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  <titleInfo>
    <title>Advances in RAS therapeutics for pancreatic cancer</title>
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  <name type="personal">
    <namePart>Der, Channing J.</namePart>
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    <role>
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  <name type="personal">
    <namePart>Yeh, Jen Jen</namePart>
  </name>
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    <extent>páginas: 1857-1861</extent>
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  <abstract>Somatic mutations in the Kirsten rat sarcoma viral oncogene homologue (KRAS) occur in more than 90% of pancreatic ductal adenocarcinomas. In this issue of the Journal, Wolpin et al. evaluated the side-effect profile of and response to a first-in-class small-molecule drug called daraxonrasib, which targets the active state of RAS (see Key Concepts) in patients with metastatic pancreatic ductal adenocarcinoma who have received at least one previous line of chemotherapy. In the context of second-line treatment, they reported an objective response according to the Response Evaluation Criteria in Solid Tumors (RECIST), version 1.1, in up to 35% of patients and a median response duration of 8.2 months.</abstract>
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    <topic>CÁNCER</topic>
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    <topic>CÁNCER DEL TRACTO GASTROINTESTINAL</topic>
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    <topic>GASTROENTEROLOGÍA</topic>
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  <subject>
    <topic>HEMATOLOGÍA</topic>
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  <subject>
    <topic>ONCOLOGÍA</topic>
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  <subject>
    <topic>GENÉTICA GENERAL</topic>
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      <title>The New England Journal of Medicine</title>
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      <publisher>Massachusetts NEJM Group</publisher>
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    <identifier>NEJM015</identifier>
    <identifier type="issn">0028-4793</identifier>
    <identifier type="local">ESSALUD</identifier>
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