockout backgrounds of $ Prf^{-/-} $, $ Cybb^{-/-} $, or $ Nos2^{-/-} $ did not completely abolish the SR/CR cancer resistant phenotype. However, the $ Nos2^{-/-} $ background did appear to weaken the resistance. Incidentally, it was also observed that the male mice in these immunocompromised backgrounds tended to be less cancer-resistant than SR/CR controls. Conclusion Despite the previously known roles of perforin, superoxide or nitric oxide in the effector mechanisms of innate immune responses, these effector mechanisms were not required for cancer-resistance in SR/CR mice. The resistance was functional when any one of these effector mechanisms was completely absent, except some noticeably reduced penetrance, but not abolishment, of the phenotype in the male background in comparison to female background. These results also indicate that some other effector mechanism(s) of granulocytes may be involved in the killing of cancer cells in SR/CR mice. Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Sanders, Anne M [verfasserIn] Stehle, John R Blanks, Michael J Riedlinger, Gregory Kim-Shapiro, Jung W Monjazeb, Arta M Adams, Jonathan M Willingham, Mark C Cui, Zheng

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2010

Schlagwörter:	Nitric Oxide Maximum Tolerate Dose Effector Mechanism S180 Cell Immunologic Synapse

Anmerkung:	© Sanders et al; licensee BioMed Central Ltd. 2010. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (

Übergeordnetes Werk:	Enthalten in: BMC cancer - London : BioMed Central, 2001, 10(2010), 1 vom: 31. März
Übergeordnetes Werk:	volume:10 ; year:2010 ; number:1 ; day:31 ; month:03

Links:	Volltext

DOI / URN:	10.1186/1471-2407-10-121

Katalog-ID:	SPR02762398X

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100	1		\|a Sanders, Anne M \|e verfasserin \|4 aut
245	1	0	\|a Cancer resistance of SR/CR mice in the genetic knockout backgrounds of leukocyte effector mechanisms: determinations for functional requirements
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520			\|a Background Spontaneous Regression/Complete Resistant (SR/CR) mice are a colony of cancer-resistant mice that can detect and rapidly destroy malignant cells with innate cellular immunity, predominately mediated by granulocytes. Our previous studies suggest that several effector mechanisms, such as perforin, granzymes, or complements, may be involved in the killing of cancer cells. However, none of these effector mechanisms is known as critical for granulocytes. Additionally, it is unclear which effector mechanisms are required for the cancer killing activity of specific leukocyte populations and the survival of SR/CR mice against the challenges of lethal cancer cells. We hypothesized that if any of these effector mechanisms was required for the resistance to cancer cells, its functional knockout in SR/CR mice should render them sensitive to cancer challenges. This was tested by cross breeding SR/CR mice into the individual genetic knockout backgrounds of perforin ($ Prf^{-/-} $), superoxide ($ Cybb^{-/} $), or inducible nitric oxide ($ Nos2^{-/} $). Methods SR/CR mice were bred into individual $ Prf^{-/-} $, $ Cybb^{-/-} $, or $ Nos2^{-/-} $ genetic backgrounds and then challenged with sarcoma 180 (S180). Their overall survival was compared to controls. The cancer killing efficiency of purified populations of macrophages and neutrophils from these immunodeficient mice was also examined. Results When these genetically engineered mice were challenged with cancer cells, the knockout backgrounds of $ Prf^{-/-} $, $ Cybb^{-/-} $, or $ Nos2^{-/-} $ did not completely abolish the SR/CR cancer resistant phenotype. However, the $ Nos2^{-/-} $ background did appear to weaken the resistance. Incidentally, it was also observed that the male mice in these immunocompromised backgrounds tended to be less cancer-resistant than SR/CR controls. Conclusion Despite the previously known roles of perforin, superoxide or nitric oxide in the effector mechanisms of innate immune responses, these effector mechanisms were not required for cancer-resistance in SR/CR mice. The resistance was functional when any one of these effector mechanisms was completely absent, except some noticeably reduced penetrance, but not abolishment, of the phenotype in the male background in comparison to female background. These results also indicate that some other effector mechanism(s) of granulocytes may be involved in the killing of cancer cells in SR/CR mice.
