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Accelerated Tumor Progression in Mice Lacking the ATP Receptor P2X7

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Harvard

Adinolfi, E, Capece, M, Franceschini, A, Falzoni, S, Giuliani, AL, Rotondo, A, Sarti, AC, Bonora, M, Syberg, S, Corigliano, D, Pinton, P, Jorgensen, NR, Abelli, L, Emionite, L, Raffaghello, L, Pistoia, V & Di Virgilio, F 2015, 'Accelerated Tumor Progression in Mice Lacking the ATP Receptor P2X7' Cancer Research, bind 75, nr. 4, s. 635-44. https://doi.org/10.1158/0008-5472.CAN-14-1259

APA

Adinolfi, E., Capece, M., Franceschini, A., Falzoni, S., Giuliani, A. L., Rotondo, A., ... Di Virgilio, F. (2015). Accelerated Tumor Progression in Mice Lacking the ATP Receptor P2X7. Cancer Research, 75(4), 635-44. https://doi.org/10.1158/0008-5472.CAN-14-1259

CBE

Adinolfi E, Capece M, Franceschini A, Falzoni S, Giuliani AL, Rotondo A, Sarti AC, Bonora M, Syberg S, Corigliano D, Pinton P, Jorgensen NR, Abelli L, Emionite L, Raffaghello L, Pistoia V, Di Virgilio F. 2015. Accelerated Tumor Progression in Mice Lacking the ATP Receptor P2X7. Cancer Research. 75(4):635-44. https://doi.org/10.1158/0008-5472.CAN-14-1259

MLA

Vancouver

Adinolfi E, Capece M, Franceschini A, Falzoni S, Giuliani AL, Rotondo A o.a. Accelerated Tumor Progression in Mice Lacking the ATP Receptor P2X7. Cancer Research. 2015 feb 15;75(4):635-44. https://doi.org/10.1158/0008-5472.CAN-14-1259

Author

Adinolfi, Elena ; Capece, Marina ; Franceschini, Alessia ; Falzoni, Simonetta ; Giuliani, Anna L ; Rotondo, Alessandra ; Sarti, Alba C ; Bonora, Massimo ; Syberg, Susanne ; Corigliano, Domenica ; Pinton, Paolo ; Jorgensen, Niklas R ; Abelli, Luigi ; Emionite, Laura ; Raffaghello, Lizzia ; Pistoia, Vito ; Di Virgilio, Francesco. / Accelerated Tumor Progression in Mice Lacking the ATP Receptor P2X7. I: Cancer Research. 2015 ; Bind 75, Nr. 4. s. 635-44.

Bibtex

@article{04810f39b6e94ed1b5baff6ebb59863a,
title = "Accelerated Tumor Progression in Mice Lacking the ATP Receptor P2X7",
abstract = "The ATP receptor P2X7 (P2X7R or P2RX7) has a key role in inflammation and immunity, but its possible roles in cancer are not firmly established. In the present study, we investigated the effect of host genetic deletion of P2X7R in the mouse on the growth of B16 melanoma or CT26 colon carcinoma cells. Tumor size and metastatic dissemination were assessed by in vivo calliper and luciferase luminescence emission measurements along with postmortem examination. In P2X7R-deficient mice, tumor growth and metastatic spreading were accelerated strongly, compared with wild-type (wt) mice. Intratumoral IL-1β and VEGF release were drastically reduced, and inflammatory cell infiltration was abrogated nearly completely. Similarly, tumor growth was also greatly accelerated in wt chimeric mice implanted with P2X7R-deficient bone marrow cells, defining hematopoietic cells as a sufficient site of P2X7R action. Finally, dendritic cells from P2X7R-deficient mice were unresponsive to stimulation with tumor cells, and chemotaxis of P2X7R-less cells was impaired. Overall, our results showed that host P2X7R expression was critical to support an antitumor immune response, and to restrict tumor growth and metastatic diffusion. Cancer Res; 75(4); 635-44. {\circledC}2014 AACR.",
author = "Elena Adinolfi and Marina Capece and Alessia Franceschini and Simonetta Falzoni and Giuliani, {Anna L} and Alessandra Rotondo and Sarti, {Alba C} and Massimo Bonora and Susanne Syberg and Domenica Corigliano and Paolo Pinton and Jorgensen, {Niklas R} and Luigi Abelli and Laura Emionite and Lizzia Raffaghello and Vito Pistoia and {Di Virgilio}, Francesco",
note = "{\circledC}2014 American Association for Cancer Research.",
year = "2015",
month = "2",
day = "15",
doi = "10.1158/0008-5472.CAN-14-1259",
language = "English",
volume = "75",
pages = "635--44",
journal = "Journal of Cancer Research",
issn = "0008-5472",
publisher = "American Association for Cancer Research (A A C R)",
number = "4",

