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      Long-lasting response to afatinib that persisted after treatment discontinuation in a case of EGFR-mutated lung adenocarcinoma

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          Abstract

          It is unknown whether tyrosine kinase inhibitors targeting epidermal growth factor receptor (EGFR) can be discontinued in patients in whom EGFR-mutated lung cancer has well stabilised. We present a case of a 73-year-old Japanese woman with no history of smoking. Right pulmonary lower lobectomy, lymph node dissection and segmental resection of the right middle lobe were performed. Additionally, she underwent adjuvant chemotherapy for stage IIIB adenocarcinoma harbouring an EGFR exon 19 deletion. Afatinib was administered for liver metastases after 15 months. A complete response of metastatic disease was achieved for 2 years. However, afatinib was unavoidably discontinued due to splenectomy for the treatment of idiopathic thrombocytopenic purpura. Although afatinib was not resumed, due to the abscess formation as surgery complication, a drug-free complete response was sustained for over 18 months. The present case suggests that exceptional and durable responses to afatinib can be achieved in individual cases.

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          Most cited references 27

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          Untangling the ErbB signalling network.

          When epidermal growth factor and its relatives bind the ErbB family of receptors, they trigger a rich network of signalling pathways, culminating in responses ranging from cell division to death, motility to adhesion. The network is often dysregulated in cancer and lends credence to the mantra that molecular understanding yields clinical benefit: over 25,000 women with breast cancer have now been treated with trastuzumab (Herceptin), a recombinant antibody designed to block the receptor ErbB2. Likewise, small-molecule enzyme inhibitors and monoclonal antibodies to ErbB1 are in advanced phases of clinical testing. What can this pathway teach us about translating basic science into clinical use?
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            EGFR mutation and resistance of non-small-cell lung cancer to gefitinib.

            Mutations of the epidermal growth factor receptor (EGFR) gene have been identified in specimens from patients with non-small-cell lung cancer who have a response to anilinoquinazoline EGFR inhibitors. Despite the dramatic responses to such inhibitors, most patients ultimately have a relapse. The mechanism of the drug resistance is unknown. Here we report the case of a patient with EGFR-mutant, gefitinib-responsive, advanced non-small-cell lung cancer who had a relapse after two years of complete remission during treatment with gefitinib. The DNA sequence of the EGFR gene in his tumor biopsy specimen at relapse revealed the presence of a second point mutation, resulting in threonine-to-methionine amino acid change at position 790 of EGFR. Structural modeling and biochemical studies showed that this second mutation led to gefitinib resistance. Copyright 2005 Massachusetts Medical Society.
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              Circulating mutant DNA to assess tumor dynamics.

              The measurement of circulating nucleic acids has transformed the management of chronic viral infections such as HIV. The development of analogous markers for individuals with cancer could similarly enhance the management of their disease. DNA containing somatic mutations is highly tumor specific and thus, in theory, can provide optimum markers. However, the number of circulating mutant gene fragments is small compared to the number of normal circulating DNA fragments, making it difficult to detect and quantify them with the sensitivity required for meaningful clinical use. In this study, we applied a highly sensitive approach to quantify circulating tumor DNA (ctDNA) in 162 plasma samples from 18 subjects undergoing multimodality therapy for colorectal cancer. We found that ctDNA measurements could be used to reliably monitor tumor dynamics in subjects with cancer who were undergoing surgery or chemotherapy. We suggest that this personalized genetic approach could be generally applied to individuals with other types of cancer.
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                Author and article information

                Journal
                BMJ Case Rep
                BMJ Case Rep
                bmjcr
                bmjcasereports
                BMJ Case Reports
                BMJ Publishing Group (BMA House, Tavistock Square, London, WC1H 9JR )
                1757-790X
                2019
                31 January 2019
                31 January 2019
                : 12
                : 1
                Affiliations
                [1 ] departmentDivision of Respirology, Department of Internal Medicine , The Jikei Daisan Hospital , Tokyo, Japan
                [2 ] departmentDivision of Respirology, Department of Internal Medicine , The Jikei University Hospital , Tokyo, Japan
                Author notes
                [Correspondence to ] Dr Yoshitaka Seki, ms97-seki@ 123456jikei.ac.jp
                bcr-2018-227383
                10.1136/bcr-2018-227383
                6357919
                30709831
                © BMJ Publishing Group Limited 2019. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.

                This is an open access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/

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                Categories
                Unexpected Outcome (Positive or Negative) Including Adverse Drug Reactions
                1506
                Case Report
                Custom metadata
                unlocked

                chemotherapy, oncology, lung cancer (oncology)

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