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Scandion Oncology
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=== Drug-resistance mechanisms are commonly reported === Cancer drug resistance is a complicated process that can occur through a variety of underlying biological mechanisms. Exhibit 4 presents a selection of common drug resistance types seen in oncology. {| class="wikitable" |+Exhibit 4: Examples of chemotherapy resistance types<ref name=":1">Source: Edison Investment Research.</ref> !Resistance type !Underlying mechanism (example) !Effect !Common drugs affected |- |Multi-drug resistance |Up-regulation of ATP Binding Cassette membrane proteins (ABC). |Increased removal of chemotherapy from tumour cells. |Doxorubicin, vinblastine, paclitaxel, irinotecan |- |Inhibition of cell death |Down-regulation of pro-cell death proteins (eg p53). Up-regulation of anti-cell death proteins (eg Bcl-2/xl). |Increased tumour cell survival, even in the presence of toxic agents. |Cisplatin, doxorubicin |- |Altered drug metabolism |Altered activity of UGT enzymes. Increased activity of cytochrome P450 enzymes. |Increased metabolism of active agents reduces effectiveness of chemotherapy. |Docetaxel, gemcitabine, cytarabine |- |Enhanced DNA repair |Increased activity of nucleotide excision repair system and homologous recombination repair mechanisms. |Repair of damaged DNA causes increase in tumour cell survival. |Cisplatin, doxorubicin |} In addition to these mechanisms, chemotherapeutic resistance can arise due to alterations to a drugβs target, gene amplifications and epigenetic alterations. Modern approaches to overcoming resistance have focused on developing new, targeted drugs and immunotherapies (for example PD-(L)1 and CTLA4 monoclonal antibodies). However, drug resistance in chemotherapy continues to be recognised as an area of unmet medical need.
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