Ivo Stárek1, Richard Salzman2, Ladislava Kučerová3, Alena Skálová4, Lukáš Hauer5. 1. Clinic of Otorhinolaryngology, University Hospital Olomouc and Faculty of Medicine and Dentistry, Palacky University Olomouc, Olomouc, Czech Republic. 2. Clinic of Otorhinolaryngology, University Hospital Olomouc and Faculty of Medicine and Dentistry, Palacky University Olomouc, Olomouc, Czech Republic. Electronic address: richard.salzman@fnol.cz. 3. Department of Clinical and Molecular Pathology, University Hospital Olomouc and Faculty of Medicine and Dentistry, Palacky University Olomouc, Olomouc, Czech Republic. 4. Department of Pathology, Charles University in Prague, Faculty of Medicine in Pilsen, Pilsen, Czech Republic. 5. Department of Stomatology, Charles University in Prague, Faculty of Medicine in Pilsen, Pilsen, Czech Republic.
Abstract
AIMS: Some human neoplasms stimulate lymphangiogenesis through the over-production of vascular endothelial growth factors C/D (VEGF-C/D). Previously little attention has been paid to the mechanisms of lymphogenous spread of salivary adenoid cystic carcinoma (SACC). The current study investigates the presence of lymphatic network and the role of VEGF-C and VEGF-D in its formation. METHODS: The retrospective study was performed in 20 (12 females and 8 males) patients diagnosed with SACC. For the evaluation of VEGF-C/D immunoreactivity, semiquantitative histoscore was calculated as a sum of positive tumor cell score (range 0-3) and staining intensity (range 0-3). Lymphatic vessel density (LVD) was determined as the number of D2-40 positive lymphatic capillaries present at "hot spots". Moreover, the values of histoscores were calculated in surrounding normal parotid parenchyma and compared to those counted in tumors. LVD in the tumor center (iLVD), in its periphery (pLVD), and in healthy gland were identified. RESULTS: VEGF-C/D expression, iLVD and pLVD were higher in SACC than in normal gland. The VEGF-C/D score correlated neither with pLVD nor with iLVD. High iLVD values were associated with poor survival. CONCLUSIONS: The authors present the first study demonstrating the existence of lymphatic vessels in SACC.
AIMS: Some humanneoplasms stimulate lymphangiogenesis through the over-production of vascular endothelial growth factors C/D (VEGF-C/D). Previously little attention has been paid to the mechanisms of lymphogenous spread of salivary adenoid cystic carcinoma (SACC). The current study investigates the presence of lymphatic network and the role of VEGF-C and VEGF-D in its formation. METHODS: The retrospective study was performed in 20 (12 females and 8 males) patients diagnosed with SACC. For the evaluation of VEGF-C/D immunoreactivity, semiquantitative histoscore was calculated as a sum of positive tumor cell score (range 0-3) and staining intensity (range 0-3). Lymphatic vessel density (LVD) was determined as the number of D2-40 positive lymphatic capillaries present at "hot spots". Moreover, the values of histoscores were calculated in surrounding normal parotid parenchyma and compared to those counted in tumors. LVD in the tumor center (iLVD), in its periphery (pLVD), and in healthy gland were identified. RESULTS:VEGF-C/D expression, iLVD and pLVD were higher in SACC than in normal gland. The VEGF-C/D score correlated neither with pLVD nor with iLVD. High iLVD values were associated with poor survival. CONCLUSIONS: The authors present the first study demonstrating the existence of lymphatic vessels in SACC.