Abstract
Resistance of rhabdomyosarcoma to current therapies remains one of the key issues in pediatric oncology. Since the success of most cytotoxic therapies in the treatment of cancer, for example, chemotherapy, depends on intact signaling pathways that mediate programmed cell death (apoptosis), defects in apoptosis programs in cancer cells may result in resistance. Evasion of apoptosis in rhabdomyosarcoma may be caused by defects in the expression or function of critical mediators of apoptosis or in aberrant expression of antiapoptotic proteins. Therefore, the identification of the molecular mechanisms that confer primary or acquired resistance to apoptosis in rhabdomyosarcoma presents a critical step for the rational development of molecular targeted drugs. This approach will likely open novel perspectives for the treatment of rhabdomyosarcoma.
Highlights
The appropriate balance between cell growth and cell death is a critical factor to maintain tissue homeostasis in multicellular organisms [1]
Defects in apoptosis programs may confer resistance to cytotoxic therapies, since the success of many anticancer therapies that are currently used in the treatment of cancer such as chemo, radio, or immunotherapy critically depends on intact cell death pathways [5]
RMS constitutes the most frequent form of soft tissue sarcoma in childhood and comprises two major histological subtypes that are characterized by typical genetic aberrations, that is, embryonal rhabdomyosarcoma (ERMS) and alveolar rhabdomyosarcoma (ARMS) [6]
Summary
The appropriate balance between cell growth and cell death is a critical factor to maintain tissue homeostasis in multicellular organisms [1]. Apoptosis is the form of programmed cell death that is currently best characterized [4]. Defects in apoptosis programs may confer resistance to cytotoxic therapies, since the success of many anticancer therapies that are currently used in the treatment of cancer such as chemo-, radio-, or immunotherapy critically depends on intact cell death pathways [5]. This implies that a better understanding of the molecular mechanisms that control cell death pathways in cancer, for example, in rhabdomyosarcoma (RMS), will likely open novel opportunities for the development of innovative treatment strategies. The deregulation of cell death programs in RMS will be discussed as well as possibilities to target cell death pathways for therapeutic purposes
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