<clinical_study>
  <!-- This xml conforms to an XML Schema at:
    https://clinicaltrials.gov/ct2/html/images/info/public.xsd -->
  <required_header>
    <download_date>ClinicalTrials.gov processed this data on September 20, 2023</download_date>
    <link_text>Link to the current ClinicalTrials.gov record.</link_text>
    <url>https://clinicaltrials.gov/ct2/show/NCT02188745</url>
  </required_header>
  <id_info>
    <org_study_id>D14122</org_study_id>
    <nct_id>NCT02188745</nct_id>
  </id_info>
  <brief_title>ER Reactivation Therapy for Breast Cancer</brief_title>
  <acronym>POLLY</acronym>
  <official_title>Phase II Pre-emptive OsciLLation of ER activitY Levels Through Alternation of Estradiol/Anti-estrogen Therapies Prior to Disease Progression in ER+/HER2- Metastatic or Advanced Breast Cancer</official_title>
  <sponsors>
    <lead_sponsor>
      <agency>Dartmouth-Hitchcock Medical Center</agency>
      <agency_class>Other</agency_class>
    </lead_sponsor>
  </sponsors>
  <source>Dartmouth-Hitchcock Medical Center</source>
  <oversight_info>
    <has_dmc>Yes</has_dmc>
  </oversight_info>
  <brief_summary>
    <textblock>
      Before anti-estrogens such as tamoxifen were developed to treat estrogen receptor&#xD;
      (ER)-positive breast cancer, high-dose estrogen therapies were used. This seems&#xD;
      counterintuitive since anti-estrogens block ER function, while estrogens increase ER&#xD;
      function, but these therapies are effective to similar extents for the treatment of&#xD;
      metastatic ER+ breast cancer. Estrogen therapies are most effective against cancers that&#xD;
      develop resistance to anti-estrogens, likely because such cancers have adapted to grow&#xD;
      without ER function, and restoring ER function (with estrogen) is damaging to the cancer&#xD;
      cells. In some patients with ER+ breast cancer that becomes resistant to anti-estrogens,&#xD;
      treatment with the estrogen 17B-estradiol induces tumor response. Furthermore, when&#xD;
      17B-estradiol-sensitive tumors eventually become resistant to 17B-estradiol, switching back&#xD;
      to anti-estrogen therapy is often effective. These observations suggest that cancers can&#xD;
      alternate between anti-estrogen-sensitive and 17B-estradiol-sensitive states. The&#xD;
      investigators hypothesize that treatment with alternating 17B-estradiol / anti-estrogen&#xD;
      therapies on a defined 8-week / 16-week schedule will more effectively prevent cancer growth&#xD;
      than continuous treatment with either type of therapy in patients with metastatic&#xD;
      anti-estrogen-resistant ER+ breast cancer.&#xD;
    </textblock>
  </brief_summary>
  <detailed_description>
    <textblock>
      Metastatic breast cancer is rarely cured by current therapies. ER+ breast cancers ultimately&#xD;
      become resistant to all available anti-estrogens. Response rates to estrogens are similar to&#xD;
      those of anti-estrogens in the metastatic setting. Given that ER+ breast cancers are often&#xD;
      responsive to anti-estrogens and estrogens, alternating anti-estrogen/estrogen therapies may&#xD;
      be more effective than continuous treatment with either type of agent. Anecdotal evidence&#xD;
      indicates that such a strategy of alternating therapies is effective in some patients.&#xD;
      Preclinical evidence suggests that anti-estrogen-resistant ER+ breast cancers are sensitized&#xD;
      to the anti-tumor effects of estrogens. Such cells harbor subpopulations that can ultimately&#xD;
      regain the ability to grow in the presence of estrogens, and revert to their&#xD;
      anti-estrogen-sensitive state. The investigators will formally test whether alternating&#xD;
      17B-estradiol/anti-estrogen therapies is effective for the management of&#xD;
      anti-estrogen-resistant metastatic ER+/HER2- breast cancer, and to identify molecular&#xD;
      biomarkers that predict tumor response to 1) 17B-estradiol and 2) alternating&#xD;
      17B-estradiol/anti-estrogen therapies. If successful, this study would present a novel&#xD;
      strategy to manage metastatic ER+/HER2- breast cancer by pre-emptively switching therapies&#xD;
      prior to disease progression.&#xD;
    </textblock>
  </detailed_description>
