Role of Osteocytes in Myeloma Bone Disease
| Status: | Recruiting |
|---|---|
| Conditions: | Blood Cancer, Hematology, Hematology |
| Therapuetic Areas: | Hematology, Oncology |
| Healthy: | No |
| Age Range: | 18 - Any |
| Updated: | 10/20/2018 |
| Start Date: | July 23, 2014 |
| End Date: | December 30, 2019 |
| Contact: | Attaya Suvannasankha, M.D. |
| Email: | asuvanna@iu.edu |
| Phone: | 317-278-9306 |
Progress in the treatment of myeloma and myeloma bone disease has substantially increased
overall survival, but relapse is inevitable and better treatment is needed. The bone
microenvironment is tremendously complex, so that targeting single interactions between tumor
and bone is unlikely to be effective. Treatments need to block centrally important,
multifunctional pathways. The investigators data point to a central role of the osteocyte to
induce heparanase, a multifunctional mediator of myeloma bone disease. Increased heparanase
due to FGF23 may make systemic inhibitors of heparanase less effective in bone than
elsewhere. FGF23 neutralizing antibodies have been developed for non-cancer conditions of
FGF23 excess, such as chronic kidney disease (Shimada & Fukamoto, 2012), and could be used in
MM alone or in combination with heparanase inhibitors. Complete neutralization of FGF23 has
adverse effects, but neutralization of FGF23 excess may be practical, or in the future,
suppression of excess FGF23 biosynthesis by osteocytes.
The investigators hope to determine serum FGF23 and heparanase, Dkk1 and plasma klotho levels
in patients with newly diagnosed and relapsed myeloma compared to healthy controls with this
exploratory study.
overall survival, but relapse is inevitable and better treatment is needed. The bone
microenvironment is tremendously complex, so that targeting single interactions between tumor
and bone is unlikely to be effective. Treatments need to block centrally important,
multifunctional pathways. The investigators data point to a central role of the osteocyte to
induce heparanase, a multifunctional mediator of myeloma bone disease. Increased heparanase
due to FGF23 may make systemic inhibitors of heparanase less effective in bone than
elsewhere. FGF23 neutralizing antibodies have been developed for non-cancer conditions of
FGF23 excess, such as chronic kidney disease (Shimada & Fukamoto, 2012), and could be used in
MM alone or in combination with heparanase inhibitors. Complete neutralization of FGF23 has
adverse effects, but neutralization of FGF23 excess may be practical, or in the future,
suppression of excess FGF23 biosynthesis by osteocytes.
The investigators hope to determine serum FGF23 and heparanase, Dkk1 and plasma klotho levels
in patients with newly diagnosed and relapsed myeloma compared to healthy controls with this
exploratory study.
Inclusion Criteria:
1. Age > 18 years but ≤ 95 years at the time of consent
2. Subjects must be English-speaking
3. Must voluntarily sign the most current informed consent and HIPAA documents prior to
study participation.
4. Have no prior history of malignancy in the past 5 years with the exception of basal
cell and squamous cell carcinoma of the skin. Other cancers with low potential for
metastasis, such as in situ cancers can also be enrolled as healthy volunteers.
5. Have no known liver or kidney disorders
Exclusion Criteria:
1. Pregnant females will be excluded from the study.
2. Subjects allergic to xylocaine will be excluded.
3. Subjects with an acute illness (Ex. upper respiratory infection, viral illness) in the
past seven days will be excluded.
4. History of bleeding disorders.
5. Subjects deemed incompetent by treating physician
6. Institutionalized, mentally disabled subjects
7. Subjects who are prisoners
We found this trial at
2
sites
Indianapolis, Indiana 46202
Principal Investigator: Attaya Suvannasankha, M.D.
Phone: 317-278-9306
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Indianapolis, Indiana 46202
Principal Investigator: Attaya Suvannasankha, M.D.
Phone: 317-278-9306
Click here to add this to my saved trials