Endometrial CancerFESPETNCT03489473
FESPET Study: Female EStrogen recePtor in Endometrial Cancer Treatment
An observational study of Endometrial Cancer, run by Radboud University Medical Center.
Trial summary
Endometrial cancer is the most common gynecological malignancy in the western world and its incidence is expected to increase in the coming years due to obesity. Major treatment modalities include surgery, radiotherapy and chemotherapy. Read more about this study
- Who is it for?
- Ages 40 years and older, women only
- Conditions the study is for
- Endometrial Cancer
- What is being tested?
- 18F-FES PET CT scan
- How many people
- 40 participants
- Where
- No sites listed yet
- Study dates
- 1 Jan 2020to 1 Dec 2021
- Phase
- Observational
- Are there results?
- None posted in the registry
Key requirements
Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.
- Ages 40 years and older
- Women only
- No healthy volunteers
- Adult, Older adult
Study population: Patient with either * Primary endometrial cancer and planned hormonal treatment * Recurrent endometrial cancer and planned hormonal treatment
Who may be able to join
- Primary or metastatic endometrial cancer in which hormonal treatment is the planned treatment
- Postmenopausal status
- All histologic types of endometrial cancer (e.g. endometrioid, clear cell, serous subtype)
- Availability of recent (micro)curettage or biopsy
Who cannot join
- Intercurrent treatment between biopsy taking and start of hormonal treatment
- Sarcoma of the uterus
- Contra-indications to perform a PET-CT scan or a CT scan with intravenous contrast
- Use of hormonal therapy in the three months preceding performance of FES PET
Trial locations and contacts
No sites are listed yet.
About this study
Endometrial cancer is the most common gynecological malignancy in the western world and its incidence is expected to increase in the coming years due to obesity. Major treatment modalities include surgery, radiotherapy and chemotherapy. Hormonal therapy can be considered in primary treatment if other treatment modalities are not feasible and in treatment for recurrent disease. Hormonal treatment has shown to be more effective in endometrial cancers expressing estrogen (ER) and progesterone receptor (PR). Tumor heterogeneity frequently causes loss of expression of ER and PR in metastasis compared to primary tumors. The FES PET CT scan combines PET-CT scan with an estrogen tracer, thus allowing non invasive visualisation of estrogen receptor, even in patients with metastasis that are difficult to reach for biopsy. FES PET has been shown to relate well to ER expression and to treatment response in breast cancer. This study explores the feasibility of the FES PET scan in endometrial cancer patients.
Read the detailed description
Endometrial carcinoma is the most common gynecological malignancy in the western world, and with a current incidence of 18/100.000 women per year in the European Union, it affects around 65,000 new women each year. Due to the increased life expectancy and obesity, the incidence of endometrial cancer has increased in the last years, and is expected to rise in the coming years. Most patients present with early stage disease and have a favorable outcome. However, patients with metastatic disease have few treatment options with a poor prognosis.
Surgery is the primary treatment modality in endometrial cancer and defines the final surgicopathological stage according to the International Federation of Gynecology and Obstetrics (FIGO) staging system. Adjuvant treatment is based on final tumor grade and FIGO stage and consists of radiotherapy and-or chemotherapy. Hormonal therapy is considered as alternative treatment modality for: 1. patients who are not suitable for surgery, 2. patients who wish to maintain fertility, and 3. patients with metastatic disease. A recent review summarizes the available evidence on the effect of hormonal therapy in patients with advanced and recurrent endometrial cancer. The overall response rate based on a single biopsy taken prior to treatment, was 22%. In ER positive tumors, the response rate was 27% compared to 9% in ER negative tumors. In PR positive tumors 36% of patients responded, compared to 12% in PR negative tumors. Thus, the presence of ER and PR receptors on the tumor cell seems to be relevant for prediction of response to hormonal treatment. Yet, data concerning the percentage of ER and PR expression are lacking, and might underestimate the response to hormonal treatment in individual cases.