  <overall_status>Active, not recruiting</overall_status>
  <start_date type="Actual">March 11, 2016</start_date>
  <completion_date type="Anticipated">April 2024</completion_date>
  <primary_completion_date type="Anticipated">October 2023</primary_completion_date>
  <phase>Phase 2</phase>
  <study_type>Interventional</study_type>
  <has_expanded_access>No</has_expanded_access>
  <study_design_info>
    <allocation>N/A</allocation>
    <intervention_model>Single Group Assignment</intervention_model>
    <primary_purpose>Treatment</primary_purpose>
    <masking>None (Open Label)</masking>
  </study_design_info>
  <primary_outcome>
    <measure>Clinical benefit</measure>
    <time_frame>12 Months</time_frame>
    <description>Determine the rate of clinical benefit from alternating 17B-estradiol/aromatase. Clinical benefit is defined as complete response, partial response or stable disease at 24 weeks per RECIST criteria.</description>
  </primary_outcome>
  <secondary_outcome>
    <measure>Objective response rate</measure>
    <time_frame>8 weeks</time_frame>
    <description>Determine the objective response rate of patients treated with 17B-estradiol therapy for 8 weeks. Objective Response is defined as complete response + partial response as per RECIST criteria; the proportion of patients experiencing objective response on 17B-estradiol will be calculated to determine objective response rate.</description>
  </secondary_outcome>
  <secondary_outcome>
    <measure>Progression-free survival</measure>
    <time_frame>12 Months</time_frame>
    <description>Determine the progression-free survival from alternating 17B-estradiol/aromatase inhibitor therapy in patients with advanced ER+ breast cancer. Progression-free survival is defined as the time period from the start of a treatment until the time of cancer progression or death from any cause. Cancer progression will be determined as per RECIST criteria.</description>
  </secondary_outcome>
  <secondary_outcome>
    <measure>Adverse event profiles</measure>
    <time_frame>12 Months</time_frame>
    <description>Determine the adverse event profiles of 17B-estradiol and aromatase inhibitors in this patient population. Adverse events will be recorded as Grade 1, 2, 3, or 4. Incidences will be compared within patients over time.</description>
  </secondary_outcome>
  <secondary_outcome>
    <measure>Predictive tumor genetic lesions</measure>
    <time_frame>12 Months</time_frame>
    <description>Determine whether specific tumor genetic lesions in ESR1 are predictive of response to 17B-estradiol and/or subsequent aromatase inhibitor therapies. The rates of clinical benefit from 17B-estradiol and/or subsequent AI therapy will be compared between patients with tumors with vs. without genetic lesions in ESR1.</description>
  </secondary_outcome>
  <number_of_arms>1</number_of_arms>
  <enrollment type="Actual">19</enrollment>
  <condition>Metastatic Breast Cancer</condition>
  <arm_group>
    <arm_group_label>Alternating Therapy</arm_group_label>
    <arm_group_type>Experimental</arm_group_type>
    <description>Study will use an 8-week/16-week alternating regimen of 17B-estradiol/AI (aromatase inhibitor) therapy. Use of only one Aromatase inhibitor throughout the study is preferred.&#xD;
17B-estradiol: One tablet containing 2 mg 17B-estradiol will be taken orally three times daily, for a total dose of 6 mg/day.&#xD;
Letrozole: One tablet containing 2.5 mg letrozole will be taken orally once per day.&#xD;
Anastrozole: One tablet containing 1 mg anastrozole will be taken orally once per day.&#xD;
Exemestane: One tablet containing 25 mg exemestane will be taken orally once per day.</description>
  </arm_group>
  <intervention>
    <intervention_type>Drug</intervention_type>
    <intervention_name>17B-estradiol</intervention_name>
    <description>Anti-estrogen</description>
    <arm_group_label>Alternating Therapy</arm_group_label>
    <other_name>aromatase inhibitor</other_name>
  </intervention>
  <intervention>
    <intervention_type>Drug</intervention_type>
    <intervention_name>Letrozole</intervention_name>
    <description>Aromatase inhibitors work by blocking estrogen receptors; they stop a key enzyme (called aromatase) from changing other hormones into estrogen. This lowers estrogen levels in the body, taking away the fuel that estrogen receptor-positive breast cancers need to grow.</description>
