Prostate-specific antigen-activated thapsigargin prodrug as targeted therapy for prostate cancer

Research output: Contribution to journal › Journal article › Research › peer-review

Standard

Prostate-specific antigen-activated thapsigargin prodrug as targeted therapy for prostate cancer. / Denmeade, Samuel R; Jakobsen, Carsten M; Janssen, Samuel; Khan, Saeed R; Garrett, Elizabeth S; Lilja, Hans; Christensen, S Brogger; Isaacs, John T.

In: National Cancer Institute. Journal (Online), Vol. 95, No. 13, 02.07.2003, p. 990-1000.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Denmeade, SR, Jakobsen, CM, Janssen, S, Khan, SR, Garrett, ES, Lilja, H, Christensen, SB & Isaacs, JT 2003, 'Prostate-specific antigen-activated thapsigargin prodrug as targeted therapy for prostate cancer', National Cancer Institute. Journal (Online), vol. 95, no. 13, pp. 990-1000.

APA

Denmeade, S. R., Jakobsen, C. M., Janssen, S., Khan, S. R., Garrett, E. S., Lilja, H., Christensen, S. B., & Isaacs, J. T. (2003). Prostate-specific antigen-activated thapsigargin prodrug as targeted therapy for prostate cancer. National Cancer Institute. Journal (Online), 95(13), 990-1000.

Vancouver

Denmeade SR, Jakobsen CM, Janssen S, Khan SR, Garrett ES, Lilja H et al. Prostate-specific antigen-activated thapsigargin prodrug as targeted therapy for prostate cancer. National Cancer Institute. Journal (Online). 2003 Jul 2;95(13):990-1000.

Author

Denmeade, Samuel R ; Jakobsen, Carsten M ; Janssen, Samuel ; Khan, Saeed R ; Garrett, Elizabeth S ; Lilja, Hans ; Christensen, S Brogger ; Isaacs, John T. / Prostate-specific antigen-activated thapsigargin prodrug as targeted therapy for prostate cancer. In: National Cancer Institute. Journal (Online). 2003 ; Vol. 95, No. 13. pp. 990-1000.

Bibtex

@article{11f355c902ac4e8cbca62edb6a0d9d0a,
title = "Prostate-specific antigen-activated thapsigargin prodrug as targeted therapy for prostate cancer",
abstract = "Standard anti-proliferative chemotherapy is relatively ineffective against slowly proliferating androgen-independent prostate cancer cells within metastatic sites. In contrast, the lipophilic cytotoxin thapsigargin, which causes apoptosis by disrupting intracellular free Ca2+ levels, is effective against both proliferative and quiescent (i.e., G0-arrested) cells. However, thapsigargin's mechanism of action indicates that it is unlikely to be selective for cancer cells or prostate cells.",
keywords = "Animals, Antineoplastic Agents, Disease Models, Animal, Humans, Hydrolysis, Male, Mice, Mice, Nude, Prodrugs, Prostate-Specific Antigen, Prostatic Neoplasms, Thapsigargin, Transplantation, Heterologous, Treatment Outcome",
author = "Denmeade, {Samuel R} and Jakobsen, {Carsten M} and Samuel Janssen and Khan, {Saeed R} and Garrett, {Elizabeth S} and Hans Lilja and Christensen, {S Brogger} and Isaacs, {John T}",
year = "2003",
month = jul,
day = "2",
language = "English",
volume = "95",
pages = "990--1000",
journal = "National Cancer Institute. Journal (Online)",
issn = "1460-2105",
publisher = "Oxford University Press",
number = "13",

}

RIS

TY - JOUR

T1 - Prostate-specific antigen-activated thapsigargin prodrug as targeted therapy for prostate cancer

AU - Denmeade, Samuel R

AU - Jakobsen, Carsten M

AU - Janssen, Samuel

AU - Khan, Saeed R

AU - Garrett, Elizabeth S

AU - Lilja, Hans

AU - Christensen, S Brogger

AU - Isaacs, John T

PY - 2003/7/2

Y1 - 2003/7/2

N2 - Standard anti-proliferative chemotherapy is relatively ineffective against slowly proliferating androgen-independent prostate cancer cells within metastatic sites. In contrast, the lipophilic cytotoxin thapsigargin, which causes apoptosis by disrupting intracellular free Ca2+ levels, is effective against both proliferative and quiescent (i.e., G0-arrested) cells. However, thapsigargin's mechanism of action indicates that it is unlikely to be selective for cancer cells or prostate cells.

AB - Standard anti-proliferative chemotherapy is relatively ineffective against slowly proliferating androgen-independent prostate cancer cells within metastatic sites. In contrast, the lipophilic cytotoxin thapsigargin, which causes apoptosis by disrupting intracellular free Ca2+ levels, is effective against both proliferative and quiescent (i.e., G0-arrested) cells. However, thapsigargin's mechanism of action indicates that it is unlikely to be selective for cancer cells or prostate cells.

KW - Animals

KW - Antineoplastic Agents

KW - Disease Models, Animal

KW - Humans

KW - Hydrolysis

KW - Male

KW - Mice

KW - Mice, Nude

KW - Prodrugs

KW - Prostate-Specific Antigen

KW - Prostatic Neoplasms

KW - Thapsigargin

KW - Transplantation, Heterologous

KW - Treatment Outcome

M3 - Journal article

C2 - 12837835

VL - 95

SP - 990

EP - 1000

JO - National Cancer Institute. Journal (Online)

JF - National Cancer Institute. Journal (Online)

SN - 1460-2105

IS - 13

ER -

ID: 44569411