<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/NCT03259152</url>
  </required_header>
  <id_info>
    <org_study_id>ZZ3592-2017</org_study_id>
    <nct_id>NCT03259152</nct_id>
  </id_info>
  <brief_title>Characteristics and Mechanism of Denosumab-treated Giant Cell Tumor of Bone</brief_title>
  <acronym>D-Gct</acronym>
  <official_title>Clinical, Pathologic Characteristics and Its Mechansim of Denosumab Treated Giant Cell Tumor of Bone</official_title>
  <sponsors>
    <lead_sponsor>
      <agency>Hebei Medical University Third Hospital</agency>
      <agency_class>Other</agency_class>
    </lead_sponsor>
  </sponsors>
  <source>Hebei Medical University Third Hospital</source>
  <oversight_info>
    <has_dmc>Yes</has_dmc>
    <is_fda_regulated_device>No</is_fda_regulated_device>
    <is_us_export>No</is_us_export>
  </oversight_info>
  <brief_summary>
    <textblock>
      Giant cell tumor of bone (GCTb) is a primary, osteolytic, benign tumor of the bone. Surgery&#xD;
      is the commonly used treatment. Discovery of RANKL and its human monoclonal antibody,&#xD;
      denosumab, led to use of denosumab for treatment of GCT. The aim of this study was to&#xD;
      evaluate clinical and pathological results of treatment of relapsed or refractoriness GCT&#xD;
      with denosumab and to assess adverse effect profile and recurrence rate.&#xD;
    </textblock>
  </brief_summary>
  <detailed_description>
    <textblock>
      Giant cell tumor of bone (GCTb) is an aggressive, benign bone tumor. GCTb, which was first&#xD;
      defined by Cooper and Travers, can produce pulmonary metastasis, albeit rarely (1-6%). GCTb&#xD;
      constitutes 5% of primary bone tumors and 20% of benign bone tumors. Histologically, the&#xD;
      tumour consists of a proliferation of mononuclear cells, accompanied by a population of&#xD;
      non-neoplastic osteoclast-like giant cells and mononuclear osteoclast precursors. Currently,&#xD;
      it is thought that proliferating neoplastic cells produce a number of cytokines and&#xD;
      mediators, including the receptor activator of nuclear factor κ-B-ligand (RANK-RANKL) system,&#xD;
      that recruit osteoclast precursors and induce their maturation into multinucleated&#xD;
      osteoclast. The standard management of GCTb is based on surgery with several local adjuvant&#xD;
      treatments like methacrylate cement, phenol or cryotherapy to reduce the risk of recurrence,&#xD;
      while bisphosphonates are used in some cases to decrease bone resorption and for pain relief&#xD;
      in inoperable tumours or metastatic disease. In the last 5 years the use of denosumab, a&#xD;
      fully human monoclonal antibody already licensed for postmenopausal osteoporosis and&#xD;
      prevention of skeletal related events in bone metastases from solid tumours, has been&#xD;
      introduced in the treatment strategy of GCTb. In this study we examined the clinical,&#xD;
      radiological, histological and underlying mechanism features of a series of GCTb, before and&#xD;
      after denosumab administration, comparing baseline and resection specimens. Moreover, we&#xD;
      examined the safety of the drug and on the angiogenesis through the determination of&#xD;
      microvascular density (MVD).&#xD;
    </textblock>
  </detailed_description>
  <overall_status>Unknown status</overall_status>
  <last_known_status>Recruiting</last_known_status>
  <start_date type="Actual">May 1, 2016</start_date>
  <completion_date type="Anticipated">May 1, 2019</completion_date>
  <primary_completion_date type="Anticipated">May 1, 2019</primary_completion_date>
  <phase>Phase 3</phase>
  <study_type>Interventional</study_type>
  <has_expanded_access>No</has_expanded_access>
  <study_design_info>
    <allocation>Randomized</allocation>
    <intervention_model>Parallel Assignment</intervention_model>
    <primary_purpose>Prevention</primary_purpose>
    <masking>None (Open Label)</masking>
  </study_design_info>
  <primary_outcome>
    <measure>Molecular analysis (Immunohistochemistry for RANKL, RANK, OPG,Col-I, VEGF)</measure>
