Multiple myeloma (MM) is a cancer that forms in a type of white blood cell called a plasma cell. It represents an incurable plasma cell malignancy that causes an annual incidence of 1% of all human cancers.
Autophagy has a dual role in cancer, acting as
a both a tumor suppressor and inducer. Autophagy actacts as a survival mechanism in response to cellular stress or increased metabolic demands during rapid cell proliferation. However, the excessive activation of autophagy could also lead to the extreme degradation of the organelles that induce autophagic cell death. In MM, autophagy actacts as a cellscell's survival mechanism and protectprotects cells from chemotherapeutic drug treatment. Several clinical trials have highlighted the potential role of autophagy modulators in the treatment of MM. A phasePhase I and Phase II clinical trials have been conducted with combination therapy of autophagy inhibitor hydroxychloroquine (HCQ) with proteasome inhibitor bortezomib and chloroquine in combination with bortezomib and cyclophosphamide relapsed or refractory MM, respectively. The promising results of these clinical studies warrant further investigation of autophagy regulatory pathwaypathways in MM. In our research, we will identify novel transcription factor which isfactors that are highly expressed and control autophagy process in MM.

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