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Nuclear survivin expression correlates with endoglin-assessed microvascularisation in laryngeal carcinoma
  1. Gino Marioni1,
  2. Giancarlo Ottaviano1,
  3. Rosario Marchese-Ragona1,
  4. Elena Fasanaro2,
  5. Giulia Tealdo1,
  6. Claudia Zanotti1,
  7. Benedetto Randon1,
  8. Luciano Giacomelli3,
  9. Edoardo Stellini4,
  10. Stella Blandamura3
  1. 1 Department of Neurosciences DNS, Otolaryngology Section, University of Padova, Padova, Italy
  2. 2 Department of Radiotherapy, Veneto Institute of Oncology, IOV-IRCCS, Padova, Italy
  3. 3 Department of Medicine DIMED, University of Padova, Italy
  4. 4 Department of Neurosciences DNS, Odontostomatology Institute, University of Padova, Padova, Italy
  1. Correspondence to Professor Gino Marioni, Department of Neurosciences DNS, Otolaryngology Section, University of Padova, Via Giustiniani 2, 35128 Padova, Italy; gino.marioni{at}


Aims Survivin—a member of the family of inhibitor of apoptosis proteins that control cell division, apoptosis and metastasis—is overexpressed in virtually all human cancers, including laryngeal squamous cell carcinoma (LSCC). Recent findings also correlate survivin expression with the regulation of angiogenesis. The novel main aim of this study was a preliminary investigation into the potential role of survivin expression in LSCC neoangiogenesis, as determined by endoglin-assessed microvascular density (MVD).

Methods Immunohistochemical expression of nuclear survivin and endoglin-assessed MVD were ascertained by image analysis in 75 consecutive LSCCs.

Results Statistical analysis disclosed a strong direct correlation between nuclear survivin expression and MVD. Patients whose nuclear survivin expression was ≥6.0% had a significantly higher LSCC recurrence rate, and a significantly shorter disease-free survival (DFS) than those with a nuclear survivin expression <6.0%. The LSCC recurrence rate was also higher and the DFS shorter in patients with endoglin-assessed MVD ≥6.89%. The OR for recurrence was 2.79 in patients with LSCC with a nuclear survivin expression ≥6.0%, and 12.31 in those with an MVD≥6.89%.

Conclusions Survivin-targeting strategies to enhance tumour cell response to apoptosis and inhibit tumour growth should receive more attention with a view to developing agents for use in multimodality advanced LSCC treatment, or combined with conventional chemotherapy. Given the present preliminary evidence in LSCC, survivin targeting should also be further investigated for anti-angiogenic purposes, to reduce tumour blood flow and induce cancer necrosis.


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  • Handling editor Tahir Pillay.

  • Contributors All authors have contributed sufficiently, read and approved the manuscript and its submission to JCP.

  • Funding This study was partly supported by grant No. 60A070199/14 (G. Marioni) from the University of Padova, Italy.

  • Competing interests None declared.

  • Ethics approval The study was approved by our Otolaryngology Section's in-house ethical committee.

  • Provenance and peer review Not commissioned; externally peer reviewed.