    <time_frame>6 month</time_frame>
    <description>For collagen RANKL (Receptor Activator for Nuclear Factor-κ B Ligand), RANK (Receptor Activator for Nuclear Factor-κ B), OPG (Osteoprotegerin), Col-I (type I Collagen), VEGF (Vascular Endothelial Growth Factor) immunohistochemistry, sections were deparaffinized, rehydrated, and immunostained with a SA1024 SABC-POD kit and Kit-0017 DAB detection kit. Briefly, antigen retrieval was performed, and endogenous peroxidases were then inactivated prior to incubation with primary antibodies overnight at 4°C. This was followed by incubation with a biotinylated secondary antibody and a streptavidin-biotin complex peroxidase solution. Diaminobenzidine (DAB) chromogen was applied and counterstained with hematoxylin for antibody detection.&#xD;
Images were captured by a microscope system at 400-magnification. The integrated optical density values of each factor were semiquantitatively analyzed using Imaging Pro Plus 6.0 software.</description>
  </primary_outcome>
  <primary_outcome>
    <measure>Molecular analysis (RT-PCR for RANKL, RANK, OPG,Col-I, VEGF)</measure>
    <time_frame>6 month</time_frame>
    <description>Tissures mRNA was extracted using TRIzol reagent (Invitrogen, Carlsbad, CA). The RNA concentration and quality were assessed using a Quawell Q5000 spectrophotometer (Quawell, San Jose, CA). Reverse transcription PCR was performed using a Gene Amp 7700 Sequence Detection System (Applied Biosystems, Foster City, CA) and custom-designed, validated primers for Col1α1, Col2α1, Aggrecan, MMP-13, and ADAMTS-4. GAPDH was used as the housekeeping gene. Relative gene expression changes were reported using the 2(-Delta Delta C(T)) method as previously described. The experiment was repeated in triplicate to ensure accuracy.</description>
  </primary_outcome>
  <secondary_outcome>
    <measure>Visual Analog Score - Pain evaluation</measure>
    <time_frame>6 months</time_frame>
    <description>Visual analog scale [VAS] is a measure of pain intensity. It is a continuous scale comprised of a horizontal (called horizontal visual analogue scale) or,vertical called vertical visual analog scale usually 10 cm or 100 mm length [both the gradations are used]. It is anchored by two verbal descriptors, one for each symptom extreme. For pain intensity, the scale is most commonly anchored by &quot;no pain&quot; (score of 0) and &quot;pain as bad as it could be&quot; or &quot;worst imaginable pain&quot; (score of 100 [on 100-mm scale]</description>
  </secondary_outcome>
  <secondary_outcome>
    <measure>Hematology test - Tartrate Resistant Acid Phosphatase</measure>
    <time_frame>6 months</time_frame>
    <description>Tartrate-resistant acid phosphatase, a bone resorption marker, is secreted from osteoclasts and this marker is reported to be high in patients with giant cell tumor of bone. We investigated the effects of denosumab and the usefulness of a tartrate-resistant acid phosphatase as a monitoring marker in the management of a refractory giant cell tumor of bone. Tartrate-resistant acid phosphatase secretion was measured in the patient's serum to monitor the response to denosumab, and a rapid normalization of the marker was observed after the first denosumab administration.</description>
  </secondary_outcome>
  <secondary_outcome>
    <measure>Follow-up for recrudescence</measure>
    <time_frame>6 month to 1 year</time_frame>
    <description>Patients were followed up regularly for local or systemic tumor recurrence by X-ray, CT, MRI, ECT.&#xD;
The follow-up period was 3 months.</description>
  </secondary_outcome>
  <secondary_outcome>
    <measure>Morphological change - HE (Hematoxylin-Eosin) staining</measure>
    <time_frame>6 month</time_frame>
    <description>For histological analysis of the adjacent intervertebral disc and fusion mass, the tissures of the Giant cell tumor of bone were fixed in 10% neutral buffered formalin, decalcified in 10% EDTA-2Na for 3 months, and then embedded in paraffin. They were subsequently cut into 5-mm sections with cationic slides. Slides of the tissures of the Giant cell tumor of bone were stained with H&amp;E and captured by a microscope system (BX53; Olympus, Tokyo, Japan).</description>