Analysis of the genomic landscape of endometrial cancer has shown marked genetic heterogeneity between biopsies of primary tumors and their corresponding metastases, suggesting that only a part of tumor cells in the primary tumor is involved in metastases. Also, loss of ER and PR expression is frequently observed in metastases from ER/PR positive primary tumors. These findings underline the relevance of obtaining a new biopsy to determine ER and PR expression in recurrent disease. This can be challenging since recurrences can be hard to reach by biopsies due to its location and multiplicity.
18F-FES PET CT (FES PET) is a novel imaging method based on positron emission tomography using a specific tracer targeting ER allowing the visualization of ER expression in tissue. FES PET allows non-invasive depiction and quantification of ER expression in all tumor lesions in a patient.
FES PET has been evaluated in breast cancer with a reported sensitivity of 69% to 100%, and a specificity of 80-100% for identifying ER positive tumor when compared to immunohistochemical expression of ER. In endometrial cancer, FES PET has been evaluated in only two studies. The first study included 19 patients with endometrial cancer with different FIGO stages that underwent FES PET prior to surgical resection. In this study a significant correlation between ER uptake on FES PET and ER immunohistochemical expression was observed. In the second study 22 patients were analyzed and classified into high risk (FIGO stage ≥Ic or grade ≥2) and low risk (FIGO stage ≤1b and grade 1) endometrioid type endometrial carcinoma. In the high risk group a significantly lower FES uptake was observed when compared to the low risk group, suggesting that FES PET could assist in identifying patients with high risk endometrial cancer. As shown by van Kruchten et al., FES PET could also be of value in the evaluation of response to hormonal therapy. In this study the results of serial FES PET scans are described in 16 patients with metastatic breast cancer treated with fulvestrant, a selective estrogen downregulator. Response to hormonal therapy was associated with reduced uptake on subsequent FES PET scans. So far, FES PET data are limited in endometrial cancer to one case report in which a decrease of estrogen uptake was observed upon medroxyprogesterone therapy in early stage endometrial cancer consistent with histological and clinical follow-up. Based on previous findings the aim of the current study is to explore the feasibility of FES PET scan in patients with endometrial cancer.
- Conditions
- Endometrial Cancer
- Being tested
- 18F-FES PET CT scan
- Keywords
- Hormonal therapy, FES PET scan, Estrogen receptor
- Medical subject headings
- Endometrial Neoplasms
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
18F-FES PET CT scanDiagnostic test
PET CT scan with estrogen tracer
What is being measured
The primary outcome is the main question the study is designed to answer.
estrogen uptake on FES PET scan
Standard uptake volume of FES
Measured: Within 1 month of inclusion
Secondary outcomes (1)
Estrogen and Progesterone Receptor expression
Percentage of tumor cells expressing estrogen and progesterone receptor through immunohistochemical analysis of tissue biopsy material
Measured: Within 1 month of inclusion
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted5 Apr 2018
- Study start1 Jan 2020 (estimated)
- Primary completion1 Dec 2021 (estimated)
- Study completion1 Dec 2021 (estimated)
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (14)Papers the sponsor has linked to this study.
- Other trials for Endometrial CancerStudies of the same condition, open and under way.
- More trials run by Radboud University Medical CenterThe sponsor's other registered studies.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Observational
- Observational model
- Case only
- Time perspective
- Prospective
- Enrolment
- 40 participants (estimated)
Sponsor and investigators
- Lead sponsor
- Radboud University Medical Center
- Sponsor type
- University, hospital or other
- Collaborators
- Academisch Medisch Centrum - Universiteit van Amsterdam (AMC-UvA), University Medical Center Groningen, Haukeland University Hospital
- Responsible party
- Sponsor
- Investigators
- JMA Pijnenborg, MD, PhD, Principal investigator, Radboud University Medical Center
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT03489473
- Sponsor's protocol ID
- FESPET
- Acronym
- FESPET
- Status last verified
- Mar 2019
- First submitted
- 12 Mar 2018
- Last updated
- 18 Apr 2019
- Results posted
- No
- Data monitoring committee
- Yes
- FDA-regulated drug
- No
- FDA-regulated device
- No
- Individual data sharing
- No: There is no plan to make individual participant data available to other researchers. This will be decided when a request for sharing of IPD is made
Publications
Basen-Engquist K, Chang M. Obesity and cancer risk: recent review and evidence. Curr Oncol Rep. 2011 Feb;13(1):71-6. doi: 10.1007/s11912-010-0139-7.
