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      A clinically practical radiomics-clinical combined model based on PET/CT data and nomogram predicts EGFR mutation in lung adenocarcinoma

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          Abstract

          <p class="first" id="d3459430e242">This study aims to develop a clinically practical model to predict EGFR mutation in lung adenocarcinoma patients according to radiomics signatures based on PET/CT and clinical risk factors. </p>

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          Intratumor Heterogeneity and Branched Evolution Revealed by Multiregion Sequencing

          Marco Gerlinger, Andrew J Rowan, Stuart Horswell … (2012)
          Intratumor heterogeneity may foster tumor evolution and adaptation and hinder personalized-medicine strategies that depend on results from single tumor-biopsy samples. To examine intratumor heterogeneity, we performed exome sequencing, chromosome aberration analysis, and ploidy profiling on multiple spatially separated samples obtained from primary renal carcinomas and associated metastatic sites. We characterized the consequences of intratumor heterogeneity using immunohistochemical analysis, mutation functional analysis, and profiling of messenger RNA expression. Phylogenetic reconstruction revealed branched evolutionary tumor growth, with 63 to 69% of all somatic mutations not detectable across every tumor region. Intratumor heterogeneity was observed for a mutation within an autoinhibitory domain of the mammalian target of rapamycin (mTOR) kinase, correlating with S6 and 4EBP phosphorylation in vivo and constitutive activation of mTOR kinase activity in vitro. Mutational intratumor heterogeneity was seen for multiple tumor-suppressor genes converging on loss of function; SETD2, PTEN, and KDM5C underwent multiple distinct and spatially separated inactivating mutations within a single tumor, suggesting convergent phenotypic evolution. Gene-expression signatures of good and poor prognosis were detected in different regions of the same tumor. Allelic composition and ploidy profiling analysis revealed extensive intratumor heterogeneity, with 26 of 30 tumor samples from four tumors harboring divergent allelic-imbalance profiles and with ploidy heterogeneity in two of four tumors. Intratumor heterogeneity can lead to underestimation of the tumor genomics landscape portrayed from single tumor-biopsy samples and may present major challenges to personalized-medicine and biomarker development. Intratumor heterogeneity, associated with heterogeneous protein function, may foster tumor adaptation and therapeutic failure through Darwinian selection. (Funded by the Medical Research Council and others.).
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            EGFR mutations in lung cancer: correlation with clinical response to gefitinib therapy.

            J G Páez (2004)
            Receptor tyrosine kinase genes were sequenced in non-small cell lung cancer (NSCLC) and matched normal tissue. Somatic mutations of the epidermal growth factor receptor gene EGFR were found in 15of 58 unselected tumors from Japan and 1 of 61 from the United States. Treatment with the EGFR kinase inhibitor gefitinib (Iressa) causes tumor regression in some patients with NSCLC, more frequently in Japan. EGFR mutations were found in additional lung cancer samples from U.S. patients who responded to gefitinib therapy and in a lung adenocarcinoma cell line that was hypersensitive to growth inhibition by gefitinib, but not in gefitinib-insensitive tumors or cell lines. These results suggest that EGFR mutations may predict sensitivity to gefitinib.
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              EGFR mutation and resistance of non-small-cell lung cancer to gefitinib.

              Susumu Kobayashi, Titus J. Boggon, Tajhal Dayaram … (2005)
              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.
              Article 0 comments Cited 399 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Title: European Radiology
                Abbreviated Title: Eur Radiol
                Publisher: Springer Science and Business Media LLC
                ISSN (Print): 0938-7994
                ISSN (Electronic): 1432-1084
                Publication date Created: August 2021
                Publication date (Electronic): February 05 2021
                Publication date (Print): August 2021
                Volume: 31
                Issue: 8
                Pages: 6259-6268
                Article
                DOI: 10.1007/s00330-020-07676-x
                PubMed ID: 33544167
                SO-VID: dfebbca4-104b-44b9-895a-df234d51aa04
                Copyright © © 2021
                License:

                https://www.springer.com/tdm

                https://www.springer.com/tdm

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