Imatinib mesylate in thymic epithelial malignancies

Palmieri, Giovannella; Marino, Mirella; Buonerba, Carlo; Federico, Piera; Conti, Salvatore; Milella, Michèle; Petillo, L.; Evoli, Amelia; Lalle, M; Ceribelli, Anna; Merola, G.; Matano, Elide; Sioletic, Stefano; Placido, Sabino De; Lorenzo, Giuseppe Di; Damiano, Vincenzo

doi:10.1007/s00280-011-1690-0

Cited by 43 publications

(29 citation statements)

References 23 publications

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“…Collectively, the percentage of c-kit positive cases averages 62.8% [3,[13][14][15][16]21,[26][27][28][29][30][31][32]. Contrary to the relatively high protein expression however, c-kit mutation is a rare event in thymic carcinomas (<10%) [13,14,19,21,26,28,29,31]. Among the mutation positive cases [13,14,19,26], two showed a partial response to treatment with the TKIs imatinib [26] and sorafenib [19].…”

Section: Oncogenesmentioning

confidence: 90%

Molecular aspects of thymic carcinoma

2012

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Section: Oncogenesmentioning

confidence: 90%

Molecular aspects of thymic carcinoma

2012

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“…The relevance of KIT mutations is even more limited in thymic carcinoma than in other cancers such as gastro-intestinal stromal tumour, as: 1) KIT mutations are far less frequent; 2) KIT expression does not correlate with the presence of KIT mutation; and 3) non pre-treated KIT mutants are not uniformly sensitive to imatinib, based on the clinical and/or the pre-clinical evidence in thymic carcinoma and/or other KIT-mutant tumours (table 6). These findings may explain why the two reported phase II trials with imatinib where patients were not selected [118], or were selected based upon histological type (B3 thymomas and thymic carcinomas) [119] or KIT staining by immunohistochemistry [120] and not upon KIT genotyping were negative. Multi-kinase inhibitors may also be of interest to target angiogenesis.…”

Section: Targeted Therapiesmentioning

confidence: 89%

Thymic epithelial tumours: from basic principles to individualised treatment strategies

Girard¹

2013

European Respiratory Review

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Thymic epithelial tumours represent a wide range of anatomical, clinical, histological and molecular malignant entities that may be aggressive and difficult to treat. The histopathological classification distinguishes thymomas from thymic carcinomas. Thymomas may be associated with autoimmune disorders.The management of thymic epithelial tumours is a paradigm of co-operation between clinicians, surgeons and pathologists, from establishing the diagnosis to organising the multimodal therapeutic strategy. Surgery is the mainstay of the curative-intent treatment, as complete resection represents the most significantly favourable prognostic factor on overall survival. In case of invasion of intra-thoracic structures and/or dissemination to the pleura and the pericardium, precluding complete resection to be achieved, primary chemotherapy has been used to reduce the tumour burden, possibly allowing subsequent surgery and/or radiotherapy.Novel strategies are needed, especially for refractory, recurrent tumours and thymic carcinomas, which carry a poor prognosis. Personalised approaches are currently being developed, as potentially ''druggable'' molecular targets are emerging from recent integrated genomic analyses. Along with the large variety of questions relative to the treatment strategy, thymic epithelial tumours represent a model of therapeutic implementation and achievement in orphan thoracic oncology, showing how the advent of new results induces new questions, as well as diversifies further clinical research directions and international collaborative initiatives.

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“…A study using EGFR inhibitor, Gefitinib, yields only one response in 26 patients (10) while another study using Erlotinib plus Bevacizumab showed no response (11). Three trials evaluating KIT inhibitor Imatinib in TETs (13–15) showed zero objective response. It is notable that although most tumors on these trials overexpressed KIT, no sensitizing mutation was found.…”

Section: Epidermal Growth Factor Receptor Kit and Src Inhibitorsmentioning

confidence: 99%