PubMed 21080117Carlson MJ, Thiel KW, Leslie KK. Past, present, and future of hormonal therapy in recurrent endometrial cancer. Int J Womens Health. 2014 May 2;6:429-35. doi: 10.2147/IJWH.S40942. eCollection 2014.
PubMed 24833920Amant F, Mirza MR, Koskas M, Creutzberg CL. Cancer of the corpus uteri. Int J Gynaecol Obstet. 2015 Oct;131 Suppl 2:S96-104. doi: 10.1016/j.ijgo.2015.06.005. No abstract available.
PubMed 26433681Ethier JL, Desautels DN, Amir E, MacKay H. Is hormonal therapy effective in advanced endometrial cancer? A systematic review and meta-analysis. Gynecol Oncol. 2017 Oct;147(1):158-166. doi: 10.1016/j.ygyno.2017.07.002. Epub 2017 Jul 6.
PubMed 28689667Gibson WJ, Hoivik EA, Halle MK, Taylor-Weiner A, Cherniack AD, Berg A, Holst F, Zack TI, Werner HM, Staby KM, Rosenberg M, Stefansson IM, Kusonmano K, Chevalier A, Mauland KK, Trovik J, Krakstad C, Giannakis M, Hodis E, Woie K, Bjorge L, Vintermyr OK, Wala JA, Lawrence MS, Getz G, Carter SL, Beroukhim R, Salvesen HB. The genomic landscape and evolution of endometrial carcinoma progression and abdominopelvic metastasis. Nat Genet. 2016 Aug;48(8):848-55. doi: 10.1038/ng.3602. Epub 2016 Jun 27.
PubMed 27348297Geels YP, van der Putten LJM, van Tilborg AAG, Nienhaus BEC, van den Berg-van Erp SH, Snijders MPLM, van der Wurff A, Massuger LFAG, Bulten J, Pijnenborg JMA. Immunohistochemical Profiles of Endometrioid Endometrial Carcinomas With and Without Metastatic Disease. Appl Immunohistochem Mol Morphol. 2018 Mar;26(3):173-179. doi: 10.1097/PAI.0000000000000402.
PubMed 27299188Vandenput I, Trovik J, Leunen K, Wik E, Stefansson I, Akslen L, Moerman P, Vergote I, Salvesen H, Amant F. Evolution in endometrial cancer: evidence from an immunohistochemical study. Int J Gynecol Cancer. 2011 Feb;21(2):316-22. doi: 10.1097/IGC.0b013e31820575f5.
PubMed 21734474Tsujikawa T, Yoshida Y, Kiyono Y, Kurokawa T, Kudo T, Fujibayashi Y, Kotsuji F, Okazawa H. Functional oestrogen receptor alpha imaging in endometrial carcinoma using 16alpha-[(1)(8)F]fluoro-17beta-oestradiol PET. Eur J Nucl Med Mol Imaging. 2011 Jan;38(1):37-45. doi: 10.1007/s00259-010-1589-8. Epub 2010 Aug 18.
PubMed 20717823Tsujikawa T, Yoshida Y, Kudo T, Kiyono Y, Kurokawa T, Kobayashi M, Tsuchida T, Fujibayashi Y, Kotsuji F, Okazawa H. Functional images reflect aggressiveness of endometrial carcinoma: estrogen receptor expression combined with 18F-FDG PET. J Nucl Med. 2009 Oct;50(10):1598-604. doi: 10.2967/jnumed.108.060145. Epub 2009 Sep 16.
PubMed 19759112van Kruchten M, de Vries EG, Glaudemans AW, van Lanschot MC, van Faassen M, Kema IP, Brown M, Schroder CP, de Vries EF, Hospers GA. Measuring residual estrogen receptor availability during fulvestrant therapy in patients with metastatic breast cancer. Cancer Discov. 2015 Jan;5(1):72-81. doi: 10.1158/2159-8290.CD-14-0697. Epub 2014 Nov 7.