  </secondary_outcome>
  <secondary_outcome>
    <measure>Micro-vessel density or area by IHC - stained slides</measure>
    <time_frame>6 month</time_frame>
    <description>IHC - stained for VEGF images were used for microvessel density (MVD) and vascular bud relative area analysis. MVD was measured by counting the number of cartilage endplate vascular buds (an average of cephalic and caudal vascular buds). The ratio of vascular bud area to the total endplate area was measured for vascular bud relative area analysis using the grid method. MVD and vascular bud relative area analyses were repeated at least three times for enhanced accuracy</description>
  </secondary_outcome>
  <secondary_outcome>
    <measure>Imaging changes by X-ray, CT, MRI, ECT.</measure>
    <time_frame>6 month</time_frame>
    <description>The patients' clinical information, images from radiographs, CT and MRI before and after Denosumab-treatment were recorded and analyzed. Tumor volume was measured on coronal, transverse, and sagital MRI or CT scansof the lesion; and maximum height, width, and depth were recorded; and the volume was calculated using the formula of an ellopsoid mass volume = [(π/6) × height × width × depth]. If CT or MRI were not available, tumor volume was measured on two-plane radiograghs.</description>
  </secondary_outcome>
  <other_outcome>
    <measure>Number of participants with treatment-related adverse events as assessed by CTCAE v4.0</measure>
    <time_frame>3 year</time_frame>
    <description>The CTCAE v.4 criteria was used to evaluate late toxicity for all patients. Toxicity scores were recalculated for patients treated before publication of CTCAE v4.0 scale.</description>
  </other_outcome>
  <number_of_arms>2</number_of_arms>
  <enrollment type="Anticipated">30</enrollment>
  <condition>Giant Cell Tumor of Bone</condition>
  <arm_group>
    <arm_group_label>Pre-Denosumab GctB</arm_group_label>
    <arm_group_type>Experimental</arm_group_type>
    <description>Specimens obtained during biopsy</description>
  </arm_group>
  <arm_group>
    <arm_group_label>Post-Denosumab GctB</arm_group_label>
    <arm_group_type>Experimental</arm_group_type>
    <description>Specimen after administration of Denosumab</description>
  </arm_group>
  <intervention>
    <intervention_type>Drug</intervention_type>
    <intervention_name>Denosumab</intervention_name>
    <description>Denosumab (trade names Prolia and Xgeva) is a human monoclonal antibody for the treatment of osteoporosis, treatment-induced bone loss, metastases to bone, and giant cell tumor of bone.Denosumab is a RANKL inhibitor, which works by preventing the development of osteoclasts which are cells that break down bone.</description>
    <arm_group_label>Post-Denosumab GctB</arm_group_label>
    <arm_group_label>Pre-Denosumab GctB</arm_group_label>
    <other_name>Xgeva or Prolia</other_name>
  </intervention>
  <eligibility>
    <criteria>
      <textblock>
        Inclusion Criteria:&#xD;
&#xD;
          -  Giant cell tumor of bone patients confirmed by clinical, medical imaging and&#xD;
             Pathology.&#xD;
&#xD;
        Exclusion Criteria:&#xD;
&#xD;
          -  (1) less than 14 patients; 2) pregnant patients; 3) A patient who receives other&#xD;
             medications during treatment.&#xD;
      </textblock>
    </criteria>
    <gender>All</gender>
    <minimum_age>14 Years</minimum_age>
    <maximum_age>60 Years</maximum_age>
    <healthy_volunteers>No</healthy_volunteers>
  </eligibility>
  <overall_official>
    <last_name>Zhuang Zhou, Ph.D</last_name>
    <role>Principal Investigator</role>
    <affiliation>Hebei Medical University Third Hospital</affiliation>
  </overall_official>
  <overall_contact>
    <last_name>Zhuang Zhou, Ph.D</last_name>
    <phone>+86 18833130669</phone>
    <email>39094572@qq.com</email>
  </overall_contact>
  <overall_contact_backup>
