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Possibilities and substantiation of re‑treatment with anti‑EGFR drugs for pre‑treated RAS wild‑type advanced colorectal cancers

03/2021 MUDr. Zdeněk Linke
Initial failure of epidermal growth factor receptor (EGFR) inhibitor therapy in advanced RAS wild-type (wt) colorectal cancers may not necessarily mean its permanent and definitive ineffectiveness. It is possible to re-apply anti-EGFR treatment after previous disease progression (rechallenge), or after a previous interruption for reasons other than progression (reintroduction), or sequence, resp. rotation between two different EGFR blockers (sequence) or an attempt to overcome the resistance of anti-EGFR treatment by increasing its dose (escalation) or the possibility of continuous EGFR blockade. Clinical data are available to demonstrate that, especially after discontinuation of primary anti-EGFR therapy and subsequent differential therapy, sensitivity to this therapy does return. This is by changing the proportion of EGFR positive RAS wt tumor cells. This occurs during another, intervening therapy, which is based on an effect different from EGFR blockade. However, a prerequisite for the effect of reintroduced anti-EGFR treatment is its effectiveness during its previous, primary application.
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Current treatment options for gastrointestinal stromal tumor

05/2017 MUDr. Zdeněk Linke
Gastrointestinal stromal tumor was one of the first solid tumors, where previous palliative treatment with chemotherapy was completely replaced by biological treatment. Imatinib mesylate was significant turning point for patients, imatinib against previous treatments significantly prolonged survival in metastatic gastrointestinal stromal tumor cases and reduced recurrence rates and prolonged survival in patients following radical resections of risk groups of patients with gastrointestinal stromal tumors. After imatinib failure, preparations such as sunitinib and regorafenib are available. In recent years, new molecules for gastrointestinal stromal tumors treatment are under research and the dependence of therapy effect on c-Kit receptor mutation status and the serum concentration of imatinib is being investigated.
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