PubMed 25380844Yoshida Y, Kurokawa T, Sawamura Y, Shinagawa A, Okazawa H, Fujibayashi Y, Kotsuji F. The positron emission tomography with F18 17beta-estradiol has the potential to benefit diagnosis and treatment of endometrial cancer. Gynecol Oncol. 2007 Mar;104(3):764-6. doi: 10.1016/j.ygyno.2006.10.024. Epub 2006 Dec 6.
PubMed 17156828Trovik J, Wik E, Werner HM, Krakstad C, Helland H, Vandenput I, Njolstad TS, Stefansson IM, Marcickiewicz J, Tingulstad S, Staff AC; MoMaTEC study group; Amant F, Akslen LA, Salvesen HB. Hormone receptor loss in endometrial carcinoma curettage predicts lymph node metastasis and poor outcome in prospective multicentre trial. Eur J Cancer. 2013 Nov;49(16):3431-41. doi: 10.1016/j.ejca.2013.06.016. Epub 2013 Aug 8.
PubMed 23932335Tangen IL, Werner HM, Berg A, Halle MK, Kusonmano K, Trovik J, Hoivik EA, Mills GB, Krakstad C, Salvesen HB. Loss of progesterone receptor links to high proliferation and increases from primary to metastatic endometrial cancer lesions. Eur J Cancer. 2014 Nov;50(17):3003-10. doi: 10.1016/j.ejca.2014.09.003. Epub 2014 Sep 30.
PubMed 25281525Eisenhauer EA, Therasse P, Bogaerts J, Schwartz LH, Sargent D, Ford R, Dancey J, Arbuck S, Gwyther S, Mooney M, Rubinstein L, Shankar L, Dodd L, Kaplan R, Lacombe D, Verweij J. New response evaluation criteria in solid tumours: revised RECIST guideline (version 1.1). Eur J Cancer. 2009 Jan;45(2):228-47. doi: 10.1016/j.ejca.2008.10.026.
PubMed 19097774
Study at a glance
From the registry record, last updated by the sponsor on 18 Apr 2019. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- FESPET Study: Female EStrogen recePtor in Endometrial Cancer Treatment
- ClinicalTrials.gov ID
- NCT03489473
- Acronym / sponsor ID
- FESPET / FESPET
- Conditions
- Endometrial Cancer
- Keywords
- Hormonal therapy, FES PET scan, Estrogen receptor
- Study type
- Observational
- Recruitment status
- Unknown status
- Enrolment
- 40 participants (estimated)
- Lead sponsor
- Radboud University Medical CenterUniversity, hospital or other
- Collaborators
- Academisch Medisch Centrum - Universiteit van Amsterdam (AMC-UvA), University Medical Center Groningen, Haukeland University Hospital
- Study start
- 1 Jan 2020 (estimated)
- Primary completion
- 1 Dec 2021 (estimated)
- Study completion
- 1 Dec 2021 (estimated)
- First posted
- 5 Apr 2018 (actual)
- Results
- Not posted in the source record
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
Endometrial cancer is the most common gynecological malignancy in the western world and its incidence is expected to increase in the coming years due to obesity. Major treatment modalities include surgery, radiotherapy and chemotherapy. Hormonal therapy can be considered in primary treatment if other treatment modalities are not feasible and in treatment for recurrent disease. Hormonal treatment has shown to be more effective in endometrial cancers expressing estrogen (ER) and progesterone receptor (PR). Tumor heterogeneity frequently causes loss of expression of ER and PR in metastasis compared to primary tumors. The FES PET CT scan combines PET-CT scan with an estrogen tracer, thus allowing non invasive visualisation of estrogen receptor, even in patients with metastasis that are difficult to reach for biopsy. FES PET has been shown to relate well to ER expression and to treatment response in breast cancer. This study explores the feasibility of the FES PET scan in endometrial cancer patients.
Detailed description
Endometrial carcinoma is the most common gynecological malignancy in the western world, and with a current incidence of 18/100.000 women per year in the European Union, it affects around 65,000 new women each year. Due to the increased life expectancy and obesity, the incidence of endometrial cancer has increased in the last years, and is expected to rise in the coming years. Most patients present with early stage disease and have a favorable outcome. However, patients with metastatic disease have few treatment options with a poor prognosis.