    <last_name>Guochuan Zhang, M.D.</last_name>
    <phone>+86 13932110889</phone>
  </overall_contact_backup>
  <location>
    <facility>
      <name>Zhuang Zhou</name>
      <address>
        <city>Shijiazhuang</city>
        <state>Hebei</state>
        <zip>050000</zip>
        <country>China</country>
      </address>
    </facility>
    <status>Recruiting</status>
    <contact>
      <last_name>Zhuang Zhou, Ph.D</last_name>
      <phone>+86 18833130669</phone>
      <email>39094572@qq.com</email>
    </contact>
    <contact_backup>
      <last_name>Guochuan Zhang, M.D.</last_name>
      <phone>+86 13932110889</phone>
    </contact_backup>
  </location>
  <location_countries>
    <country>China</country>
  </location_countries>
  <link>
    <url>https://en.wikipedia.org/wiki/Denosumab</url>
    <description>Description of Denosumab</description>
  </link>
  <reference>
    <citation>Girolami I, Mancini I, Simoni A, Baldi GG, Simi L, Campanacci D, Beltrami G, Scoccianti G, D'Arienzo A, Capanna R, Franchi A. Denosumab treated giant cell tumour of bone: a morphological, immunohistochemical and molecular analysis of a series. J Clin Pathol. 2016 Mar;69(3):240-7. doi: 10.1136/jclinpath-2015-203248. Epub 2015 Sep 3.</citation>
    <PMID>26338802</PMID>
  </reference>
  <reference>
    <citation>Deveci MA, Paydas S, Gonlusen G, Ozkan C, Bicer OS, Tekin M. Clinical and pathological results of denosumab treatment for giant cell tumors of bone: Prospective study of 14 cases. Acta Orthop Traumatol Turc. 2017 Jan;51(1):1-6. doi: 10.1016/j.aott.2016.03.004. Epub 2016 Oct 24.</citation>
    <PMID>27784623</PMID>
  </reference>
  <reference>
    <citation>Rutkowski P, Ferrari S, Grimer RJ, Stalley PD, Dijkstra SP, Pienkowski A, Vaz G, Wunder JS, Seeger LL, Feng A, Roberts ZJ, Bach BA. Surgical downstaging in an open-label phase II trial of denosumab in patients with giant cell tumor of bone. Ann Surg Oncol. 2015 Sep;22(9):2860-8. doi: 10.1245/s10434-015-4634-9. Epub 2015 Jun 2.</citation>
    <PMID>26033180</PMID>
  </reference>
  <verification_date>May 2017</verification_date>
  <study_first_submitted>August 17, 2017</study_first_submitted>
  <study_first_submitted_qc>August 19, 2017</study_first_submitted_qc>
  <study_first_posted type="Actual">August 23, 2017</study_first_posted>
  <last_update_submitted>August 23, 2017</last_update_submitted>
  <last_update_submitted_qc>August 23, 2017</last_update_submitted_qc>
  <last_update_posted type="Actual">August 24, 2017</last_update_posted>
  <responsible_party>
    <responsible_party_type>Sponsor</responsible_party_type>
  </responsible_party>
  <keyword>Giant cell tumor of bone</keyword>
  <keyword>Denousmab</keyword>
  <keyword>Pathologic</keyword>
  <keyword>Clinical</keyword>
  <keyword>Mechansim</keyword>
  <condition_browse>
    <!-- CAUTION:  The following MeSH terms are assigned with an imperfect algorithm            -->
    <mesh_term>Giant Cell Tumors</mesh_term>
    <mesh_term>Bone Neoplasms</mesh_term>
    <mesh_term>Giant Cell Tumor of Bone</mesh_term>
  </condition_browse>
  <intervention_browse>
    <!-- CAUTION:  The following MeSH terms are assigned with an imperfect algorithm            -->
    <mesh_term>Denosumab</mesh_term>
  </intervention_browse>
  <patient_data>
    <sharing_ipd>No</sharing_ipd>
    <ipd_description>We have not yet planned to to make individual participant data (IPD) available to other researchers.</ipd_description>
  </patient_data>
  <!-- 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/NCT03259152
org study id: ZZ3592-2017
nct id: NCT03259152
lead sponsor: 
has dmc: Yes
is fda regulated device: No
is us export: No
Giant cell tumor of bone (GCTb) is a primary, osteolytic, benign tumor of the bone. Surgery
      is the commonly used treatment. Discovery of RANKL and its human monoclonal antibody,
      denosumab, led to use of denosumab for treatment of GCT. The aim of this study was to
      evaluate clinical and pathological results of treatment of relapsed or refractoriness GCT
      with denosumab and to assess adverse effect profile and recurrence rate.