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700	1		\|a Stehle, John R \|4 aut
700	1		\|a Blanks, Michael J \|4 aut
700	1		\|a Riedlinger, Gregory \|4 aut
700	1		\|a Kim-Shapiro, Jung W \|4 aut
700	1		\|a Monjazeb, Arta M \|4 aut
700	1		\|a Adams, Jonathan M \|4 aut
700	1		\|a Willingham, Mark C \|4 aut
700	1		\|a Cui, Zheng \|4 aut
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allfields	10.1186/1471-2407-10-121 doi (DE-627)SPR02762398X (SPR)1471-2407-10-121-e DE-627 ger DE-627 rakwb eng Sanders, Anne M verfasserin aut Cancer resistance of SR/CR mice in the genetic knockout backgrounds of leukocyte effector mechanisms: determinations for functional requirements 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Sanders et al; licensee BioMed Central Ltd. 2010. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Background Spontaneous Regression/Complete Resistant (SR/CR) mice are a colony of cancer-resistant mice that can detect and rapidly destroy malignant cells with innate cellular immunity, predominately mediated by granulocytes. Our previous studies suggest that several effector mechanisms, such as perforin, granzymes, or complements, may be involved in the killing of cancer cells. However, none of these effector mechanisms is known as critical for granulocytes. Additionally, it is unclear which effector mechanisms are required for the cancer killing activity of specific leukocyte populations and the survival of SR/CR mice against the challenges of lethal cancer cells. We hypothesized that if any of these effector mechanisms was required for the resistance to cancer cells, its functional knockout in SR/CR mice should render them sensitive to cancer challenges. This was tested by cross breeding SR/CR mice into the individual genetic knockout backgrounds of perforin ($ Prf^{-/-} $), superoxide ($ Cybb^{-/} $), or inducible nitric oxide ($ Nos2^{-/} $). Methods SR/CR mice were bred into individual $ Prf^{-/-} $, $ Cybb^{-/-} $, or $ Nos2^{-/-} $ genetic backgrounds and then challenged with sarcoma 180 (S180). Their overall survival was compared to controls. The cancer killing efficiency of purified populations of macrophages and neutrophils from these immunodeficient mice was also examined. Results When these genetically engineered mice were challenged with cancer cells, the knockout backgrounds of $ Prf^{-/-} $, $ Cybb^{-/-} $, or $ Nos2^{-/-} $ did not completely abolish the SR/CR cancer resistant phenotype. However, the $ Nos2^{-/-} $ background did appear to weaken the resistance. Incidentally, it was also observed that the male mice in these immunocompromised backgrounds tended to be less cancer-resistant than SR/CR controls. Conclusion Despite the previously known roles of perforin, superoxide or nitric oxide in the effector mechanisms of innate immune responses, these effector mechanisms were not required for cancer-resistance in SR/CR mice. The resistance was functional when any one of these effector mechanisms was completely absent, except some noticeably reduced penetrance, but not abolishment, of the phenotype in the male background in comparison to female background. These results also indicate that some other effector mechanism(s) of granulocytes may be involved in the killing of cancer cells in SR/CR mice. Nitric Oxide (dpeaa)DE-He213 Maximum Tolerate Dose (dpeaa)DE-He213 Effector Mechanism (dpeaa)DE-He213 S180 Cell (dpeaa)DE-He213 Immunologic Synapse (dpeaa)DE-He213 Stehle, John R aut Blanks, Michael J aut Riedlinger, Gregory aut Kim-Shapiro, Jung W aut Monjazeb, Arta M aut Adams, Jonathan M aut Willingham, Mark C aut Cui, Zheng aut Enthalten in BMC cancer London : BioMed Central, 2001 10(2010), 1 vom: 31. März (DE-627)326643710 (DE-600)2041352-X 1471-2407 nnns volume:10 year:2010 number:1 day:31 month:03 https://dx.doi.org/10.1186/1471-2407-10-121 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 10 2010 1 31 03
spelling	10.1186/1471-2407-10-121 doi (DE-627)SPR02762398X (SPR)1471-2407-10-121-e DE-627 ger DE-627 rakwb eng Sanders, Anne M verfasserin aut Cancer resistance of SR/CR mice in the genetic knockout backgrounds of leukocyte effector mechanisms: determinations for functional requirements 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Sanders et al; licensee BioMed Central Ltd. 2010. