To discriminate the acquired anti-hormonal resistance phenotypes in patients based on ER expression levels by FES-PET in order to select patients eligible for estrogen therapy.
ID
Source
Brief title
Condition
- Breast neoplasms malignant and unspecified (incl nipple)
Synonym
Research involving
Sponsors and support
Intervention
Outcome measures
Primary outcome
Clinical/biochemical/radiological response on Estradiol versus ER expression
on FES-PET signal preferable with an ER expressions density measured on recent
taken tumor tissue
Secondary outcome
Physical burden of FES-PET
Background summary
Title: Imaging of ER density to guide and improve tailored therapy for acquired
anti-hormonal resistant breast cancer
Breast cancer is the most frequent tumor among women in the Netherlands. In
metastatic disease standard systemic treatment options are hormonal therapy and
chemotherapy. Hormonal treatment is effective for breast tumors with a hormone
receptor positive breast cancer. The interference in the estrogen signaling
pathway with tamoxifen, aromatase inhibitors or faslodex is an important
intervention modality with relatively mild side effects. However, eventually
this therapy becomes ineffective, as all patients will acquire hormonal
resistance. For metastatic estrogen receptor (ER) positive breast cancer,
interference in the estrogen signaling pathway with tamoxifen, aromatase
inhibitors or faslodex is an important intervention modality with relatively
mild side effects. However, eventually this therapy becomes ineffective, as
all patients will acquire resistance. Three types of resistance can be
identified in-vitro: resistance in which ER expression is negative (ER-; mainly
epigenetically silenced; 20% of patients), resistance in which ER expression is
preserved and tumors still require estrogen for their growth (ER+; 50% of
patients) and resistance , in which ER expression is increased and tumors are
hypersensitive to estrogens (ER++; 30% of patients). Early identification of
the resistance phenotypes (ER expression levels) could govern optimal treatment
decision-making, as most likely ER+ and ER++ phenotypes will benefit best form
additional anti-hormonal therapy and estrogen treatment, respectively, whereas
chemotherapy remains for ER-.
Study objective
To discriminate the acquired anti-hormonal resistance phenotypes in patients
based on ER expression levels by FES-PET in order to select patients eligible
for estrogen therapy.
Study design
Observational study
Study burden and risks
Extra stralingsbelasting van 4.4 mSv.
Hanzeplein 1
Groningen 9713 GZ
NL
Hanzeplein 1
Groningen 9713 GZ
NL
Listed location countries
Age
Inclusion criteria
1. Acquired antihormonal resistant advanced breast cancer showing progression after two or more lines of antihormonal treatment.
2. Treatment with estradiol.
3. Age >= 18 years
4. ECOG performance status 0-2
5. Signed written informed consent
6. Able to comply with the protocol
Exclusion criteria
1. Life-expectancy <= 3 months
2. Uncontrolled CNS metastases
3. Uncontrolled hypercalcemia
4. Treatment with any investigational drug within 30 days before start of study
5. Pregnant or lactating women. Documentation of a negative pregnancy test must be available for pre-menopausal women with intact reproductive organs and for women less than two years after menopause
6. Women of childbearing potential unless (1) surgically sterile or (2) using adequate measures of contraception
7. One of the relative contra-indications underneath, unless estradiol is the only available treatment option available:
a. Serious uncontrolled concurrent illness, e.g. autoimmune disorders
b. New York Heart Association (NYHA) class III/IV congestive heart failure
c. Dyspnea at rest due to any cause
d. Diabetes mellitus
e. History of thrombosis
Design
Recruitment
Followed up by the following (possibly more current) registration
No registrations found.
Other (possibly less up-to-date) registrations in this register
No registrations found.
In other registers
| Register | ID |
|---|---|
| EudraCT | EUCTR2008-002657-20-NL |
| CCMO | NL23268.042.08 |