Heat shock proteins as a new, promising target of multiple myeloma therapy

ABSTRACT

Introduction: The results of therapy of the multiple myeloma (MM) patients remain unsatisfactory despite the constantly observed progress in treatment.

Areas covered: It has been shown that mechanisms regulated by heat shock proteins (HSPs) play an important role in pathogenesis of MM and resistance developing to treatment, which constitute a protective shield against external damaging factors in healthy and cancerous cells.

Expert opinion: Inhibiting these mechanisms seems to be the natural way of therapy in MM patients. In vitro studies have shown promising effects in the form of an increase in the apoptosis index of MM cells exposed to HSP inhibitors. The observations are very promising in the early stages of clinical trials with HSP inhibitors, such as tanespimycin, in the relapsed/refractory MM patients. Effects were more pronounced when combined with bortezomib. It seems that enriching the range of anti-myeloma drugs with HSP inhibitors may be the next step in the future of extending life of patients with multiple myeloma.

KEYWORDS:

• Heat shock protein
• multiple myeloma
• HSP
• MM
• treatment
• bortezomib

Article highlights

• Heat shock proteins are key elements in pathogenesis and are responsible for the development of resistance to multiple myeloma treatment.

• Inhibiting these mechanisms seems to be the natural way of MM therapy.

• Results of the early phase of clinical studies with HSP inhibitors are promising, and the combination with bortezomib enhances the proapoptotic effect

• HSP inhibitors give hope for further progress in the treatment of patients with multiple myeloma.

Declaration of interest

The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

Reviewer disclosures

Peer reviewers on this manuscript have no relevant financial or other relationships to disclose.

Additional information

Funding

This paper was not funded.