Researchers Develop New Treatment For Recurring Multiple Myeloma

One of the most common forms of cancer is multiple myeloma, which affects the plasma cells, a type of immune cell found in the bone marrow. This form of cancer weakens the immune system, leads to kidney damage and causes weak bones. With the advancement in treatment, the cancer gets cured but the chances of relapse are high as the cancer cells become drug resistant over a period of time.

A team of researchers in Berlin were successful in unravelling an earlier unknown mechanism, which can lead to this type of relapse. This was done using latest improvements for a method known as proteomics.

Commenting on the developments, Prof. Jan Krönke of the Department of Hematology, Oncology and Cancer Immunology on Campus Benjamin Franklin, said, "We were able to show that production of CDK6, a cell division-promoting cell cycle regulator, is particularly high once the cancer has become resistant to treatment. Based on our data, we believe that CDK6 inhibition could represent a new treatment approach in relapsed multiple myeloma."

In spite of there being extensive DNA sequencing studies, treatment resistance in multiple myeloma has only rarely been linked to changes at the genetic level, like gene mutations or gene deletions.

Researchers said that this indicates that the changes taking place within the cancer cell which would explain this relapse must take place at a different level. The cancer cells' growth potential may also be subject to various means of control at the protein level. Here, we observed this type of effect in relation to the protein CDK6.

Researchers used cutting-edge mass spectrometry technology to understand whether changes at the protein level are responsible for the cancer becoming drug resistant. With the help of both pre- and post-relapse samples from patients with multiple myeloma, the researchers were able to quantify more than 6,000 different proteins.

By comparing cancer cells collected before and after relapse, researchers found that a range of proteins were present at either higher or lower concentrations post-relapse. Using statistical and bioinformatics analyses, the researchers were able to trace most of the drug resistance to a single protein namely cyclin-dependent kinase 6, or CDK6, an enzyme, which controls the cell's entry into the cell division phase of the cell cycle.

As a first step, the researchers used cell cultures to demonstrate that CDK6 plays a key role in the development of treatment resistance in multiple myeloma. The researchers were able to confirm this effect in an animal model, where the combination of cancer drug pomalidomide with a CDK6 inhibitor significantly improved the odds of survival. "These data suggest that patients with treatment-resistant multiple myeloma may also benefit from the addition of CDK6 inhibitors," researchers said.

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