Ignite Creation Date:
2024-05-05 @ 7:15 PM
Last Modification Date:
2024-10-26 @ 9:46 AM
Study NCT ID:
NCT00634647
Status:
COMPLETED
Last Update Posted:
2018-10-02
First Post:
2008-03-12
Brief Title:
Satraplatin and Prednisone to Treat Prostate Cancer
Sponsor:
National Cancer Institute NCI
Organization:
National Institutes of Health Clinical Center CC
Study Overview
Official Title:
A Phase II Study of Satraplatin and Prednisone in Metastatic Androgen Independent Prostate Cancer AIPC
Status:
COMPLETED
Status Verified Date:
2018-08
Last Known Status:
None
Delayed Posting:
No
If Stopped, Why?:
Not Stopped
Has Expanded Access:
False
If Expanded Access, NCT#:
N/A
Has Expanded Access, NCT# Status:
N/A
Acronym:
None
Brief Summary:
Background
Satraplatin is an experimental drug that may be of benefit to patients with prostate cancer
Prednisone is approved for treating prostate cancer
The gene excision repair cross-complementing rodent repair deficiency complementation group 1 ERCC1 helps repair cell damage caused by satraplatin It is possible that patients who have a variant of this gene will not benefit from treatment with satraplatin because the drug will not be able to damage the cancer cells effectively
Objectives
To determine if satraplatin may help treat prostate cancer in patients with certain variants of the ERCC1 gene
Eligibility
Patients with advanced androgen-independent prostate cancer whose disease has not responded to hormonal therapy or at least one type of chemotherapy and whose x-rays scans or other tests have shown their cancer to be spreading
Design
Participants have a blood test to determine if they have a variant of the ERCC1 gene
Participants take satraplatin by mouth every day for 5 consecutive days out of every 35 days and prednisone by mouth every day These 35-day treatment cycles may continue for 6 months or longer depending on the benefits and side effects of the treatment
During the treatment period patients undergo the following tests and procedures
Blood tests on days 1 of the treatment cycle
Weekly blood draws for the first 3 treatment cycles
Imaging studies eg bone scans computed tomography CT scans every two cycles to determine the response to treatment
Surgical or medical suppression of testosterone in patients whose cancer cells continue to grow due to exposure to the hormone
Satraplatin is an experimental drug that may be of benefit to patients with prostate cancer
Prednisone is approved for treating prostate cancer
The gene excision repair cross-complementing rodent repair deficiency complementation group 1 ERCC1 helps repair cell damage caused by satraplatin It is possible that patients who have a variant of this gene will not benefit from treatment with satraplatin because the drug will not be able to damage the cancer cells effectively
Objectives
To determine if satraplatin may help treat prostate cancer in patients with certain variants of the ERCC1 gene
Eligibility
Patients with advanced androgen-independent prostate cancer whose disease has not responded to hormonal therapy or at least one type of chemotherapy and whose x-rays scans or other tests have shown their cancer to be spreading
Design
Participants have a blood test to determine if they have a variant of the ERCC1 gene
Participants take satraplatin by mouth every day for 5 consecutive days out of every 35 days and prednisone by mouth every day These 35-day treatment cycles may continue for 6 months or longer depending on the benefits and side effects of the treatment
During the treatment period patients undergo the following tests and procedures
Blood tests on days 1 of the treatment cycle
Weekly blood draws for the first 3 treatment cycles
Imaging studies eg bone scans computed tomography CT scans every two cycles to determine the response to treatment
Surgical or medical suppression of testosterone in patients whose cancer cells continue to grow due to exposure to the hormone
Detailed Description:
Background
Satraplatin is an oral third-generation platinum analog that has recently been shown to increase prostatic specific antigen PSA decline rates and progression-free survival in hormone-resistant prostate cancer
Satraplatin acts by binding to deoxyribonucleic acid DNA forming intra- and interstrand cross links DNA adducts resulting in cell-cycle arrest in G2 phase and eventual apoptosis One of the mechanisms that bring about resistance to platinum-based chemotherapy is removal of the platinum-DNA adducts by DNA repair pathways called nucleotide excision repair NER and base excision repair BER pathways
