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Drug resistance: 2 case reports In a study of 32 patients, a 66-year-old patient and a 55-year-old patient [sexes not stated] exhibited drug resistance, while being treated with cetuximab, dabrafenib or trametinib [dosages and routes not stated]. The 66-year-old patient, with neoplasm of rectosigmoid junction tumour was found to be KRAS wildtype. Subsequently, The patient started receiving cetuximab, along with fluorouracil, folinic-acid and irinotecan (FOLFIRI). However, after 2 years, the patient exhibited resistance to cetuximab. Sequencing showed MET amplification, which was a known mechanism of resistance to cetuximab treatment. Later on, RNA expression analysis revealed 44-fold increase in MET expression, along with overexpression of AREG and EREG. The 55-year-old patient, with metastatic pancreatic cancers treated with unspecified standard chemotherapy. However, upon disease progression, the patient was sequenced, and based on presence of BRAF V600E, treatment with trametinib and dabrafenib was initiated. But, the patient exhibited resistance to dabrafenib and trametinib. Thus, following disease progression on BRAF/MEK inhibitors (dabrafenib and trametinib), metastatic sample was resequenced, and RNA expression analysis found increased expression of MET, MACC1 and SMAD7 and 4-fold decrease in PTEN, which potentially caused resistance to BRAF/MEK inhibitors. Basu GD, et al. Whole exome and transcriptome sequencing of colorectal and pancreatic cancer. Journal of Clinical Oncology 38: no pagination, No. 15, Jan 2020. Available 803503384 from: URL: http://doi.org/10.1200/JCO.2020.38.15_suppl.e15666 [abstract]

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Reactions 26 Sep 2020 No. 1823