Pulmonary cavitation in patients with thyroid cancer receiving antiangiogenic agents
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RESEARCH ARTICLE
Open Access
Pulmonary cavitation in patients with thyroid cancer receiving antiangiogenic agents Saumil Datar1, Maria Cabanillas2, Ramona Dadu3, David Ost3 and Horiana B. Grosu3*
Abstract Background: Thyroid malignancies are among the most common endocrine cancers worldwide. Owing to the angiogenic nature of these malignancies, tyrosine kinase inhibitors (TKIs) are an attractive potential treatment. However, TKIs have been associated with an increased risk of tumor cavitation, in turn linked to poor outcomes, in patients with malignancies in the lungs, where thyroid cancer commonly metastasizes. Method: We performe d a retrospective cohort study of patients with thyroid cancer and evidence of metastatic disease to the lung that were treated with multi-targeted antiangiogenic TKIs. The primary objective of this study was to determine the incidence of pulmonary cavitation. The secondary objective was to evaluate the effect of pulmonary cavitation on survival. Results: Of the 83 patients with pulmonary nodules, 10 developed cavitation during treatment. Of these 83 patients, two patients had to stop the treatment due to pneumothorax. Additionally, cavitation did not demonstrate any significant effect on survival. Conclusion: In patients with thyroid cancer and evidence of metastatic disease to the chest, the use of multitargeted TKIs led to cavitations that were not uncommon but clinical consequences were marginal. Treatment was stopped only in two patients that developed pneumothorax, however the small sample is a strong limitation of our study. Keywords: Thyroid malignancy, Antiangiogenic agent, Tyrosine kinase inhibitors
Background Thyroid cancer is the most common endocrine malignancy and is the ninth most common cancer overall [1]. The formation of new blood vessels, or angiogenesis, is important for tumor growth, and vascular endothelial growth factor (VEGF) has an important role in this process [2]. Thyroid tumors are highly vascular and overexpress VEGF; thus, therapy targeting VEGF receptors (VEGFRs), by which VEGF mediates its effects on * Correspondence: [email protected] 3 Department of Pulmonary Medicine, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Blvd, Houston, TX 77030, USA Full list of author information is available at the end of the article
angiogenesis, was found to be promising [3]. Another approach to blocking the VEGF pathway is preventing activation of VEGFRs using tyrosine kinase inhibitors (TKIs) [2]. Recent trials with multi-targeted TKIs have shown better survival outcomes for patients with metastatic thyroid cancer [4–8]. However, patients with lung cancer treated with antiangiogenic agents commonly develop cavitation in their lung lesions—that is, a gas-filled area in the center of a lung nodule [9–11]. Cavitation of malignant tissue may be caused by treatment-related necrosis, cyst formation, or desquamation and then liquefaction of tumor cells within the lesion [12]. In 2008, Marom et al. reported
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