Surgery is the primary treatment modality in endometrial cancer and defines the final surgicopathological stage according to the International Federation of Gynecology and Obstetrics (FIGO) staging system. Adjuvant treatment is based on final tumor grade and FIGO stage and consists of radiotherapy and-or chemotherapy. Hormonal therapy is considered as alternative treatment modality for: 1. patients who are not suitable for surgery, 2. patients who wish to maintain fertility, and 3. patients with metastatic disease. A recent review summarizes the available evidence on the effect of hormonal therapy in patients with advanced and recurrent endometrial cancer. The overall response rate based on a single biopsy taken prior to treatment, was 22%. In ER positive tumors, the response rate was 27% compared to 9% in ER negative tumors. In PR positive tumors 36% of patients responded, compared to 12% in PR negative tumors. Thus, the presence of ER and PR receptors on the tumor cell seems to be relevant for prediction of response to hormonal treatment. Yet, data concerning the percentage of ER and PR expression are lacking, and might underestimate the response to hormonal treatment in individual cases.
Analysis of the genomic landscape of endometrial cancer has shown marked genetic heterogeneity between biopsies of primary tumors and their corresponding metastases, suggesting that only a part of tumor cells in the primary tumor is involved in metastases. Also, loss of ER and PR expression is frequently observed in metastases from ER/PR positive primary tumors. These findings underline the relevance of obtaining a new biopsy to determine ER and PR expression in recurrent disease. This can be challenging since recurrences can be hard to reach by biopsies due to its location and multiplicity.
18F-FES PET CT (FES PET) is a novel imaging method based on positron emission tomography using a specific tracer targeting ER allowing the visualization of ER expression in tissue. FES PET allows non-invasive depiction and quantification of ER expression in all tumor lesions in a patient.
FES PET has been evaluated in breast cancer with a reported sensitivity of 69% to 100%, and a specificity of 80-100% for identifying ER positive tumor when compared to immunohistochemical expression of ER. In endometrial cancer, FES PET has been evaluated in only two studies. The first study included 19 patients with endometrial cancer with different FIGO stages that underwent FES PET prior to surgical resection. In this study a significant correlation between ER uptake on FES PET and ER immunohistochemical expression was observed. In the second study 22 patients were analyzed and classified into high risk (FIGO stage ≥Ic or grade ≥2) and low risk (FIGO stage ≤1b and grade 1) endometrioid type endometrial carcinoma. In the high risk group a significantly lower FES uptake was observed when compared to the low risk group, suggesting that FES PET could assist in identifying patients with high risk endometrial cancer. As shown by van Kruchten et al., FES PET could also be of value in the evaluation of response to hormonal therapy. In this study the results of serial FES PET scans are described in 16 patients with metastatic breast cancer treated with fulvestrant, a selective estrogen downregulator. Response to hormonal therapy was associated with reduced uptake on subsequent FES PET scans. So far, FES PET data are limited in endometrial cancer to one case report in which a decrease of estrogen uptake was observed upon medroxyprogesterone therapy in early stage endometrial cancer consistent with histological and clinical follow-up. Based on previous findings the aim of the current study is to explore the feasibility of FES PET scan in patients with endometrial cancer.
Study design
- Observational model
- Case only
- Time perspective
- Prospective
Who may qualify
- Ages
- 40 years and older
- Sex
- Female only
- Healthy volunteers
- Not accepted
- Age groups
- Adult, Older adult
- Study population
- Patient with either * Primary endometrial cancer and planned hormonal treatment * Recurrent endometrial cancer and planned hormonal treatment
Key inclusion criteria (4 listed)
- Primary or metastatic endometrial cancer in which hormonal treatment is the planned treatment
- Postmenopausal status
- All histologic types of endometrial cancer (e.g. endometrioid, clear cell, serous subtype)
- Availability of recent (micro)curettage or biopsy
Key exclusion criteria (4 listed)
- Intercurrent treatment between biopsy taking and start of hormonal treatment
- Sarcoma of the uterus
- Contra-indications to perform a PET-CT scan or a CT scan with intravenous contrast
- Use of hormonal therapy in the three months preceding performance of FES PET
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Interventions
| Intervention | Type | Arms |
|---|---|---|
| 18F-FES PET CT scanPET CT scan with estrogen tracer | Diagnostic test | – |
Primary outcome
estrogen uptake on FES PET scan
Time frame: Within 1 month of inclusion
Standard uptake volume of FES
1 secondary outcome
Estrogen and Progesterone Receptor expression
Time frame: Within 1 month of inclusion
Results and safety
Results are not available in the source record.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 18 Apr 2019.
