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Use of macrophages to target therapeutic adenovirus to human prostate tumors

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Use of macrophages to target therapeutic adenovirus to human prostate tumors. / Muthana, Munitta; Giannoudis, Athina; Scott, Simon D; Fang, Hsin-Yu; Coffelt, Seth B; Morrow, Fiona J; Murdoch, Craig; Burton, Julian; Cross, Neil; Burke, Bernard; Mistry, Roshna; Hamdy, Freddie; Brown, Nicola J; Georgopoulos, Lindsay; Hoskin, Peter; Essand, Magnus; Lewis, Claire E; Maitland, Norman J.

In: Cancer research, Vol. 71, No. 5, 01.03.2011, p. 1805-1815.

Research output: Contribution to journalArticle

Harvard

Muthana, M, Giannoudis, A, Scott, SD, Fang, H-Y, Coffelt, SB, Morrow, FJ, Murdoch, C, Burton, J, Cross, N, Burke, B, Mistry, R, Hamdy, F, Brown, NJ, Georgopoulos, L, Hoskin, P, Essand, M, Lewis, CE & Maitland, NJ 2011, 'Use of macrophages to target therapeutic adenovirus to human prostate tumors', Cancer research, vol. 71, no. 5, pp. 1805-1815. https://doi.org/10.1158/0008-5472.CAN-10-2349

APA

Muthana, M., Giannoudis, A., Scott, S. D., Fang, H-Y., Coffelt, S. B., Morrow, F. J., ... Maitland, N. J. (2011). Use of macrophages to target therapeutic adenovirus to human prostate tumors. Cancer research, 71(5), 1805-1815. https://doi.org/10.1158/0008-5472.CAN-10-2349

Vancouver

Muthana M, Giannoudis A, Scott SD, Fang H-Y, Coffelt SB, Morrow FJ et al. Use of macrophages to target therapeutic adenovirus to human prostate tumors. Cancer research. 2011 Mar 1;71(5):1805-1815. https://doi.org/10.1158/0008-5472.CAN-10-2349

Author

Muthana, Munitta ; Giannoudis, Athina ; Scott, Simon D ; Fang, Hsin-Yu ; Coffelt, Seth B ; Morrow, Fiona J ; Murdoch, Craig ; Burton, Julian ; Cross, Neil ; Burke, Bernard ; Mistry, Roshna ; Hamdy, Freddie ; Brown, Nicola J ; Georgopoulos, Lindsay ; Hoskin, Peter ; Essand, Magnus ; Lewis, Claire E ; Maitland, Norman J. / Use of macrophages to target therapeutic adenovirus to human prostate tumors. In: Cancer research. 2011 ; Vol. 71, No. 5. pp. 1805-1815.

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@article{e27a0115dc924c02b947d5b9c4f98dfb,
title = "Use of macrophages to target therapeutic adenovirus to human prostate tumors",
abstract = "New therapies are required to target hypoxic areas of tumors as these sites are highly resistant to conventional cancer therapies. Monocytes continuously extravasate from the bloodstream into tumors where they differentiate into macrophages and accumulate in hypoxic areas, thereby opening up the possibility of using these cells as vehicles to deliver gene therapy to these otherwise inaccessible sites. We describe a new cell-based method that selectively targets an oncolytic adenovirus to hypoxic areas of prostate tumors. In this approach, macrophages were cotransduced with a hypoxia-regulated E1A/B construct and an E1A-dependent oncolytic adenovirus, whose proliferation is restricted to prostate tumor cells using prostate-specific promoter elements from the TARP, PSA, and PMSA genes. When such cotransduced cells reach an area of extreme hypoxia, the E1A/B proteins are expressed, thereby activating replication of the adenovirus. The virus is subsequently released by the host macrophage and infects neighboring tumor cells. Following systemic injection into mice bearing subcutaneous or orthotopic prostate tumors, cotransduced macrophages migrated into hypoxic tumor areas, upregulated E1A protein, and released multiple copies of adenovirus. The virus then infected neighboring cells but only proliferated and was cytotoxic in prostate tumor cells, resulting in the marked inhibition of tumor growth and reduction of pulmonary metastases. This novel delivery system employs 3 levels of tumor specificity: the natural {"}homing{"} of macrophages to hypoxic tumor areas, hypoxia-induced proliferation of the therapeutic adenovirus in host macrophages, and targeted replication of oncolytic virus in prostate tumor cells.",
keywords = "Adenoviridae, Adenovirus E1A Proteins, Animals, Cell Hypoxia, Electrophoresis, Polyacrylamide Gel, Humans, Macrophages, Male, Mice, Mice, Nude, Oncolytic Virotherapy, Oncolytic Viruses, Prostatic Neoplasms, Transduction, Genetic, Xenograft Model Antitumor Assays",
author = "Munitta Muthana and Athina Giannoudis and Scott, {Simon D} and Hsin-Yu Fang and Coffelt, {Seth B} and Morrow, {Fiona J} and Craig Murdoch and Julian Burton and Neil Cross and Bernard Burke and Roshna Mistry and Freddie Hamdy and Brown, {Nicola J} and Lindsay Georgopoulos and Peter Hoskin and Magnus Essand and Lewis, {Claire E} and Maitland, {Norman J}",
note = "{\circledC}2011 AACR.",
year = "2011",
month = "3",
day = "1",
doi = "10.1158/0008-5472.CAN-10-2349",
language = "English",
volume = "71",
pages = "1805--1815",
journal = "Cancer research",
issn = "0008-5472",
publisher = "American Association for Cancer Research Inc.",
number = "5",