Giant cell tumor of bone (GCTb) is an aggressive, benign bone tumor. GCTb, which was first
      defined by Cooper and Travers, can produce pulmonary metastasis, albeit rarely (1-6%). GCTb
      constitutes 5% of primary bone tumors and 20% of benign bone tumors. Histologically, the
      tumour consists of a proliferation of mononuclear cells, accompanied by a population of
      non-neoplastic osteoclast-like giant cells and mononuclear osteoclast precursors. Currently,
      it is thought that proliferating neoplastic cells produce a number of cytokines and
      mediators, including the receptor activator of nuclear factor κ-B-ligand (RANK-RANKL) system,
      that recruit osteoclast precursors and induce their maturation into multinucleated
      osteoclast. The standard management of GCTb is based on surgery with several local adjuvant
      treatments like methacrylate cement, phenol or cryotherapy to reduce the risk of recurrence,
      while bisphosphonates are used in some cases to decrease bone resorption and for pain relief
      in inoperable tumours or metastatic disease. In the last 5 years the use of denosumab, a
      fully human monoclonal antibody already licensed for postmenopausal osteoporosis and
      prevention of skeletal related events in bone metastases from solid tumours, has been
      introduced in the treatment strategy of GCTb. In this study we examined the clinical,
      radiological, histological and underlying mechanism features of a series of GCTb, before and
      after denosumab administration, comparing baseline and resection specimens. Moreover, we
      examined the safety of the drug and on the angiogenesis through the determination of
      microvascular density (MVD).
allocation: Randomized
intervention model: Parallel Assignment
primary purpose: Prevention
masking: None (Open Label)
measure: Molecular analysis (Immunohistochemistry for RANKL, RANK, OPG,Col-I, VEGF)
time frame: 6 month
description: For collagen RANKL (Receptor Activator for Nuclear Factor-κ B Ligand), RANK (Receptor Activator for Nuclear Factor-κ B), OPG (Osteoprotegerin), Col-I (type I Collagen), VEGF (Vascular Endothelial Growth Factor) immunohistochemistry, sections were deparaffinized, rehydrated, and immunostained with a SA1024 SABC-POD kit and Kit-0017 DAB detection kit. Briefly, antigen retrieval was performed, and endogenous peroxidases were then inactivated prior to incubation with primary antibodies overnight at 4°C. This was followed by incubation with a biotinylated secondary antibody and a streptavidin-biotin complex peroxidase solution. Diaminobenzidine (DAB) chromogen was applied and counterstained with hematoxylin for antibody detection.
Images were captured by a microscope system at 400-magnification. The integrated optical density values of each factor were semiquantitatively analyzed using Imaging Pro Plus 6.0 software.
measure: Molecular analysis (RT-PCR for RANKL, RANK, OPG,Col-I, VEGF)
time frame: 6 month
description: Tissures mRNA was extracted using TRIzol reagent (Invitrogen, Carlsbad, CA). The RNA concentration and quality were assessed using a Quawell Q5000 spectrophotometer (Quawell, San Jose, CA). Reverse transcription PCR was performed using a Gene Amp 7700 Sequence Detection System (Applied Biosystems, Foster City, CA) and custom-designed, validated primers for Col1α1, Col2α1, Aggrecan, MMP-13, and ADAMTS-4. GAPDH was used as the housekeeping gene. Relative gene expression changes were reported using the 2(-Delta Delta C(T)) method as previously described. The experiment was repeated in triplicate to ensure accuracy.
measure: Visual Analog Score - Pain evaluation
time frame: 6 months
description: Visual analog scale [VAS] is a measure of pain intensity. It is a continuous scale comprised of a horizontal (called horizontal visual analogue scale) or,vertical called vertical visual analog scale usually 10 cm or 100 mm length [both the gradations are used]. It is anchored by two verbal descriptors, one for each symptom extreme. For pain intensity, the scale is most commonly anchored by "no pain" (score of 0) and "pain as bad as it could be" or "worst imaginable pain" (score of 100 [on 100-mm scale]
measure: Hematology test - Tartrate Resistant Acid Phosphatase
time frame: 6 months
description: Tartrate-resistant acid phosphatase, a bone resorption marker, is secreted from osteoclasts and this marker is reported to be high in patients with giant cell tumor of bone. We investigated the effects of denosumab and the usefulness of a tartrate-resistant acid phosphatase as a monitoring marker in the management of a refractory giant cell tumor of bone. Tartrate-resistant acid phosphatase secretion was measured in the patient's serum to monitor the response to denosumab, and a rapid normalization of the marker was observed after the first denosumab administration.
measure: Follow-up for recrudescence
time frame: 6 month to 1 year
description: Patients were followed up regularly for local or systemic tumor recurrence by X-ray, CT, MRI, ECT.
