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Beacon NewsFlashes – August 5, 2013

By: Sruti Krishna; Published: August 5, 2013 @ 4:23 pm | Comments Disabled

Phase 2 Clinical Trial To Examine If Natural Killer Cells Slow Progression Of Smoldering Myeloma – Researchers from the University of Arkansas for Medical Sciences, in collaboration with Millennium Pharmaceuticals, have launched a Phase 2 clinical trial to determine if treating smoldering multiple myeloma patients with natural killer cells slows disease progression to active multiple myeloma.  A natural killer cell is a type of immune cell that fights infected cells and cancerous cells. In this trial, the researchers will collect natural killer cells from the patient’s blood and grow and multiply the cells under laboratory conditions. Once this expanded population of natural killer cells is re-infused into the patient, the researchers will monitor the patient to make sure the treatment is safe, that the cells persist in the body after infusion, and that the cells continue to multiple in the body. In addition, the researchers will monitor the patient’s time to progression from smoldering myeloma to symptomatic myeloma, and compare it against historical data from smoldering myeloma patients who did not receive any therapy. Patients with high-risk smoldering myeloma, who have not received prior treatment, are eligible to participate in the study.  Smoldering, or asymptomatic, multiple myeloma is a precursor to multiple myeloma in which the patient experiences none of the symptoms typically associated with active (symptomatic) multiple myeloma, such as ele­vated calcium levels, kidney failure, anemia, or bone lesions. For more information about the study or how to enroll, please see the clinical trial [1] description.

Phase 1/2 Clinical Trial To Study Treatment With Modified Lymphocytes In Relapsed / Refractory Myeloma Patients – A Phase 1/2 clinical trial to be conducted in China will test if modified lymphocytes stimulate an anti-cancer immune response in patients with relapsed / refractory myeloma. The study design involves T lymphocytes, a type of immune cell that can kill infected cells and cancerous cells. Relapsed / refractory myeloma patients whose cancer cells produce the CD138 protein are eligible to participate in this study. The patient’s own T-cells or T-cells from a donor will be harvested, genetically modified under laboratory conditions, and infused into the patient. These genetic modifications will allow the T-cells to identify myeloma cells with CD138 on their surface and trigger an immune response that kills the myeloma cells. The researchers will monitor the survival of the modified T-cells in the patients and the immune response generated against the cancer cells. Other studies have used this approach before, generating modified T-cells that are able to recognize other proteins on myeloma cells and other types of cancer cells. For more information on the ongoing Chinese trial, please see the clinical trial [2] description.

Preclinical Study Shows Blocking Heat Shock Protein 70 May Be An Effective Treatment Option For Multiple Myeloma – Results from a preclinical study show that inhibiting Heat shock protein 70 (Hsp70) can significantly slow the division of myeloma cells and promote their death. Based on these findings, the study investigators, who are from the United Kingdom, suggest that blocking Hsp70 could represent a novel therapeutic approach for multiple myeloma. Heat shock proteins are involved in a number of vital processes within the cell, including the folding and unfolding of other proteins. Tanespimycin [3] (17-AAG), which inhibits another member of the heat shock protein family known as Hsp90, has been tested in clinical trials for anti-myeloma activity, but the drug is no longer being developed (see related Beacon [4] news). In the current study, the researchers used a small molecule, Ver-155008, that blocks Hsp70 function. Ver-155008 significantly reduced the division of myeloma cells with limited effects on normal blood cells. The researchers also found that a combination of Ver-155008 plus tanespimycin blocked myeloma cell division more effectively than either molecule alone. For more information, please see the study in Cancer Letters [5].

UCL67022 Shows Anti-Myeloma Activity In Preclinical Study – Results from a recent preclinical study suggest that a new agent, UCL67022, has potent activity against multiple myeloma and non-Hodgkin lymphoma. UCL67022 belongs to a class of compounds called histone deacetylase (HDAC) inhibitors that interrupt division of cancer cells and cause cell death. Several other HDAC inhibitors – such as  Zolinza [6] (vorinostat), panobinostat [7], and quisinostat [8] – are being studied in clinical trials for the treatment of multiple myeloma. In the current study, researchers from the U.K. found that UCL67022 was toxic to myeloma cells and non-Hodgkin lymphoma cells at 10-fold lower concentrations than previously demonstrated with Zolinza. UCL67022 was not toxic to blood cells or bone marrow cells at this concentration. The investigators also found that UCL67022 increased Velcade’s ability to kill myeloma and non-Hodgkin lymphoma cells. Based on these findings, they recommended that UCL67022 be evaluated further in clinical trials. For more information, please see the study in the British Journal of Hematology [9].


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URL to article: https://myelomabeacon.org/news/2013/08/05/beacon-newsflashes-august-5-2013/

URLs in this post:

[1] clinical trial: http://clinicaltrials.gov/ct2/show/NCT01884688

[2] clinical trial: http://clinicaltrials.gov/ct2/show/NCT01886976

[3] Tanespimycin: https://myelomabeacon.org/resources/2008/10/15/tanespimycin/

[4] Beacon: https://myelomabeacon.org/news/2010/07/22/tanespimycin-development-halted/

[5] Cancer Letters: http://www.sciencedirect.com/science/article/pii/S0304383513005430

[6] Zolinza: https://myelomabeacon.org/resources/2009/11/04/zolinza/

[7] panobinostat: https://myelomabeacon.org/tag/panobinostat

[8] quisinostat: https://myelomabeacon.org/tag/quisinostat/

[9] British Journal of Hematology: http://onlinelibrary.wiley.com/doi/10.1111/bjh.12456/full

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