Considering the need to treat advanced TC more effectively, disparate findings in predictive molecular markers (eg, KIT mutations in TSCC, but not in thymomas) suggest that targeted treatments will have to be different in thymomas and TC.
Apart from their different morphology, TC and thymomas differ also in functional terms (TC, in contrast to thymomas, have lost the capacity to promote the maturation of intratumorous lymphocytes), have different genetic features (discussed in this review), a different immunoprofile (most TC overexpress c-KIT, whereas thymomas are consistently negative), and different clinical features (TC, in contrast to thymomas, are not associated with paraneoplastic myasthenia gravis).
Imatinib upregulates compensatory integrin signaling in a mouse model of gastrointestinal stromal tumor and is more effective when combined with dasatinib.
In summary, COX-2 is expressed in all subtypes of thymomas and thymic carcinomas and thus represents, in addition to EGFR and KIT, a potential therapeutic target.
Association of KIT exon 9 mutations with nongastric primary site and aggressive behavior: KIT mutation analysis and clinical correlates of 120 gastrointestinal stromal tumors.