    <arm_group_label>Alternating Therapy</arm_group_label>
    <other_name>Letrozole (Aromatase inhibitor)</other_name>
  </intervention>
  <intervention>
    <intervention_type>Drug</intervention_type>
    <intervention_name>Anastrozole</intervention_name>
    <description>Aromatase inhibitors work differently from tamoxifen and raloxifene. Instead of blocking the estrogen receptors, they stop a key enzyme (called aromatase) from changing other hormones into estrogen. This lowers estrogen levels in the body, taking away the fuel that estrogen receptor-positive breast cancers need to grow.</description>
    <arm_group_label>Alternating Therapy</arm_group_label>
    <other_name>Aromatase inhibitor</other_name>
  </intervention>
  <intervention>
    <intervention_type>Drug</intervention_type>
    <intervention_name>Exemestane</intervention_name>
    <description>Aromatase inhibitors work differently from tamoxifen and raloxifene. Instead of blocking the estrogen receptors, they stop a key enzyme (called aromatase) from changing other hormones into estrogen. This lowers estrogen levels in the body, taking away the fuel that estrogen receptor-positive breast cancers need to grow.</description>
    <arm_group_label>Alternating Therapy</arm_group_label>
    <other_name>Aromatase inhibitor</other_name>
  </intervention>
  <eligibility>
    <criteria>
      <textblock>
        Inclusion Criteria:&#xD;
&#xD;
          1. Women ≥18 years of age with clinical stage IV ER+/HER2- breast cancer, or with locally&#xD;
             recurrent ER+/HER2- disease not amenable to therapy for curative intent.&#xD;
&#xD;
          2. Patient must have been treated with an anti-estrogen at any time in their disease&#xD;
             history. Combination regimens that include an anti-estrogen and any biologic, or&#xD;
             targeted therapy, are permitted (e.g., any CDK inhibitor, everolimus, or any other&#xD;
             novel biologics), and are considered to be a single hormonal therapy based regimen.&#xD;
&#xD;
               -  Any number of prior lines of anti-estrogen (i.e., hormonal) therapy is&#xD;
                  permissible.&#xD;
&#xD;
               -  One line of prior chemotherapy for advanced/metastatic disease is permissible.&#xD;
&#xD;
          3. Histologic documentation of ER strongly+/HER2- breast cancer by core needle biopsy,&#xD;
             fine needle aspiration, incisional biopsy, or surgical biopsy of ≥1 site(s) of&#xD;
             metastatic or locally advanced disease performed as standard of care within the past 4&#xD;
             months for assessment of eligibility for study participation (except as noted below in&#xD;
             c/d/e).&#xD;
&#xD;
               1. ER strongly+ status defined as ER staining by immunohistochemistry in ≥50% of&#xD;
                  malignant cell nuclei with an intensity ≥2+ on a scale of 0-3+. These criteria&#xD;
                  are equivalent to an Allred score ≥6.&#xD;
&#xD;
               2. HER2-negative status is defined as immunohistochemistry score of 0-1+, or with a&#xD;
                  FISH ratio of &lt;2 if IHC is 2+ or if IHC has not been done (as per ASCO/CAP&#xD;
                  definitions). In cases of borderline or equivocal HER2 status, eligibility will&#xD;
                  be determined by the PI.&#xD;
&#xD;
               3. Archived tumor specimens: Excess tumor tissue must be available for research&#xD;
                  purposes. This will include tumor tissue sufficient to make ≥10 five-micron&#xD;
                  sections; more tumor tissue is preferred.&#xD;
&#xD;
                  Freshly acquired tumor specimens: As part of a clinically indicated biopsy&#xD;
                  procedure, an additional 1-3 cores or tissue fragments will be obtained by core&#xD;
                  needle or surgical biopsy for research purposes and FFPE.&#xD;
&#xD;
               4. Patients with bone-only metastatic disease with a history of ER+/HER2- breast&#xD;
                  cancer are eligible, and bone biopsy is not required, providing their primary&#xD;
                  cancer is consistent with the above-described ER and HER2 criteria.&#xD;
