{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,19]],"date-time":"2026-06-19T16:25:32Z","timestamp":1781886332170,"version":"3.54.5"},"reference-count":145,"publisher":"American Society of Clinical Oncology (ASCO)","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Am Soc Clin Oncol Educ Book"],"published-print":{"date-parts":[[2025,6]]},"abstract":"<jats:p>\n            In cancer genomics, there is the realization that some very frequently mutated genes like\n            <jats:italic toggle=\"yes\">TP53<\/jats:italic>\n            or\n            <jats:italic toggle=\"yes\">KRAS<\/jats:italic>\n            are extremely hard to approach from a therapeutic perspective. In the realm of cancer treatment, the development of agents capable of transforming these alterations into actionable targets would be like capturing unicorns. These unicorns of oncology\u2014drugs targeting undruggable targets that span various cancer types\u2014offer an exciting opportunity for the development of histology-agnostic therapies. Among these, recent developments in targeting\n            <jats:italic toggle=\"yes\">TP53<\/jats:italic>\n            mutations,\n            <jats:italic toggle=\"yes\">KRAS<\/jats:italic>\n            alterations, and\n            <jats:italic toggle=\"yes\">MTAP<\/jats:italic>\n            loss mark pivotal advancements for innovative treatment strategies.\n            <jats:italic toggle=\"yes\">TP53<\/jats:italic>\n            mutations, which occur in nearly every cancer type, are central to tumorigenesis and contribute to resistance against conventional therapies.\n            <jats:italic toggle=\"yes\">KRAS<\/jats:italic>\n            mutations, especially in cancers like pancreatic and lung cancers, are notoriously difficult to target but are now yielding promising therapeutic avenues. Similarly,\n            <jats:italic toggle=\"yes\">MTAP<\/jats:italic>\n            is frequently deleted in cancers such as lung, pancreatic, and mesothelioma and plays a critical role in cellular metabolism and epigenetics, making its loss a significant vulnerability in tumor cells. Recent developments in drug discovery provide a broad foundation for the clinical testing of drugs that target common mechanisms across diverse tumor types, offering hope for a more universal approach to cancer treatment.\n          <\/jats:p>","DOI":"10.1200\/edbk-25-473616","type":"journal-article","created":{"date-parts":[[2025,5,28]],"date-time":"2025-05-28T21:05:50Z","timestamp":1748466350000},"source":"Crossref","is-referenced-by-count":4,"title":["Capturing Unicorns: Targeting Cancers With\n            <i>TP53<\/i>\n            Mutations,\n            <i>RAS<\/i>\n            Alterations Beyond G12C, and\n            <i>MTAP<\/i>\n            Loss\u2014No Target Is Out of the Realm of Possibility"],"prefix":"10.1200","volume":"45","author":[{"given":"Pooja A.","family":"Shah","sequence":"first","affiliation":[{"name":"Department of Investigational Cancer Therapeutics, The University of Texas MD Anderson Cancer Center, Houston, TX"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Klas G.","family":"Wiman","sequence":"additional","affiliation":[{"name":"Department of Oncology-Pathology, Karolinska Institutet, Stockholm, Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Karen","family":"Cichowski","sequence":"additional","affiliation":[{"name":"Division of Genetics, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA"},{"name":"Ludwig Center at Harvard, Boston, MA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6467-3632","authenticated-orcid":true,"given":"Jordi","family":"Rodon Ahnert","sequence":"additional","affiliation":[{"name":"Department of Investigational Cancer Therapeutics, The University of Texas MD Anderson Cancer Center, Houston, TX"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"233","reference":[{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1038\/278261a0"},{"key":"e_1_3_3_3_2","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(79)90293-9"},{"key":"e_1_3_3_4_2","doi-asserted-by":"publisher","DOI":"10.1128\/jvi.31.2.472-483.1979"},{"key":"e_1_3_3_5_2","doi-asserted-by":"publisher","DOI":"10.1128\/jvi.31.2.463-471.1979"},{"key":"e_1_3_3_6_2","doi-asserted-by":"publisher","DOI":"10.1016\/0092-8674(89)90045-7"},{"key":"e_1_3_3_7_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.86.22.8763"},{"key":"e_1_3_3_8_2","doi-asserted-by":"publisher","DOI":"10.1038\/342705a0"},{"key":"e_1_3_3_9_2","doi-asserted-by":"publisher","DOI":"10.1126\/science.2649981"},{"key":"e_1_3_3_10_2","doi-asserted-by":"publisher","DOI":"10.1038\/356215a0"},{"key":"e_1_3_3_11_2","doi-asserted-by":"publisher","DOI":"10.1038\/352345a0"},{"key":"e_1_3_3_12_2","first-page":"1689","article-title":"UV irradiation stimulates levels of P53 cellular tumor-antigen in nontransformed mouse cells","volume":"4","author":"Maltzman W","year":"1984","unstructured":"Maltzman W, Czyzyk L: UV irradiation stimulates levels of P53 cellular tumor-antigen in nontransformed mouse cells. 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