}

RIS

TY - JOUR

T1 - Accelerated Tumor Progression in Mice Lacking the ATP Receptor P2X7

AU - Adinolfi, Elena

AU - Capece, Marina

AU - Franceschini, Alessia

AU - Falzoni, Simonetta

AU - Giuliani, Anna L

AU - Rotondo, Alessandra

AU - Sarti, Alba C

AU - Bonora, Massimo

AU - Syberg, Susanne

AU - Corigliano, Domenica

AU - Pinton, Paolo

AU - Jorgensen, Niklas R

AU - Abelli, Luigi

AU - Emionite, Laura

AU - Raffaghello, Lizzia

AU - Pistoia, Vito

AU - Di Virgilio, Francesco

N1 - ©2014 American Association for Cancer Research.

PY - 2015/2/15

Y1 - 2015/2/15

N2 - The ATP receptor P2X7 (P2X7R or P2RX7) has a key role in inflammation and immunity, but its possible roles in cancer are not firmly established. In the present study, we investigated the effect of host genetic deletion of P2X7R in the mouse on the growth of B16 melanoma or CT26 colon carcinoma cells. Tumor size and metastatic dissemination were assessed by in vivo calliper and luciferase luminescence emission measurements along with postmortem examination. In P2X7R-deficient mice, tumor growth and metastatic spreading were accelerated strongly, compared with wild-type (wt) mice. Intratumoral IL-1β and VEGF release were drastically reduced, and inflammatory cell infiltration was abrogated nearly completely. Similarly, tumor growth was also greatly accelerated in wt chimeric mice implanted with P2X7R-deficient bone marrow cells, defining hematopoietic cells as a sufficient site of P2X7R action. Finally, dendritic cells from P2X7R-deficient mice were unresponsive to stimulation with tumor cells, and chemotaxis of P2X7R-less cells was impaired. Overall, our results showed that host P2X7R expression was critical to support an antitumor immune response, and to restrict tumor growth and metastatic diffusion. Cancer Res; 75(4); 635-44. ©2014 AACR.

AB - The ATP receptor P2X7 (P2X7R or P2RX7) has a key role in inflammation and immunity, but its possible roles in cancer are not firmly established. In the present study, we investigated the effect of host genetic deletion of P2X7R in the mouse on the growth of B16 melanoma or CT26 colon carcinoma cells. Tumor size and metastatic dissemination were assessed by in vivo calliper and luciferase luminescence emission measurements along with postmortem examination. In P2X7R-deficient mice, tumor growth and metastatic spreading were accelerated strongly, compared with wild-type (wt) mice. Intratumoral IL-1β and VEGF release were drastically reduced, and inflammatory cell infiltration was abrogated nearly completely. Similarly, tumor growth was also greatly accelerated in wt chimeric mice implanted with P2X7R-deficient bone marrow cells, defining hematopoietic cells as a sufficient site of P2X7R action. Finally, dendritic cells from P2X7R-deficient mice were unresponsive to stimulation with tumor cells, and chemotaxis of P2X7R-less cells was impaired. Overall, our results showed that host P2X7R expression was critical to support an antitumor immune response, and to restrict tumor growth and metastatic diffusion. Cancer Res; 75(4); 635-44. ©2014 AACR.

U2 - 10.1158/0008-5472.CAN-14-1259

DO - 10.1158/0008-5472.CAN-14-1259

M3 - Journal article

VL - 75

SP - 635

EP - 644

JO - Journal of Cancer Research

JF - Journal of Cancer Research

SN - 0008-5472

IS - 4

ER -

ID: 44991935