Antisense treatment of IGF-IR induces apoptosis and enhances chemosensitivity in central nervous system atypical teratoid/rhabdoid tumours cells.

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Antisense treatment of IGF-IR induces apoptosis and enhances chemosensitivity in central nervous system atypical teratoid/rhabdoid tumours cells. / D'cunja, J; Shalaby, T; Rivera, P; von Bueren, André; Patti, R; Heppner, F L; Arcaro, A; Rorke-Adams, L B; Phillips, P C; Grotzer, M A.

In: EUR J CANCER, Vol. 43, No. 10, 10, 2007, p. 1581-1589.

Research output: SCORING: Contribution to journalSCORING: Journal articleResearchpeer-review

Harvard

D'cunja, J, Shalaby, T, Rivera, P, von Bueren, A, Patti, R, Heppner, FL, Arcaro, A, Rorke-Adams, LB, Phillips, PC & Grotzer, MA 2007, 'Antisense treatment of IGF-IR induces apoptosis and enhances chemosensitivity in central nervous system atypical teratoid/rhabdoid tumours cells.', EUR J CANCER, vol. 43, no. 10, 10, pp. 1581-1589. <http://www.ncbi.nlm.nih.gov/pubmed/17446062?dopt=Citation>

APA

D'cunja, J., Shalaby, T., Rivera, P., von Bueren, A., Patti, R., Heppner, F. L., Arcaro, A., Rorke-Adams, L. B., Phillips, P. C., & Grotzer, M. A. (2007). Antisense treatment of IGF-IR induces apoptosis and enhances chemosensitivity in central nervous system atypical teratoid/rhabdoid tumours cells. EUR J CANCER, 43(10), 1581-1589. [10]. http://www.ncbi.nlm.nih.gov/pubmed/17446062?dopt=Citation

Vancouver

Bibtex

@article{227305b6d6f8455a9390c758752becb8,
title = "Antisense treatment of IGF-IR induces apoptosis and enhances chemosensitivity in central nervous system atypical teratoid/rhabdoid tumours cells.",
abstract = "Central nervous system (CNS) atypical teratoid/rhabdoid tumours (AT/RT) are among the paediatric malignant tumours with the worst prognosis and fatal outcome. Insulin-like growth factor I receptor (IGF-IR) protects cancer cells from apoptosis induced by a variety of anticancer drugs and radiation. In the present study, IGF-IR was expressed in 8/8 primary AT/RT as detected by immunohistochemistry. Moreover, we found IGF-I and IGF-II mRNA in BT-16 CNS AT/RT cells and IGF-II mRNA in BT-12 CNS AT/RT cells, and autophosphorylated IGF-IR in both cell lines, indicating the potential presence of an autocrine/paracrine IGF-I/II/IGF-IR loop in CNS AT/RT. IGF-IR antisense oligonucleotide treatment of human CNS AT/RT cells resulted in significant down-regulation of IGF-IR mRNA and protein expression, induction of apoptosis, and chemosensitisation to doxorubicin and cisplatin. These studies provide evidence for the influence of IGF-IR on cellular responses to chemotherapy and raise the possibility that curability of selected CNS AT/RT may be improved by pharmaceutical strategies directed towards the IGF-IR.",
author = "J D'cunja and T Shalaby and P Rivera and {von Bueren}, Andr{\'e} and R Patti and Heppner, {F L} and A Arcaro and Rorke-Adams, {L B} and Phillips, {P C} and Grotzer, {M A}",
year = "2007",
language = "Deutsch",
volume = "43",
pages = "1581--1589",
journal = "EUR J CANCER",
issn = "0959-8049",
publisher = "Elsevier Limited",
number = "10",

}

RIS

TY - JOUR

T1 - Antisense treatment of IGF-IR induces apoptosis and enhances chemosensitivity in central nervous system atypical teratoid/rhabdoid tumours cells.

AU - D'cunja, J

AU - Shalaby, T

AU - Rivera, P

AU - von Bueren, André

AU - Patti, R

AU - Heppner, F L

AU - Arcaro, A

AU - Rorke-Adams, L B

AU - Phillips, P C

AU - Grotzer, M A

PY - 2007

Y1 - 2007

N2 - Central nervous system (CNS) atypical teratoid/rhabdoid tumours (AT/RT) are among the paediatric malignant tumours with the worst prognosis and fatal outcome. Insulin-like growth factor I receptor (IGF-IR) protects cancer cells from apoptosis induced by a variety of anticancer drugs and radiation. In the present study, IGF-IR was expressed in 8/8 primary AT/RT as detected by immunohistochemistry. Moreover, we found IGF-I and IGF-II mRNA in BT-16 CNS AT/RT cells and IGF-II mRNA in BT-12 CNS AT/RT cells, and autophosphorylated IGF-IR in both cell lines, indicating the potential presence of an autocrine/paracrine IGF-I/II/IGF-IR loop in CNS AT/RT. IGF-IR antisense oligonucleotide treatment of human CNS AT/RT cells resulted in significant down-regulation of IGF-IR mRNA and protein expression, induction of apoptosis, and chemosensitisation to doxorubicin and cisplatin. These studies provide evidence for the influence of IGF-IR on cellular responses to chemotherapy and raise the possibility that curability of selected CNS AT/RT may be improved by pharmaceutical strategies directed towards the IGF-IR.

AB - Central nervous system (CNS) atypical teratoid/rhabdoid tumours (AT/RT) are among the paediatric malignant tumours with the worst prognosis and fatal outcome. Insulin-like growth factor I receptor (IGF-IR) protects cancer cells from apoptosis induced by a variety of anticancer drugs and radiation. In the present study, IGF-IR was expressed in 8/8 primary AT/RT as detected by immunohistochemistry. Moreover, we found IGF-I and IGF-II mRNA in BT-16 CNS AT/RT cells and IGF-II mRNA in BT-12 CNS AT/RT cells, and autophosphorylated IGF-IR in both cell lines, indicating the potential presence of an autocrine/paracrine IGF-I/II/IGF-IR loop in CNS AT/RT. IGF-IR antisense oligonucleotide treatment of human CNS AT/RT cells resulted in significant down-regulation of IGF-IR mRNA and protein expression, induction of apoptosis, and chemosensitisation to doxorubicin and cisplatin. These studies provide evidence for the influence of IGF-IR on cellular responses to chemotherapy and raise the possibility that curability of selected CNS AT/RT may be improved by pharmaceutical strategies directed towards the IGF-IR.

M3 - SCORING: Zeitschriftenaufsatz

VL - 43

SP - 1581

EP - 1589

JO - EUR J CANCER

JF - EUR J CANCER

SN - 0959-8049

IS - 10

M1 - 10

ER -