- Background: PubMed 21080117Basen-Engquist K, Chang M. Obesity and cancer risk: recent review and evidence. Curr Oncol Rep. 2011 Feb;13(1):71-6. doi: 10.1007/s11912-010-0139-7.
- Background: PubMed 24833920Carlson MJ, Thiel KW, Leslie KK. Past, present, and future of hormonal therapy in recurrent endometrial cancer. Int J Womens Health. 2014 May 2;6:429-35. doi: 10.2147/IJWH.S40942. eCollection 2014.
- Background: PubMed 26433681Amant F, Mirza MR, Koskas M, Creutzberg CL. Cancer of the corpus uteri. Int J Gynaecol Obstet. 2015 Oct;131 Suppl 2:S96-104. doi: 10.1016/j.ijgo.2015.06.005. No abstract available.
- Background: PubMed 28689667Ethier JL, Desautels DN, Amir E, MacKay H. Is hormonal therapy effective in advanced endometrial cancer? A systematic review and meta-analysis. Gynecol Oncol. 2017 Oct;147(1):158-166. doi: 10.1016/j.ygyno.2017.07.002. Epub 2017 Jul 6.
- Background: PubMed 27348297Gibson WJ, Hoivik EA, Halle MK, Taylor-Weiner A, Cherniack AD, Berg A, Holst F, Zack TI, Werner HM, Staby KM, Rosenberg M, Stefansson IM, Kusonmano K, Chevalier A, Mauland KK, Trovik J, Krakstad C, Giannakis M, Hodis E, Woie K, Bjorge L, Vintermyr OK, Wala JA, Lawrence MS, Getz G, Carter SL, Beroukhim R, Salvesen HB. The genomic landscape and evolution of endometrial carcinoma progression and abdominopelvic metastasis. Nat Genet. 2016 Aug;48(8):848-55. doi: 10.1038/ng.3602. Epub 2016 Jun 27.
- Background: PubMed 27299188Geels YP, van der Putten LJM, van Tilborg AAG, Nienhaus BEC, van den Berg-van Erp SH, Snijders MPLM, van der Wurff A, Massuger LFAG, Bulten J, Pijnenborg JMA. Immunohistochemical Profiles of Endometrioid Endometrial Carcinomas With and Without Metastatic Disease. Appl Immunohistochem Mol Morphol. 2018 Mar;26(3):173-179. doi: 10.1097/PAI.0000000000000402.
- Background: PubMed 21734474Vandenput I, Trovik J, Leunen K, Wik E, Stefansson I, Akslen L, Moerman P, Vergote I, Salvesen H, Amant F. Evolution in endometrial cancer: evidence from an immunohistochemical study. Int J Gynecol Cancer. 2011 Feb;21(2):316-22. doi: 10.1097/IGC.0b013e31820575f5.
- Background: PubMed 20717823Tsujikawa T, Yoshida Y, Kiyono Y, Kurokawa T, Kudo T, Fujibayashi Y, Kotsuji F, Okazawa H. Functional oestrogen receptor alpha imaging in endometrial carcinoma using 16alpha-[(1)(8)F]fluoro-17beta-oestradiol PET. Eur J Nucl Med Mol Imaging. 2011 Jan;38(1):37-45. doi: 10.1007/s00259-010-1589-8. Epub 2010 Aug 18.
- Background: PubMed 19759112Tsujikawa T, Yoshida Y, Kudo T, Kiyono Y, Kurokawa T, Kobayashi M, Tsuchida T, Fujibayashi Y, Kotsuji F, Okazawa H. Functional images reflect aggressiveness of endometrial carcinoma: estrogen receptor expression combined with 18F-FDG PET. J Nucl Med. 2009 Oct;50(10):1598-604. doi: 10.2967/jnumed.108.060145. Epub 2009 Sep 16.