Polymorphisms in the DNA repair genes causing impaired NER and BER capability has recently been shown in some cancers including head and neck squamous cell carcinoma non-small cell lung carcinoma and ovarian carcinoma to predict better treatment outcome and response to platinum treatment
Objectives
Primary objective of this single arm study is to determine if the presence of ERCC1 variant gene polymorphism which is involved with DNA damage repair may be associated with an impact on the progression-free survival of patients with metastatic prostate cancer
Secondary objectives of this study includes demonstration of biologic effect by the drug satraplatin in the patient and in the tumor whenever possible by obtaining tissue biopsy and white blood cell collections to determine correlation of biologic or clinical effects with PSA progression evaluate correlations between genotype expression repair pathways and clinical events and obtain laboratory correlates which will include pharmacogenetic analysis of prostate cancer patients with genotyping using Polymerase chain reaction PCR followed by either restriction fragment length polymorphism or direct sequencing to genotype single nucleotide polymorphisms of ERCC1 x-ray repair cross-complementing protein 1 XRCC1 and poly ADP-ribose polymerase 1 PARP1
Eligibility
Patients with metastatic androgen-independent prostate cancer
Had docetaxel-based chemotherapy but no more than 1 previous cytotoxic chemotherapy line
Good organ function
Design
Phase II trial with single stage design and a planned accrual of 66 patients
Progression-free survival will be determined using a Fishers exact test
Will treat all enrolled patients with oral satraplatin 80 mgm2 dose on days 1-5 of every 35-days cycle plus Prednisone 5 mg twice daily every 35 days
Genotyping will be performed after the first 20 patients to determine if the proportion for wild-type ERCC1 and variants follow a 2080 split
Satraplatin is an oral third-generation platinum analog that has recently been shown to increase prostatic specific antigen PSA decline rates and progression-free survival in hormone-resistant prostate cancer
Satraplatin acts by binding to deoxyribonucleic acid DNA forming intra- and interstrand cross links DNA adducts resulting in cell-cycle arrest in G2 phase and eventual apoptosis One of the mechanisms that bring about resistance to platinum-based chemotherapy is removal of the platinum-DNA adducts by DNA repair pathways called nucleotide excision repair NER and base excision repair BER pathways
Polymorphisms in the DNA repair genes causing impaired NER and BER capability has recently been shown in some cancers including head and neck squamous cell carcinoma non-small cell lung carcinoma and ovarian carcinoma to predict better treatment outcome and response to platinum treatment
Objectives
Primary objective of this single arm study is to determine if the presence of ERCC1 variant gene polymorphism which is involved with DNA damage repair may be associated with an impact on the progression-free survival of patients with metastatic prostate cancer
Secondary objectives of this study includes demonstration of biologic effect by the drug satraplatin in the patient and in the tumor whenever possible by obtaining tissue biopsy and white blood cell collections to determine correlation of biologic or clinical effects with PSA progression evaluate correlations between genotype expression repair pathways and clinical events and obtain laboratory correlates which will include pharmacogenetic analysis of prostate cancer patients with genotyping using Polymerase chain reaction PCR followed by either restriction fragment length polymorphism or direct sequencing to genotype single nucleotide polymorphisms of ERCC1 x-ray repair cross-complementing protein 1 XRCC1 and poly ADP-ribose polymerase 1 PARP1
Eligibility
Patients with metastatic androgen-independent prostate cancer
Had docetaxel-based chemotherapy but no more than 1 previous cytotoxic chemotherapy line
Good organ function
Design
Phase II trial with single stage design and a planned accrual of 66 patients
Progression-free survival will be determined using a Fishers exact test
Will treat all enrolled patients with oral satraplatin 80 mgm2 dose on days 1-5 of every 35-days cycle plus Prednisone 5 mg twice daily every 35 days
Genotyping will be performed after the first 20 patients to determine if the proportion for wild-type ERCC1 and variants follow a 2080 split
Study Oversight
Has Oversight DMC:
None
Is a FDA Regulated Drug?:
True
Is a FDA Regulated Device?:
False
Is an Unapproved Device?:
None
Is a PPSD?:
None
Is a US Export?:
None
Is an FDA AA801 Violation?:
None
Secondary IDs
| Secondary ID | Type | Domain | Link |
|---|---|---|---|
| 08-C-0074 | None | None | None |