&#xD;
               5. Patients with non-bone metastatic disease in whom a safe and accurate biopsy of&#xD;
                  recurrent/metastatic disease cannot be readily obtained are also eligible,&#xD;
                  providing their primary cancer is consistent with the above-described ER and HER2&#xD;
                  criteria.&#xD;
&#xD;
          4. Patient must be a candidate for treatment with 17B-estradiol and an aromatase&#xD;
             inhibitor.&#xD;
&#xD;
          5. If the most recent therapy was in the adjuvant setting, the recurrence-free interval&#xD;
             (time from initiation of adjuvant anti-estrogen therapy to clinical evidence of&#xD;
             disease recurrence) must have been ≥2 years.&#xD;
&#xD;
             If the most recent therapy was in the advanced/metastatic setting, the&#xD;
             progression-free interval must have been ≥3 months (except in the case of&#xD;
             investigational hormonal therapies).&#xD;
&#xD;
          6. Patient must be post-menopausal based on either a history of an oophorectomy, or ≥1&#xD;
             year of amenorrhea. An elevated serum gonadotropin level and estradiol level in the&#xD;
             postmenopausal range (as locally defined) can be used to confirm menopausal status in&#xD;
             a subject with &lt;1 year of amenorrhea.&#xD;
&#xD;
          7. Baseline radiographic staging, including specifically either PET/CT, or CT (CAP) and&#xD;
             bone scan.&#xD;
&#xD;
          8. Patient must be capable and willing to provide informed written consent for study&#xD;
             participation.&#xD;
&#xD;
          9. The following laboratory values must be confirmed for eligibility within 28 days prior&#xD;
             to initiation of study therapy:&#xD;
&#xD;
        Hematology panel&#xD;
&#xD;
          -  hemoglobin &gt; 9 g/dL&#xD;
&#xD;
          -  white blood cell (WBC) count (≥ 2,000/uL)&#xD;
&#xD;
          -  platelet count ≥ 75,000/uL Serum biochemistry/metabolic panel&#xD;
&#xD;
          -  creatinine ≤ 1.5 x upper limits of normal (ULN)&#xD;
&#xD;
          -  total bilirubin ≤ 1.5 x upper limits of normal (ULN)&#xD;
&#xD;
          -  ALT and AST ≤ 3.0 x upper limits of normal (ULN) For patients with liver metastasis: &lt;&#xD;
             5 x upper limits of normal (ULN)&#xD;
&#xD;
        Exclusion Criteria:&#xD;
&#xD;
          1. Treatment with fulvestrant within 16 weeks prior to study enrollment.&#xD;
&#xD;
          2. Any other concurrent systemic anti-cancer treatments, including conventional&#xD;
             chemotherapeutic agents and biological agents, during the study period.&#xD;
&#xD;
             Anti-resorptive bone therapies (e.g., bisphosphonates, denosumab) are permitted.&#xD;
&#xD;
          3. Any investigational cancer therapy in the last 3 weeks.&#xD;
&#xD;
          4. Known CNS disease, unless clinically stable for ≥ 3 months.&#xD;
&#xD;
          5. History of any of the following:&#xD;
&#xD;
               -  deep venous thrombosis&#xD;
&#xD;
               -  pulmonary embolism&#xD;
&#xD;
               -  stroke&#xD;
&#xD;
               -  acute myocardial infarction&#xD;
&#xD;
               -  congestive heart failure&#xD;
&#xD;
               -  previous malignancy not treated with curative intent, or with an estimated&#xD;
                  recurrence risk ≥30%&#xD;
      </textblock>
    </criteria>
    <gender>Female</gender>
    <minimum_age>18 Years</minimum_age>
    <maximum_age>N/A</maximum_age>
    <healthy_volunteers>No</healthy_volunteers>
  </eligibility>
  <overall_official>
    <last_name>Gary N Schwartz, MD</last_name>
    <role>Principal Investigator</role>
    <affiliation>Dartmouth-Hitchcock Medical Center</affiliation>
  </overall_official>
  <location>
    <facility>
      <name>Baystate Medical Center</name>
      <address>
        <city>Springfield</city>
        <state>Massachusetts</state>
        <zip>01199</zip>
        <country>United States</country>
      </address>
    </facility>
  </location>
  <location>
    <facility>
      <name>Mayo Clinic Cancer Center</name>
      <address>
        <city>Rochester</city>
        <state>Minnesota</state>
        <zip>55905</zip>
        <country>United States</country>
      </address>
