Background:
Chemotherapy-induced peripheral neuropathy (CIPN) is a painful condition, experienced by patients undergoing chemotherapy with some specific drugs, such as platinum-based agents, taxanes, and vinca alkaloids. Painful CIPN may lead to dose interruptions and discontinuation of chemotherapy and can negatively impact on the quality of life and clinical outcome of these patients. Due to a lack of a practical medical therapy for CIPN, it is necessary to further explore and identify novel therapeutic options.
Methods:
We have reviewed PubMed and EMBASE libraries to gather data on the mechanism-based pharmacological management of chemotherapy-induced neuropathic pain.
Result:
This review has focused on the potential mechanisms by which these chemotherapeutic agents may be involved in the development of CIPN, and explains how this may be translated into clinical management. Additionally, we have presented an overview of emerging candidates for the prevention and treatment of CIPN in preclinical and clinical studies.
Conclusion:
Taken together, due to the debilitating consequences of CIPN for the quality of life and clinical outcome of cancer survivors, future studies should focus on identifying underlying mechanisms contributing to CIPN as well as developing effective pharmacological interventions based on these mechanistic insights.
Background:
Colorectal cancer (CRC) is the third most common cause of cancer deaths, and metastasis is a major cause of mortalities. The survival rate of patients diagnosed with metastasis remains disappointing. Therefore, the prevention of tumor dissemination as well as treatment of existing metastatic lesions is an important focus of new cancer therapies. Epithelial-to-mesenchymal transition (EMT) is defined as a cellular transition from an epithelial to a mesenchymal state and determines cancer lethal characteristics consisting of invasiveness, metastasis formation, and drug resistance.
Methods:
We reviewed PubMed and EMBASE libraries to gather data about pharmacological targeting of Epithelial-to-Mesenchymal Transition in colorectal cancer to prevent the tumor metastatic distribution and improve survival of patients with CRC.
Result:
We provided an overview of the available EMT-based therapies in CRC, summarized FDA-approved and under-clinical trial drugs with EMT-inhibiting property in metastatic CRC, and described several agents preventing EMT-associated progression and metastasis in preclinical studies. Although various preclinical and clinical findings have proven that inhibiting EMT via different pharmacological approaches can reduce aggressive features of many cancers, not all agents possessing EMT-inhibiting function in preclinical research exhibit improvement in clinical studies.
Conclusion:
Combating EMT as a therapeutic intervention with the aim of preventing tumor dissemination, eliminating exiting metastasis, and promoting resistance to therapy may be a novel and effective strategy in the treatment of CRC. Our hope is that further exploration about EMT-related mechanisms and EMT-inhibiting drugs provide more opportunities for us to treat CRC efficiently.
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