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Background Spontaneous Regression/Complete Resistant (SR/CR) mice are a colony of cancer-resistant mice that can detect and rapidly destroy malignant cells with innate cellular immunity, predominately mediated by granulocytes. Our previous studies suggest that several effector mechanisms, such as perforin, granzymes, or complements, may be involved in the killing of cancer cells. However, none of these effector mechanisms is known as critical for granulocytes. Additionally, it is unclear which effector mechanisms are required for the cancer killing activity of specific leukocyte populations and the survival of SR/CR mice against the challenges of lethal cancer cells. We hypothesized that if any of these effector mechanisms was required for the resistance to cancer cells, its functional knockout in SR/CR mice should render them sensitive to cancer challenges. This was tested by cross breeding SR/CR mice into the individual genetic knockout backgrounds of perforin ($ Prf^{-/-} $), superoxide ($ Cybb^{-/} $), or inducible nitric oxide ($ Nos2^{-/} $). Methods SR/CR mice were bred into individual $ Prf^{-/-} $, $ Cybb^{-/-} $, or $ Nos2^{-/-} $ genetic backgrounds and then challenged with sarcoma 180 (S180). Their overall survival was compared to controls. The cancer killing efficiency of purified populations of macrophages and neutrophils from these immunodeficient mice was also examined. Results When these genetically engineered mice were challenged with cancer cells, the knockout backgrounds of $ Prf^{-/-} $, $ Cybb^{-/-} $, or $ Nos2^{-/-} $ did not completely abolish the SR/CR cancer resistant phenotype. However, the $ Nos2^{-/-} $ background did appear to weaken the resistance. Incidentally, it was also observed that the male mice in these immunocompromised backgrounds tended to be less cancer-resistant than SR/CR controls. Conclusion Despite the previously known roles of perforin, superoxide or nitric oxide in the effector mechanisms of innate immune responses, these effector mechanisms were not required for cancer-resistance in SR/CR mice. The resistance was functional when any one of these effector mechanisms was completely absent, except some noticeably reduced penetrance, but not abolishment, of the phenotype in the male background in comparison to female background. These results also indicate that some other effector mechanism(s) of granulocytes may be involved in the killing of cancer cells in SR/CR mice. Nitric Oxide (dpeaa)DE-He213 Maximum Tolerate Dose (dpeaa)DE-He213 Effector Mechanism (dpeaa)DE-He213 S180 Cell (dpeaa)DE-He213 Immunologic Synapse (dpeaa)DE-He213 Stehle, John R aut Blanks, Michael J aut Riedlinger, Gregory aut Kim-Shapiro, Jung W aut Monjazeb, Arta M aut Adams, Jonathan M aut Willingham, Mark C aut Cui, Zheng aut Enthalten in BMC cancer London : BioMed Central, 2001 10(2010), 1 vom: 31. März (DE-627)326643710 (DE-600)2041352-X 1471-2407 nnns volume:10 year:2010 number:1 day:31 month:03 https://dx.doi.org/10.1186/1471-2407-10-121 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 10 2010 1 31 03
allfields_unstemmed	10.1186/1471-2407-10-121 doi (DE-627)SPR02762398X (SPR)1471-2407-10-121-e DE-627 ger DE-627 rakwb eng Sanders, Anne M verfasserin aut Cancer resistance of SR/CR mice in the genetic knockout backgrounds of leukocyte effector mechanisms: determinations for functional requirements 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Sanders et al; licensee BioMed Central Ltd. 2010. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Background Spontaneous Regression/Complete Resistant (SR/CR) mice are a colony of cancer-resistant mice that can detect and rapidly destroy malignant cells with innate cellular immunity, predominately mediated by granulocytes. Our previous studies suggest that several effector mechanisms, such as perforin, granzymes, or complements, may be involved in the killing of cancer cells. However, none of these effector mechanisms is known as critical for granulocytes. Additionally, it is unclear which effector mechanisms are required for the cancer killing activity of specific leukocyte populations and the survival of SR/CR mice against the challenges of lethal cancer cells. We hypothesized that if any of these effector mechanisms was required for the resistance to cancer cells, its functional knockout in SR/CR mice should render them sensitive to cancer challenges. This was tested by cross breeding SR/CR mice into the individual genetic knockout backgrounds of perforin ($ Prf^{-/-} $), superoxide ($ Cybb^{-/} $), or inducible nitric oxide ($ Nos2^{-/} $). Methods SR/CR mice were bred into individual $ Prf^{-/-} $, $ Cybb^{-/-} $, or $ Nos2^{-/-} $ genetic backgrounds and then challenged with sarcoma 180 (S180). Their overall survival was compared to controls. The cancer killing efficiency of purified populations of macrophages and neutrophils from these immunodeficient mice was also examined. Results When these genetically engineered mice were challenged with cancer cells, the knockout backgrounds of $ Prf^{-/-} $, $ Cybb^{-/-} $, or $ Nos2^{-/-} $ did not completely abolish the SR/CR cancer resistant phenotype. However, the $ Nos2^{-/-} $ background did appear to weaken the resistance. Incidentally, it was also observed that the male mice in these immunocompromised backgrounds tended to be less cancer-resistant than SR/CR controls. Conclusion Despite the previously known roles of perforin, superoxide or nitric oxide