Androgen Receptor Gene Amplification
in a Recurrent Prostate Cancer after
Monotherapy with the Nonsteroidal
Potent Antiandrogen Casodex
(Bicalutamide) with a Subsequent
Favorable Response to Maximal
Androgen Blockade

Palmberg, Christian; Koivisto, PA; Hyytinen, E.; Isola, J; Visakorpi, Tapio; Kallioniemi, Olli-Pekka; Tammela, T.L.J.

doi:10.1159/000474453

Cited by 66 publications

(37 citation statements)

References 11 publications

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“…Their response to secondary hormonal therapy (such as maximal androgen blockade) may also be favourable. 22 …”

Section: Discussionmentioning

confidence: 99%

Aneuploidy and rapid cell proliferation in recurrent prostate cancers with androgen receptor gene amplification

Koivisto

1997

Prostate Cancer Prostatic Dis

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Mechanisms of prostate cancer recurrence during androgen deprivation are poorly understood. We recently described androgen receptor (AR) gene ampli®-cation in 28% of recurrent prostate carcinomas from hormone-refractory prostate cancer patients. To investigate the hypothesis that ampli®cation of the AR gene promotes the growth of hormone-refractory prostate carcinomas, DNA¯ow cytometric (FCM) studies were carried out to compare matched, primary and hormone-refractory recurrent samples from 31 prostate cancer patients. Recurrent tumours had a higher (P 0.05) S-phase fraction (SPF) (10.6 AE 4.6) than corresponding primary tumours from the same patients (7.0 AE 4.1) and the frequency of aneuploidy also increased from 8±55%. Recurrent tumours with AR gene ampli®cation had a signi®cantly higher (P 0.02) SPF (14.0 AE 6.5) than those with no ampli®cation (9.0 AE 2.9). The results suggest that clinical progression of prostate cancer during androgen withdrawal therapy is often associated with increased cell proliferation rate and formation of DNA aneuploidy. AR ampli®-cation may be an important molecular mechanism underlying the increase in proliferation rate of some recurrent tumours.

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“…Their response to secondary hormonal therapy (such as maximal androgen blockade) may also be favourable. 22 …”

Section: Discussionmentioning

confidence: 99%

Aneuploidy and rapid cell proliferation in recurrent prostate cancers with androgen receptor gene amplification

Koivisto

1997

Prostate Cancer Prostatic Dis

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“…Although an increased DNA copy number of Xp was frequently detected in EULMSs and gastric cancers (El-Rifai et al, 1998;Otano-Joos et al, 1998;Sakakura et al, 1999), high-level amplification of Xp has not been reported in these tumors. The X chromosome amplicon was identified only in a recurrent prostate cancer (Palmberg et al, 1997); however, this amplicon is located in the nearby region Xp11-q13, where the androgen receptor is located. There are two putative oncogenes, ELK1 and ARAF1, located in the Xp11 region near the synovial sarcoma breakpoint.…”

Section: Gains Of Dna Copy Numbers and Novel Amplicons In Ulmsmentioning

confidence: 98%

Genomic alterations in uterine leiomyosarcomas: Potential markers for clinical diagnosis and prognosis

Khanna

Jones

et al. 2001

Genes Chromosomes & Cancer

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Genomic alterations were analyzed in 21 uterine leiomyosarcomas (ULMSs) by comparative genomic hybridization. DNA copy number changes were detected in all 21 tumors. The most frequent losses were 13q (16/21 = 76%), 10q (13/21 = 62%), 16q (8/21 = 38%), 12p (7/21 = 33%), and 2p (9/21 = 43%). The most common gains were 17p (8/21 = 38%), Xp (7/21 = 33%), and 1q (7/21 = 33%). High-copy-number gains (ratio > 1.5) were identified in Xp, 1q, and 17p. Loss of 13q was identified in both low-grade and high-grade tumors. Inactivation of a tumor suppressor gene in 13q may be an early event in the development of leiomyosarcomas. Loss of 10q, 2p, and 12p and gains of 1q as well as 17p were frequently found in high-grade tumors and recurrent tumors. Inactivation of tumor suppressor genes and activation of oncogenes in these regions may be associated with a more aggressive behavior of ULMS. Patients with only loss of 13q and without the other alterations listed above had longer survival times. Gains of Xp, 17p, and 1q and losses of 13q, 10q, 16q, 12p, and 2p have been reported in extra-uterine leiomyosarcomas. Our findings indicate that the pathogenesis of uterine leiomyosarcomas and extra-uterine leiomyosarcomas follows the same genetic pathways.

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“…The AR-mediated growth despite low androgen levels could also be achieved via an increased expression of AR itself, mostly by AR gene amplification, leading to an enhanced ligand occupied AR. Support for this hypothesis comes from the observation that about a third of tumors that become hormone refractory after ablation therapy have an amplified AR gene, compared with none in the primary tumors from the same patients (17)(18)(19)(20)(21).…”

Section: Ar and Prostate Cancermentioning

confidence: 99%

Androgen Receptor Coregulators in Prostate Cancer

Rahman

Miyamoto

Chang

2004

Clinical Cancer Research

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Androgen Receptor Gene Amplification in a Recurrent Prostate Cancer after Monotherapy with the Nonsteroidal Potent Antiandrogen Casodex (Bicalutamide) with a Subsequent Favorable Response to Maximal Androgen Blockade

Cited by 66 publications

References 11 publications

Aneuploidy and rapid cell proliferation in recurrent prostate cancers with androgen receptor gene amplification

Aneuploidy and rapid cell proliferation in recurrent prostate cancers with androgen receptor gene amplification

Genomic alterations in uterine leiomyosarcomas: Potential markers for clinical diagnosis and prognosis

Androgen Receptor Coregulators in Prostate Cancer

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