The follow-up period was 3 months.
measure: Morphological change - HE (Hematoxylin-Eosin) staining
time frame: 6 month
description: For histological analysis of the adjacent intervertebral disc and fusion mass, the tissures of the Giant cell tumor of bone were fixed in 10% neutral buffered formalin, decalcified in 10% EDTA-2Na for 3 months, and then embedded in paraffin. They were subsequently cut into 5-mm sections with cationic slides. Slides of the tissures of the Giant cell tumor of bone were stained with H&E and captured by a microscope system (BX53; Olympus, Tokyo, Japan).
measure: Micro-vessel density or area by IHC - stained slides
time frame: 6 month
description: IHC - stained for VEGF images were used for microvessel density (MVD) and vascular bud relative area analysis. MVD was measured by counting the number of cartilage endplate vascular buds (an average of cephalic and caudal vascular buds). The ratio of vascular bud area to the total endplate area was measured for vascular bud relative area analysis using the grid method. MVD and vascular bud relative area analyses were repeated at least three times for enhanced accuracy
measure: Imaging changes by X-ray, CT, MRI, ECT.
time frame: 6 month
description: The patients' clinical information, images from radiographs, CT and MRI before and after Denosumab-treatment were recorded and analyzed. Tumor volume was measured on coronal, transverse, and sagital MRI or CT scansof the lesion; and maximum height, width, and depth were recorded; and the volume was calculated using the formula of an ellopsoid mass volume = [(π/6) × height × width × depth]. If CT or MRI were not available, tumor volume was measured on two-plane radiograghs.
measure: Number of participants with treatment-related adverse events as assessed by CTCAE v4.0
time frame: 3 year
description: The CTCAE v.4 criteria was used to evaluate late toxicity for all patients. Toxicity scores were recalculated for patients treated before publication of CTCAE v4.0 scale.
arm group label: Pre-Denosumab GctB
arm group type: Experimental
description: Specimens obtained during biopsy
arm group label: Post-Denosumab GctB
arm group type: Experimental
description: Specimen after administration of Denosumab
intervention type: Drug
intervention name: Denosumab
description: Denosumab (trade names Prolia and Xgeva) is a human monoclonal antibody for the treatment of osteoporosis, treatment-induced bone loss, metastases to bone, and giant cell tumor of bone.Denosumab is a RANKL inhibitor, which works by preventing the development of osteoclasts which are cells that break down bone.
arm group label: Post-Denosumab GctB
arm group label: Pre-Denosumab GctB
other name: Xgeva or Prolia
criteria: 
gender: All
minimum age: 14 Years
maximum age: 60 Years
healthy volunteers: No
last name: Zhuang Zhou, Ph.D
role: Principal Investigator
affiliation: Hebei Medical University Third Hospital
last name: Zhuang Zhou, Ph.D
phone: +86 18833130669
email: 39094572@qq.com
last name: Guochuan Zhang, M.D.
phone: +86 13932110889
facility: 
status: Recruiting
contact: 
contact backup: 
country: China
url: https://en.wikipedia.org/wiki/Denosumab
description: Description of Denosumab
citation: Girolami I, Mancini I, Simoni A, Baldi GG, Simi L, Campanacci D, Beltrami G, Scoccianti G, D'Arienzo A, Capanna R, Franchi A. Denosumab treated giant cell tumour of bone: a morphological, immunohistochemical and molecular analysis of a series. J Clin Pathol. 2016 Mar;69(3):240-7. doi: 10.1136/jclinpath-2015-203248. Epub 2015 Sep 3.
PMID: 26338802
citation: Deveci MA, Paydas S, Gonlusen G, Ozkan C, Bicer OS, Tekin M. Clinical and pathological results of denosumab treatment for giant cell tumors of bone: Prospective study of 14 cases. Acta Orthop Traumatol Turc. 2017 Jan;51(1):1-6. doi: 10.1016/j.aott.2016.03.004. Epub 2016 Oct 24.
PMID: 27784623
citation: Rutkowski P, Ferrari S, Grimer RJ, Stalley PD, Dijkstra SP, Pienkowski A, Vaz G, Wunder JS, Seeger LL, Feng A, Roberts ZJ, Bach BA. Surgical downstaging in an open-label phase II trial of denosumab in patients with giant cell tumor of bone. Ann Surg Oncol. 2015 Sep;22(9):2860-8. doi: 10.1245/s10434-015-4634-9. Epub 2015 Jun 2.
PMID: 26033180
responsible party type: Sponsor
mesh term: Giant Cell Tumors
mesh term: Bone Neoplasms
mesh term: Giant Cell Tumor of Bone
mesh term: Denosumab
sharing ipd: No
ipd description: We have not yet planned to to make individual participant data (IPD) available to other researchers.