in the effector mechanisms of innate immune responses, these effector mechanisms were not required for cancer-resistance in SR/CR mice. The resistance was functional when any one of these effector mechanisms was completely absent, except some noticeably reduced penetrance, but not abolishment, of the phenotype in the male background in comparison to female background. These results also indicate that some other effector mechanism(s) of granulocytes may be involved in the killing of cancer cells in SR/CR mice. Nitric Oxide (dpeaa)DE-He213 Maximum Tolerate Dose (dpeaa)DE-He213 Effector Mechanism (dpeaa)DE-He213 S180 Cell (dpeaa)DE-He213 Immunologic Synapse (dpeaa)DE-He213 Stehle, John R aut Blanks, Michael J aut Riedlinger, Gregory aut Kim-Shapiro, Jung W aut Monjazeb, Arta M aut Adams, Jonathan M aut Willingham, Mark C aut Cui, Zheng aut Enthalten in BMC cancer London : BioMed Central, 2001 10(2010), 1 vom: 31. März (DE-627)326643710 (DE-600)2041352-X 1471-2407 nnns volume:10 year:2010 number:1 day:31 month:03 https://dx.doi.org/10.1186/1471-2407-10-121 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 10 2010 1 31 03
allfieldsGer	10.1186/1471-2407-10-121 doi (DE-627)SPR02762398X (SPR)1471-2407-10-121-e DE-627 ger DE-627 rakwb eng Sanders, Anne M verfasserin aut Cancer resistance of SR/CR mice in the genetic knockout backgrounds of leukocyte effector mechanisms: determinations for functional requirements 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Sanders et al; licensee BioMed Central Ltd. 2010. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Background Spontaneous Regression/Complete Resistant (SR/CR) mice are a colony of cancer-resistant mice that can detect and rapidly destroy malignant cells with innate cellular immunity, predominately mediated by granulocytes. Our previous studies suggest that several effector mechanisms, such as perforin, granzymes, or complements, may be involved in the killing of cancer cells. However, none of these effector mechanisms is known as critical for granulocytes. Additionally, it is unclear which effector mechanisms are required for the cancer killing activity of specific leukocyte populations and the survival of SR/CR mice against the challenges of lethal cancer cells. We hypothesized that if any of these effector mechanisms was required for the resistance to cancer cells, its functional knockout in SR/CR mice should render them sensitive to cancer challenges. This was tested by cross breeding SR/CR mice into the individual genetic knockout backgrounds of perforin ($ Prf^{-/-} $), superoxide ($ Cybb^{-/} $), or inducible nitric oxide ($ Nos2^{-/} $). Methods SR/CR mice were bred into individual $ Prf^{-/-} $, $ Cybb^{-/-} $, or $ Nos2^{-/-} $ genetic backgrounds and then challenged with sarcoma 180 (S180). Their overall survival was compared to controls. The cancer killing efficiency of purified populations of macrophages and neutrophils from these immunodeficient mice was also examined. Results When these genetically engineered mice were challenged with cancer cells, the knockout backgrounds of $ Prf^{-/-} $, $ Cybb^{-/-} $, or $ Nos2^{-/-} $ did not completely abolish the SR/CR cancer resistant phenotype. However, the $ Nos2^{-/-} $ background did appear to weaken the resistance. Incidentally, it was also observed that the male mice in these immunocompromised backgrounds tended to be less cancer-resistant than SR/CR controls. Conclusion Despite the previously known roles of perforin, superoxide or nitric oxide in the effector mechanisms of innate immune responses, these effector mechanisms were not required for cancer-resistance in SR/CR mice. The resistance was functional when any one of these effector mechanisms was completely absent, except some noticeably reduced penetrance, but not abolishment, of the phenotype in the male background in comparison to female background. These results also indicate that some other effector mechanism(s) of granulocytes may be involved in the killing of cancer cells in SR/CR mice. Nitric Oxide (dpeaa)DE-He213 Maximum Tolerate Dose (dpeaa)DE-He213 Effector Mechanism (dpeaa)DE-He213 S180 Cell (dpeaa)DE-He213 Immunologic Synapse (dpeaa)DE-He213 Stehle, John R aut Blanks, Michael J aut Riedlinger, Gregory aut Kim-Shapiro, Jung W aut Monjazeb, Arta M aut Adams, Jonathan M aut Willingham, Mark C aut Cui, Zheng aut Enthalten in BMC cancer London : BioMed Central, 2001 10(2010), 1 vom: 31. März (DE-627)326643710 (DE-600)2041352-X 1471-2407 nnns volume:10 year:2010 number:1 day:31 month:03 https://dx.doi.org/10.1186/1471-2407-10-121 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 10 2010 1 31 03