- Background: PubMed 25380844van Kruchten M, de Vries EG, Glaudemans AW, van Lanschot MC, van Faassen M, Kema IP, Brown M, Schroder CP, de Vries EF, Hospers GA. Measuring residual estrogen receptor availability during fulvestrant therapy in patients with metastatic breast cancer. Cancer Discov. 2015 Jan;5(1):72-81. doi: 10.1158/2159-8290.CD-14-0697. Epub 2014 Nov 7.
- Background: PubMed 17156828Yoshida Y, Kurokawa T, Sawamura Y, Shinagawa A, Okazawa H, Fujibayashi Y, Kotsuji F. The positron emission tomography with F18 17beta-estradiol has the potential to benefit diagnosis and treatment of endometrial cancer. Gynecol Oncol. 2007 Mar;104(3):764-6. doi: 10.1016/j.ygyno.2006.10.024. Epub 2006 Dec 6.
- Background: PubMed 23932335Trovik J, Wik E, Werner HM, Krakstad C, Helland H, Vandenput I, Njolstad TS, Stefansson IM, Marcickiewicz J, Tingulstad S, Staff AC; MoMaTEC study group; Amant F, Akslen LA, Salvesen HB. Hormone receptor loss in endometrial carcinoma curettage predicts lymph node metastasis and poor outcome in prospective multicentre trial. Eur J Cancer. 2013 Nov;49(16):3431-41. doi: 10.1016/j.ejca.2013.06.016. Epub 2013 Aug 8.
- Individual participant dataSharing planned: No. There is no plan to make individual participant data available to other researchers. This will be decided when a request for sharing of IPD is made
Related trials for Endometrial Cancer
Recruiting
Methylation Profiling in Self-Samples for Identification of (Epi)Genetic Biomarkers for Gynecological Cancers
Gynaecological Cancers, Ovarian Cancer
Active, not recruitingPhase 3
Endometrial Cancer Patientes MMR Deficient Comparing Chemotherapy vs Dostarlimab in First Line
Endometrial Cancer
RecruitingPhase 3
Testing the Addition of an Antiangiogenic Drug (Bevacizumab) to Chemotherapy (Carboplatin and Paclitaxel) Combined With Immunotherapy (Pembrolizumab) for pMMR, TP53 Mutated Endometrial Cancer
Advanced Endometrial Carcinoma, Recurrent Endometrial Carcinoma
RecruitingPhase 2
At-Home Cancer Directed Therapy Versus in Clinic for the Treatment of Patients With Advanced Cancer
Advanced Anal Carcinoma, Advanced Biliary Tract Carcinoma
RecruitingPhase 3
Impact of Sentinel Lymph Node Mapping on Patient Reported Lower Extremity Limb Dysfunction in Stage I Endometrial Cancer
Stage I Uterine Corpus Carcinoma or Carcinosarcoma AJCC v8
Referral and contact
AzTrials does not enrol participants or take referrals. Contact the study team or a site listed below; they decide who can take part. This study is not recruiting at the moment.
JMA Pijnenborg, MD, PhD principal investigator
Radboud University Medical Center
Questions about this trial
What is this clinical trial studying?
An observational study of Endometrial Cancer, run by Radboud University Medical Center.
The full registered description is in the About this study section and the official record.
Who may be eligible to take part?
The sponsor lists 4 inclusion and 4 exclusion criteria. Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: status not confirmed, as of the sponsor's last update on 18 Apr 2019. Status can change between updates, so confirm with the study contact before making plans.
What are the possible benefits and risks?
They depend on the study and the treatment, and no study can promise a benefit. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
Are results available for this study?
Results are not available in the source record.
How can a doctor refer a patient or contact the research team?
Contact Willem Jan van Weelden, MD (0031643274577, willemjan.vanweelden@radboudumc.nl), or a site near the patient. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
estrogen uptake on FES PET scan (time frame: Within 1 month of inclusion). It is what the study was designed to measure, not a finding.
Where can I read the original study information?
On the ClinicalTrials.gov record for NCT03489473, which also lists 14 linked publications.
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 18 Apr 2019.