    </facility>
  </location>
  <location>
    <facility>
      <name>Dartmouth Hitchcock Medical Center</name>
      <address>
        <city>Lebanon</city>
        <state>New Hampshire</state>
        <zip>03756</zip>
        <country>United States</country>
      </address>
    </facility>
  </location>
  <location_countries>
    <country>United States</country>
  </location_countries>
  <verification_date>July 2023</verification_date>
  <study_first_submitted>June 24, 2014</study_first_submitted>
  <study_first_submitted_qc>July 11, 2014</study_first_submitted_qc>
  <study_first_posted type="Estimate">July 14, 2014</study_first_posted>
  <last_update_submitted>July 17, 2023</last_update_submitted>
  <last_update_submitted_qc>July 17, 2023</last_update_submitted_qc>
  <last_update_posted type="Actual">July 18, 2023</last_update_posted>
  <responsible_party>
    <responsible_party_type>Principal Investigator</responsible_party_type>
    <investigator_affiliation>Dartmouth-Hitchcock Medical Center</investigator_affiliation>
    <investigator_full_name>Gary Schwartz</investigator_full_name>
    <investigator_title>Associate Professor of Medicine</investigator_title>
  </responsible_party>
  <keyword>metastatic</keyword>
  <keyword>locally advanced</keyword>
  <keyword>ER+</keyword>
  <keyword>Estrogen therapy</keyword>
  <keyword>Estradiol therapy</keyword>
  <condition_browse>
    <!-- CAUTION:  The following MeSH terms are assigned with an imperfect algorithm            -->
    <mesh_term>Breast Neoplasms</mesh_term>
  </condition_browse>
  <intervention_browse>
    <!-- CAUTION:  The following MeSH terms are assigned with an imperfect algorithm            -->
    <mesh_term>Letrozole</mesh_term>
    <mesh_term>Anastrozole</mesh_term>
    <mesh_term>Exemestane</mesh_term>
    <mesh_term>Estradiol</mesh_term>
    <mesh_term>Aromatase Inhibitors</mesh_term>
  </intervention_browse>
  <!-- Results have not yet been posted for this study                                          -->
</clinical_study>


download date: ClinicalTrials.gov processed this data on September 20, 2023
link text: Link to the current ClinicalTrials.gov record.
url: https://clinicaltrials.gov/ct2/show/NCT02188745
org study id: D14122
nct id: NCT02188745
lead sponsor: 
has dmc: Yes
Before anti-estrogens such as tamoxifen were developed to treat estrogen receptor
      (ER)-positive breast cancer, high-dose estrogen therapies were used. This seems
      counterintuitive since anti-estrogens block ER function, while estrogens increase ER
      function, but these therapies are effective to similar extents for the treatment of
      metastatic ER+ breast cancer. Estrogen therapies are most effective against cancers that
      develop resistance to anti-estrogens, likely because such cancers have adapted to grow
      without ER function, and restoring ER function (with estrogen) is damaging to the cancer
      cells. In some patients with ER+ breast cancer that becomes resistant to anti-estrogens,
      treatment with the estrogen 17B-estradiol induces tumor response. Furthermore, when
      17B-estradiol-sensitive tumors eventually become resistant to 17B-estradiol, switching back
      to anti-estrogen therapy is often effective. These observations suggest that cancers can
      alternate between anti-estrogen-sensitive and 17B-estradiol-sensitive states. The
      investigators hypothesize that treatment with alternating 17B-estradiol / anti-estrogen
      therapies on a defined 8-week / 16-week schedule will more effectively prevent cancer growth
      than continuous treatment with either type of therapy in patients with metastatic
      anti-estrogen-resistant ER+ breast cancer.
Metastatic breast cancer is rarely cured by current therapies. ER+ breast cancers ultimately
      become resistant to all available anti-estrogens. Response rates to estrogens are similar to
      those of anti-estrogens in the metastatic setting. Given that ER+ breast cancers are often
      responsive to anti-estrogens and estrogens, alternating anti-estrogen/estrogen therapies may
      be more effective than continuous treatment with either type of agent. Anecdotal evidence
      indicates that such a strategy of alternating therapies is effective in some patients.