allfieldsSound	10.1186/1471-2407-10-121 doi (DE-627)SPR02762398X (SPR)1471-2407-10-121-e DE-627 ger DE-627 rakwb eng Sanders, Anne M verfasserin aut Cancer resistance of SR/CR mice in the genetic knockout backgrounds of leukocyte effector mechanisms: determinations for functional requirements 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Sanders et al; licensee BioMed Central Ltd. 2010. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( Background Spontaneous Regression/Complete Resistant (SR/CR) mice are a colony of cancer-resistant mice that can detect and rapidly destroy malignant cells with innate cellular immunity, predominately mediated by granulocytes. Our previous studies suggest that several effector mechanisms, such as perforin, granzymes, or complements, may be involved in the killing of cancer cells. However, none of these effector mechanisms is known as critical for granulocytes. Additionally, it is unclear which effector mechanisms are required for the cancer killing activity of specific leukocyte populations and the survival of SR/CR mice against the challenges of lethal cancer cells. We hypothesized that if any of these effector mechanisms was required for the resistance to cancer cells, its functional knockout in SR/CR mice should render them sensitive to cancer challenges. This was tested by cross breeding SR/CR mice into the individual genetic knockout backgrounds of perforin ($ Prf^{-/-} $), superoxide ($ Cybb^{-/} $), or inducible nitric oxide ($ Nos2^{-/} $). Methods SR/CR mice were bred into individual $ Prf^{-/-} $, $ Cybb^{-/-} $, or $ Nos2^{-/-} $ genetic backgrounds and then challenged with sarcoma 180 (S180). Their overall survival was compared to controls. The cancer killing efficiency of purified populations of macrophages and neutrophils from these immunodeficient mice was also examined. Results When these genetically engineered mice were challenged with cancer cells, the knockout backgrounds of $ Prf^{-/-} $, $ Cybb^{-/-} $, or $ Nos2^{-/-} $ did not completely abolish the SR/CR cancer resistant phenotype. However, the $ Nos2^{-/-} $ background did appear to weaken the resistance. Incidentally, it was also observed that the male mice in these immunocompromised backgrounds tended to be less cancer-resistant than SR/CR controls. Conclusion Despite the previously known roles of perforin, superoxide or nitric oxide in the effector mechanisms of innate immune responses, these effector mechanisms were not required for cancer-resistance in SR/CR mice. The resistance was functional when any one of these effector mechanisms was completely absent, except some noticeably reduced penetrance, but not abolishment, of the phenotype in the male background in comparison to female background. These results also indicate that some other effector mechanism(s) of granulocytes may be involved in the killing of cancer cells in SR/CR mice. Nitric Oxide (dpeaa)DE-He213 Maximum Tolerate Dose (dpeaa)DE-He213 Effector Mechanism (dpeaa)DE-He213 S180 Cell (dpeaa)DE-He213 Immunologic Synapse (dpeaa)DE-He213 Stehle, John R aut Blanks, Michael J aut Riedlinger, Gregory aut Kim-Shapiro, Jung W aut Monjazeb, Arta M aut Adams, Jonathan M aut Willingham, Mark C aut Cui, Zheng aut Enthalten in BMC cancer London : BioMed Central, 2001 10(2010), 1 vom: 31. März (DE-627)326643710 (DE-600)2041352-X 1471-2407 nnns volume:10 year:2010 number:1 day:31 month:03 https://dx.doi.org/10.1186/1471-2407-10-121 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 10 2010 1 31 03
language	English
source	Enthalten in BMC cancer 10(2010), 1 vom: 31. März volume:10 year:2010 number:1 day:31 month:03
sourceStr	Enthalten in BMC cancer 10(2010), 1 vom: 31. März volume:10 year:2010 number:1 day:31 month:03
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Nitric Oxide Maximum Tolerate Dose Effector Mechanism S180 Cell Immunologic Synapse
isfreeaccess_bool	true
container_title	BMC cancer
authorswithroles_txt_mv	Sanders, Anne M @@aut@@ Stehle, John R @@aut@@ Blanks, Michael J @@aut@@ Riedlinger, Gregory @@aut@@ Kim-Shapiro, Jung W @@aut@@ Monjazeb, Arta M @@aut@@ Adams, Jonathan M @@aut@@ Willingham, Mark C @@aut@@ Cui, Zheng @@aut@@
publishDateDaySort_date	2010-03-31T00:00:00Z
hierarchy_top_id	326643710
id	SPR02762398X
language_de	englisch
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This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Background Spontaneous Regression/Complete Resistant (SR/CR) mice are a colony of cancer-resistant mice that can detect and rapidly destroy malignant cells with innate cellular immunity, predominately mediated by granulocytes. Our previous studies suggest that several effector mechanisms, such as perforin, granzymes, or complements, may be involved in the killing of cancer cells. However, none of these effector mechanisms is known as critical for granulocytes. Additionally, it is unclear which effector mechanisms are required for the cancer killing activity of specific leukocyte populations and the survival of SR/CR mice against the challenges of lethal cancer cells. We hypothesized that if any of these effector mechanisms was required for the resistance