}

RIS (suitable for import to EndNote) - Download

TY - JOUR

T1 - Use of macrophages to target therapeutic adenovirus to human prostate tumors

AU - Muthana, Munitta

AU - Giannoudis, Athina

AU - Scott, Simon D

AU - Fang, Hsin-Yu

AU - Coffelt, Seth B

AU - Morrow, Fiona J

AU - Murdoch, Craig

AU - Burton, Julian

AU - Cross, Neil

AU - Burke, Bernard

AU - Mistry, Roshna

AU - Hamdy, Freddie

AU - Brown, Nicola J

AU - Georgopoulos, Lindsay

AU - Hoskin, Peter

AU - Essand, Magnus

AU - Lewis, Claire E

AU - Maitland, Norman J

N1 - ©2011 AACR.

PY - 2011/3/1

Y1 - 2011/3/1

N2 - New therapies are required to target hypoxic areas of tumors as these sites are highly resistant to conventional cancer therapies. Monocytes continuously extravasate from the bloodstream into tumors where they differentiate into macrophages and accumulate in hypoxic areas, thereby opening up the possibility of using these cells as vehicles to deliver gene therapy to these otherwise inaccessible sites. We describe a new cell-based method that selectively targets an oncolytic adenovirus to hypoxic areas of prostate tumors. In this approach, macrophages were cotransduced with a hypoxia-regulated E1A/B construct and an E1A-dependent oncolytic adenovirus, whose proliferation is restricted to prostate tumor cells using prostate-specific promoter elements from the TARP, PSA, and PMSA genes. When such cotransduced cells reach an area of extreme hypoxia, the E1A/B proteins are expressed, thereby activating replication of the adenovirus. The virus is subsequently released by the host macrophage and infects neighboring tumor cells. Following systemic injection into mice bearing subcutaneous or orthotopic prostate tumors, cotransduced macrophages migrated into hypoxic tumor areas, upregulated E1A protein, and released multiple copies of adenovirus. The virus then infected neighboring cells but only proliferated and was cytotoxic in prostate tumor cells, resulting in the marked inhibition of tumor growth and reduction of pulmonary metastases. This novel delivery system employs 3 levels of tumor specificity: the natural "homing" of macrophages to hypoxic tumor areas, hypoxia-induced proliferation of the therapeutic adenovirus in host macrophages, and targeted replication of oncolytic virus in prostate tumor cells.

AB - New therapies are required to target hypoxic areas of tumors as these sites are highly resistant to conventional cancer therapies. Monocytes continuously extravasate from the bloodstream into tumors where they differentiate into macrophages and accumulate in hypoxic areas, thereby opening up the possibility of using these cells as vehicles to deliver gene therapy to these otherwise inaccessible sites. We describe a new cell-based method that selectively targets an oncolytic adenovirus to hypoxic areas of prostate tumors. In this approach, macrophages were cotransduced with a hypoxia-regulated E1A/B construct and an E1A-dependent oncolytic adenovirus, whose proliferation is restricted to prostate tumor cells using prostate-specific promoter elements from the TARP, PSA, and PMSA genes. When such cotransduced cells reach an area of extreme hypoxia, the E1A/B proteins are expressed, thereby activating replication of the adenovirus. The virus is subsequently released by the host macrophage and infects neighboring tumor cells. Following systemic injection into mice bearing subcutaneous or orthotopic prostate tumors, cotransduced macrophages migrated into hypoxic tumor areas, upregulated E1A protein, and released multiple copies of adenovirus. The virus then infected neighboring cells but only proliferated and was cytotoxic in prostate tumor cells, resulting in the marked inhibition of tumor growth and reduction of pulmonary metastases. This novel delivery system employs 3 levels of tumor specificity: the natural "homing" of macrophages to hypoxic tumor areas, hypoxia-induced proliferation of the therapeutic adenovirus in host macrophages, and targeted replication of oncolytic virus in prostate tumor cells.

KW - Adenoviridae

KW - Adenovirus E1A Proteins

KW - Animals

KW - Cell Hypoxia

KW - Electrophoresis, Polyacrylamide Gel

KW - Humans

KW - Macrophages

KW - Male

KW - Mice

KW - Mice, Nude

KW - Oncolytic Virotherapy

KW - Oncolytic Viruses

KW - Prostatic Neoplasms

KW - Transduction, Genetic

KW - Xenograft Model Antitumor Assays

UR - http://www.scopus.com/inward/record.url?scp=79952233838&partnerID=8YFLogxK

U2 - 10.1158/0008-5472.CAN-10-2349

DO - 10.1158/0008-5472.CAN-10-2349

M3 - Article

VL - 71

SP - 1805

EP - 1815

JO - Cancer research

T2 - Cancer research

JF - Cancer research

SN - 0008-5472

IS - 5

ER -