      Preclinical evidence suggests that anti-estrogen-resistant ER+ breast cancers are sensitized
      to the anti-tumor effects of estrogens. Such cells harbor subpopulations that can ultimately
      regain the ability to grow in the presence of estrogens, and revert to their
      anti-estrogen-sensitive state. The investigators will formally test whether alternating
      17B-estradiol/anti-estrogen therapies is effective for the management of
      anti-estrogen-resistant metastatic ER+/HER2- breast cancer, and to identify molecular
      biomarkers that predict tumor response to 1) 17B-estradiol and 2) alternating
      17B-estradiol/anti-estrogen therapies. If successful, this study would present a novel
      strategy to manage metastatic ER+/HER2- breast cancer by pre-emptively switching therapies
      prior to disease progression.
allocation: N/A
intervention model: Single Group Assignment
primary purpose: Treatment
masking: None (Open Label)
measure: Clinical benefit
time frame: 12 Months
description: Determine the rate of clinical benefit from alternating 17B-estradiol/aromatase. Clinical benefit is defined as complete response, partial response or stable disease at 24 weeks per RECIST criteria.
measure: Objective response rate
time frame: 8 weeks
description: Determine the objective response rate of patients treated with 17B-estradiol therapy for 8 weeks. Objective Response is defined as complete response + partial response as per RECIST criteria; the proportion of patients experiencing objective response on 17B-estradiol will be calculated to determine objective response rate.
measure: Progression-free survival
time frame: 12 Months
description: Determine the progression-free survival from alternating 17B-estradiol/aromatase inhibitor therapy in patients with advanced ER+ breast cancer. Progression-free survival is defined as the time period from the start of a treatment until the time of cancer progression or death from any cause. Cancer progression will be determined as per RECIST criteria.
measure: Adverse event profiles
time frame: 12 Months
description: Determine the adverse event profiles of 17B-estradiol and aromatase inhibitors in this patient population. Adverse events will be recorded as Grade 1, 2, 3, or 4. Incidences will be compared within patients over time.
measure: Predictive tumor genetic lesions
time frame: 12 Months
description: Determine whether specific tumor genetic lesions in ESR1 are predictive of response to 17B-estradiol and/or subsequent aromatase inhibitor therapies. The rates of clinical benefit from 17B-estradiol and/or subsequent AI therapy will be compared between patients with tumors with vs. without genetic lesions in ESR1.
arm group label: Alternating Therapy
arm group type: Experimental
description: Study will use an 8-week/16-week alternating regimen of 17B-estradiol/AI (aromatase inhibitor) therapy. Use of only one Aromatase inhibitor throughout the study is preferred.
17B-estradiol: One tablet containing 2 mg 17B-estradiol will be taken orally three times daily, for a total dose of 6 mg/day.
Letrozole: One tablet containing 2.5 mg letrozole will be taken orally once per day.
Anastrozole: One tablet containing 1 mg anastrozole will be taken orally once per day.
Exemestane: One tablet containing 25 mg exemestane will be taken orally once per day.
intervention type: Drug
intervention name: 17B-estradiol
description: Anti-estrogen
arm group label: Alternating Therapy
other name: aromatase inhibitor
intervention type: Drug
intervention name: Letrozole
description: Aromatase inhibitors work by blocking estrogen receptors; they stop a key enzyme (called aromatase) from changing other hormones into estrogen. This lowers estrogen levels in the body, taking away the fuel that estrogen receptor-positive breast cancers need to grow.
arm group label: Alternating Therapy
other name: Letrozole (Aromatase inhibitor)
intervention type: Drug
intervention name: Anastrozole
description: Aromatase inhibitors work differently from tamoxifen and raloxifene. Instead of blocking the estrogen receptors, they stop a key enzyme (called aromatase) from changing other hormones into estrogen. This lowers estrogen levels in the body, taking away the fuel that estrogen receptor-positive breast cancers need to grow.
arm group label: Alternating Therapy
other name: Aromatase inhibitor
intervention type: Drug
intervention name: Exemestane
description: Aromatase inhibitors work differently from tamoxifen and raloxifene. Instead of blocking the estrogen receptors, they stop a key enzyme (called aromatase) from changing other hormones into estrogen. This lowers estrogen levels in the body, taking away the fuel that estrogen receptor-positive breast cancers need to grow.
arm group label: Alternating Therapy
other name: Aromatase inhibitor
criteria: 
gender: Female
minimum age: 18 Years
maximum age: N/A
healthy volunteers: No
last name: Gary N Schwartz, MD
role: Principal Investigator
affiliation: Dartmouth-Hitchcock Medical Center
facility: 
facility: 
facility: 
country: United States
responsible party type: Principal Investigator
investigator affiliation: Dartmouth-Hitchcock Medical Center
investigator full name: Gary Schwartz
investigator title: Associate Professor of Medicine
mesh term: Breast Neoplasms
mesh term: Letrozole
mesh term: Anastrozole
mesh term: Exemestane
mesh term: Estradiol
mesh term: Aromatase Inhibitors