to cancer cells, its functional knockout in SR/CR mice should render them sensitive to cancer challenges. This was tested by cross breeding SR/CR mice into the individual genetic knockout backgrounds of perforin ($ Prf^{-/-} $), superoxide ($ Cybb^{-/} $), or inducible nitric oxide ($ Nos2^{-/} $). Methods SR/CR mice were bred into individual $ Prf^{-/-} $, $ Cybb^{-/-} $, or $ Nos2^{-/-} $ genetic backgrounds and then challenged with sarcoma 180 (S180). Their overall survival was compared to controls. The cancer killing efficiency of purified populations of macrophages and neutrophils from these immunodeficient mice was also examined. Results When these genetically engineered mice were challenged with cancer cells, the knockout backgrounds of $ Prf^{-/-} $, $ Cybb^{-/-} $, or $ Nos2^{-/-} $ did not completely abolish the SR/CR cancer resistant phenotype. 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author	Sanders, Anne M
spellingShingle	Sanders, Anne M misc Nitric Oxide misc Maximum Tolerate Dose misc Effector Mechanism misc S180 Cell misc Immunologic Synapse Cancer resistance of SR/CR mice in the genetic knockout backgrounds of leukocyte effector mechanisms: determinations for functional requirements
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topic_title	Cancer resistance of SR/CR mice in the genetic knockout backgrounds of leukocyte effector mechanisms: determinations for functional requirements Nitric Oxide (dpeaa)DE-He213 Maximum Tolerate Dose (dpeaa)DE-He213 Effector Mechanism (dpeaa)DE-He213 S180 Cell (dpeaa)DE-He213 Immunologic Synapse (dpeaa)DE-He213
topic	misc Nitric Oxide misc Maximum Tolerate Dose misc Effector Mechanism misc S180 Cell misc Immunologic Synapse
topic_unstemmed	misc Nitric Oxide misc Maximum Tolerate Dose misc Effector Mechanism misc S180 Cell misc Immunologic Synapse
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title	Cancer resistance of SR/CR mice in the genetic knockout backgrounds of leukocyte effector mechanisms: determinations for functional requirements
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title_full	Cancer resistance of SR/CR mice in the genetic knockout backgrounds of leukocyte effector mechanisms: determinations for functional requirements
author_sort	Sanders, Anne M
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author_browse	Sanders, Anne M Stehle, John R Blanks, Michael J Riedlinger, Gregory Kim-Shapiro, Jung W Monjazeb, Arta M Adams, Jonathan M Willingham, Mark C Cui, Zheng
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title_sort	cancer resistance of sr/cr mice in the genetic knockout backgrounds of leukocyte effector mechanisms: determinations for functional requirements
title_auth	Cancer resistance of SR/CR mice in the genetic knockout backgrounds of leukocyte effector mechanisms: determinations for functional requirements
abstract	Background Spontaneous Regression/Complete Resistant (SR/CR) mice are a colony of cancer-resistant mice that can detect and rapidly destroy malignant cells with innate cellular immunity, predominately mediated by granulocytes. Our previous studies suggest that several effector mechanisms, such as perforin, granzymes, or complements, may be involved in the killing of cancer cells. However, none of these effector mechanisms is known as critical for granulocytes. Additionally, it is unclear which effector mechanisms are required for the cancer killing activity of specific leukocyte populations and the survival of SR/CR mice against the challenges of lethal cancer cells. We hypothesized that if any of these effector mechanisms was required for the resistance to cancer cells, its functional knockout in SR/CR mice should render them sensitive to cancer challenges. This was tested by cross breeding SR/CR mice into the individual genetic knockout backgrounds of perforin ($ Prf^{-/-} $), superoxide ($ Cybb^{-/} $), or inducible nitric oxide ($ Nos2^{-/} $). Methods SR/CR mice were bred into individual $ Prf^{-/-} $, $ Cybb^{-/-} $, or $ Nos2^{-/-} $ genetic backgrounds and then challenged with sarcoma 180 (S180). Their overall survival was compared to controls. The cancer killing efficiency of purified populations of macrophages and neutrophils from these immunodeficient mice was also examined. Results When these genetically engineered mice were challenged with cancer cells, the knockout backgrounds of $ Prf^{-/-} $, $ Cybb^{-/-} $, or $ Nos2^{-/-} $ did not completely abolish the SR/CR cancer resistant phenotype. However, the $ Nos2^{-/-} $ background did appear to weaken the resistance. Incidentally, it was also observed that the male mice in these immunocompromised backgrounds tended to be less cancer-resistant than SR/CR controls. Conclusion Despite the previously known roles of perforin, superoxide or nitric oxide in the effector mechanisms of innate immune responses, these effector mechanisms were not required for cancer-resistance in SR/CR mice. The resistance was functional when any one of these effector mechanisms was completely absent, except some noticeably reduced penetrance, but not abolishment, of the phenotype in the male background in comparison to female background. These results also indicate that some other effector mechanism(s) of granulocytes may be involved in the killing of cancer cells in SR/CR mice. © Sanders et al; licensee BioMed Central Ltd. 2010. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (
abstractGer	Background Spontaneous Regression/Complete Resistant (SR/CR) mice are a colony of cancer-resistant mice that can detect and rapidly destroy malignant cells with innate cellular immunity, predominately mediated by granulocytes. Our previous studies suggest that several effector mechanisms, such as perforin, granzymes, or complements, may be involved in the killing of cancer cells. However, none of these effector mechanisms is known as critical for granulocytes. Additionally, it is unclear which effector mechanisms are required for the cancer killing activity of specific leukocyte populations and the survival of SR/CR mice against the challenges of lethal cancer cells. We hypothesized that if any of these effector mechanisms was required for the resistance to cancer cells, its functional knockout in SR/CR mice should render them sensitive to cancer challenges. This was tested by cross breeding SR/CR mice into the individual genetic knockout backgrounds of perforin ($ Prf^{-/-} $), superoxide ($ Cybb^{-/} $), or inducible nitric oxide ($ Nos2^{-/} $). Methods SR/CR mice were bred into individual $ Prf^{-/-} $, $ Cybb^{-/-} $, or $ Nos2^{-/-} $ genetic backgrounds and then challenged with sarcoma 180 (S180). Their overall survival was compared to controls. The cancer killing efficiency of purified populations of macrophages and neutrophils from these immunodeficient mice was also examined. Results When these genetically engineered mice were challenged with cancer cells, the knockout backgrounds of $ Prf^{-/-} $, $ Cybb^{-/-} $, or $ Nos2^{-/-} $ did not completely abolish the SR/CR cancer resistant phenotype. However, the $ Nos2^{-/-} $ background did appear to weaken the resistance. Incidentally, it was also observed that the male mice in these immunocompromised backgrounds tended to be less cancer-resistant than SR/CR controls. Conclusion Despite the previously known roles of perforin, superoxide or nitric oxide in the effector mechanisms of innate immune responses, these effector mechanisms were not required for cancer-resistance in SR/CR mice. The resistance was functional when any one of these effector mechanisms was completely absent, except some noticeably reduced penetrance, but not abolishment, of the phenotype in the male background in comparison to female background. These results also indicate that some other effector mechanism(s) of granulocytes may be involved in the killing of cancer cells in SR/CR mice. © Sanders et al; licensee BioMed Central Ltd. 2010. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (
abstract_unstemmed	Background Spontaneous Regression/Complete Resistant (SR/CR) mice are a colony of cancer-resistant mice that can detect and rapidly destroy malignant cells with innate cellular immunity, predominately mediated by granulocytes. Our previous studies suggest that several effector mechanisms, such as perforin, granzymes, or complements, may be involved in the killing of cancer cells. However, none of these effector mechanisms is known as critical for granulocytes. Additionally, it is unclear which effector mechanisms are required for the cancer killing activity of specific leukocyte populations and the survival of SR/CR mice against the challenges of lethal cancer cells. We hypothesized that if any of these effector mechanisms was required for the resistance to cancer cells, its functional knockout in SR/CR mice should render them sensitive to cancer challenges. This was tested by cross breeding SR/CR mice into the individual genetic knockout backgrounds of perforin ($ Prf^{-/-} $), superoxide ($ Cybb^{-/} $), or inducible nitric oxide ($ Nos2^{-/} $). Methods SR/CR mice were bred into individual $ Prf^{-/-} $, $ Cybb^{-/-} $, or $ Nos2^{-/-} $ genetic backgrounds and then challenged with sarcoma 180 (S180). Their overall survival was compared to controls. The cancer killing efficiency of purified populations of macrophages and neutrophils from these immunodeficient mice was also examined. Results When these genetically engineered mice were challenged with cancer cells, the knockout backgrounds of $ Prf^{-/-} $, $ Cybb^{-/-} $, or $ Nos2^{-/-} $ did not completely abolish the SR/CR cancer resistant phenotype. However, the $ Nos2^{-/-} $ background did appear to weaken the resistance. Incidentally, it was also observed that the male mice in these immunocompromised backgrounds tended to be less cancer-resistant than SR/CR controls. Conclusion Despite the previously known roles of perforin, superoxide or nitric oxide in the effector mechanisms of innate immune responses, these effector mechanisms were not required for cancer-resistance in SR/CR mice. The resistance was functional when any one of these effector mechanisms was completely absent, except some noticeably reduced penetrance, but not abolishment, of the phenotype in the male background in comparison to female background. These results also indicate that some other effector mechanism(s) of granulocytes may be involved in the killing of cancer cells in SR/CR mice. © Sanders et al; licensee BioMed Central Ltd. 2010. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (
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title_short	Cancer resistance of SR/CR mice in the genetic knockout backgrounds of leukocyte effector mechanisms: determinations for functional requirements
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This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Background Spontaneous Regression/Complete Resistant (SR/CR) mice are a colony of cancer-resistant mice that can detect and rapidly destroy malignant cells with innate cellular immunity, predominately mediated by granulocytes. Our previous studies suggest that several effector mechanisms, such as perforin, granzymes, or complements, may be involved in the killing of cancer cells. However, none of these effector mechanisms is known as critical for granulocytes. Additionally, it is unclear which effector mechanisms are required for the cancer killing activity of specific leukocyte populations and the survival of SR/CR mice against the challenges of lethal cancer cells. We hypothesized that if any of these effector mechanisms was required for the resistance to cancer cells, its functional knockout in SR/CR mice should render them sensitive to cancer challenges. This was tested by cross breeding SR/CR mice into the individual genetic knockout backgrounds of perforin ($ Prf^{-/-} $), superoxide ($ Cybb^{-/} $), or inducible nitric oxide ($ Nos2^{-/} $). Methods SR/CR mice were bred into individual $ Prf^{-/-} $, $ Cybb^{-/-} $, or $ Nos2^{-/-} $ genetic backgrounds and then challenged with sarcoma 180 (S180). Their overall survival was compared to controls. The cancer killing efficiency of purified populations of macrophages and neutrophils from these immunodeficient mice was also examined. Results When these genetically engineered mice were challenged with cancer cells, the knockout backgrounds of $ Prf^{-/-} $, $ Cybb^{-/-} $, or $ Nos2^{-/-} $ did not completely abolish the SR/CR cancer resistant phenotype. However, the $ Nos2^{-/-} $ background did appear to weaken the resistance. Incidentally, it was also observed that the male mice in these immunocompromised backgrounds tended to be less cancer-resistant than SR/CR controls. Conclusion Despite the previously known roles of perforin, superoxide or nitric oxide in the effector mechanisms of innate immune responses, these effector mechanisms were not required for cancer-resistance in SR/CR mice. The resistance was functional when any one of these effector mechanisms was completely absent, except some noticeably reduced penetrance, but not abolishment, of the phenotype in the male background in comparison to female background. These results also indicate that some other effector mechanism(s) of granulocytes may be involved in the killing of cancer cells in SR/CR mice.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Nitric Oxide</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Maximum Tolerate Dose</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Effector Mechanism</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">S180 Cell</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Immunologic Synapse</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Stehle, John R</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Blanks, Michael J</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Riedlinger, Gregory</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Kim-Shapiro, Jung W</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Monjazeb, Arta M</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Adams, Jonathan M</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Willingham, Mark C</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Cui, Zheng</subfield><subfield code="4">aut</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="t">BMC cancer</subfield><subfield code="d">London : BioMed Central, 2001</subfield><subfield code="g">10(2010), 1 vom: 31. 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Cancer resistance of SR/CR mice in the genetic knockout backgrounds of leukocyte effector mechanisms: determinations for functional requirements

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